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Laganà A, Visalli G, Di Pietro A, Facciolà A. Vaccinomics and adversomics: key elements for a personalized vaccinology. Clin Exp Vaccine Res 2024; 13:105-120. [PMID: 38752004 PMCID: PMC11091437 DOI: 10.7774/cevr.2024.13.2.105] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/14/2023] [Revised: 02/07/2024] [Accepted: 03/12/2024] [Indexed: 05/18/2024] Open
Abstract
Vaccines are one of the most important and effective tools in the prevention of infectious diseases and research about all the aspects of vaccinology are essential to increase the number of available vaccines more and more safe and effective. Despite the unquestionable value of vaccinations, vaccine hesitancy has spread worldwide compromising the success of vaccinations. Currently, the main purpose of vaccination campaigns is the immunization of whole populations with the same vaccine formulations and schedules for all individuals. A personalized vaccinology approach could improve modern vaccinology counteracting vaccine hesitancy and giving great benefits for human health. This ambitious purpose would be possible by facing and deepening the areas of vaccinomics and adversomics, two innovative areas of study investigating the role of a series of variables able to influence the immune response to vaccinations and the development of serious side effects, respectively. We reviewed the recent scientific knowledge about these innovative sciences focusing on genetic and non-genetic basis involved in the individual response to vaccines in terms of both immune response and side effects.
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Affiliation(s)
- Antonio Laganà
- Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, Messina, Italy
- Istituto Clinico Polispecialistico C.O.T., Cure Ortopediche Traumatologiche S.P.A., Messina, Italy
| | - Giuseppa Visalli
- Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, Messina, Italy
| | - Angela Di Pietro
- Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, Messina, Italy
| | - Alessio Facciolà
- Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, Messina, Italy
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Wang M, Gu H, Zhai Y, Li X, Huang L, Li H, Xie Z, Wen C. Vaccination and the risk of systemic lupus erythematosus: a meta-analysis of observational studies. Arthritis Res Ther 2024; 26:60. [PMID: 38433222 PMCID: PMC10910799 DOI: 10.1186/s13075-024-03296-8] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/03/2024] [Accepted: 02/26/2024] [Indexed: 03/05/2024] Open
Abstract
OBJECTIVE This meta-analysis aims to explore the potential link between vaccines and systemic lupus erythematosus (SLE). METHODS We systematically searched PubMed, Cochrane Library, and Embase for observational studies from inception to September 3, 2023, using medical subject headings (MeSH) and keywords. Study quality was assessed using the NOS scale. Statistical analyses were conducted using STATA software (version 14.0). Publication bias was evaluated using funnel plots and Egger's regression. RESULTS The meta-analysis incorporated 17 studies, encompassing 45,067,349 individuals with follow-up periods ranging from 0.5 to 2 years. The pooled analysis revealed no significant association between vaccinations and an increased risk of SLE [OR = 1.14, 95% CI (0.86-1.52), I2 = 78.1%, P = 0.348]. Subgroup analyses indicated that HBV vaccination was significantly associated with an elevated risk of SLE [OR =2.11, 95% CI (1.11-4.00), I2 = 63.3%, P = 0.02], HPV vaccination was slightly associated with an increased risk of SLE [OR = 1.43, 95% CI (0.88-2.31), I2 = 72.4%, P = 0.148], influenza vaccination showed no association with an increased risk of SLE [OR = 0.96, 95% CI (0.82-1.12), I2 = 0.0%, P = 0.559], and COVID-19 vaccine was marginally associated with a decreased risk of SLE [OR = 0.44, 95% CI (0.18-1.21), I2 = 91.3%, P = 0.118]. CONCLUSIONS This study suggests that vaccinations are not linked to an increased risk of SLE. Our meta-analysis results provide valuable insights, alleviating concerns about SLE risk post-vaccination and supporting further vaccine development efforts.
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Affiliation(s)
- Meijiao Wang
- Research Institute of Chinese Medicine Clinical Foundation and Immunology, School of Basic Medicine Sciences, Zhejiang Chinese Medical University, Binwen Road, Binjiang Dsitrict, Hangzhou, China
| | - Huanpeng Gu
- Research Institute of Chinese Medicine Clinical Foundation and Immunology, School of Basic Medicine Sciences, Zhejiang Chinese Medical University, Binwen Road, Binjiang Dsitrict, Hangzhou, China
| | - Yingqi Zhai
- Research Institute of Chinese Medicine Clinical Foundation and Immunology, School of Basic Medicine Sciences, Zhejiang Chinese Medical University, Binwen Road, Binjiang Dsitrict, Hangzhou, China
| | - Xuanlin Li
- Research Institute of Chinese Medicine Clinical Foundation and Immunology, School of Basic Medicine Sciences, Zhejiang Chinese Medical University, Binwen Road, Binjiang Dsitrict, Hangzhou, China
| | - Lin Huang
- Research Institute of Chinese Medicine Clinical Foundation and Immunology, School of Basic Medicine Sciences, Zhejiang Chinese Medical University, Binwen Road, Binjiang Dsitrict, Hangzhou, China
| | - Haichang Li
- Research Institute of Chinese Medicine Clinical Foundation and Immunology, School of Basic Medicine Sciences, Zhejiang Chinese Medical University, Binwen Road, Binjiang Dsitrict, Hangzhou, China
| | - Zhijun Xie
- Research Institute of Chinese Medicine Clinical Foundation and Immunology, School of Basic Medicine Sciences, Zhejiang Chinese Medical University, Binwen Road, Binjiang Dsitrict, Hangzhou, China.
| | - Chengping Wen
- Research Institute of Chinese Medicine Clinical Foundation and Immunology, School of Basic Medicine Sciences, Zhejiang Chinese Medical University, Binwen Road, Binjiang Dsitrict, Hangzhou, China.
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Moriyama M, Noda K, Ito H, Matsushita T, Kurosaka D. Clinical features of newly diagnosed systemic lupus erythematosus after SARS-CoV-2 vaccination. Mod Rheumatol Case Rep 2023; 8:63-68. [PMID: 37348045 DOI: 10.1093/mrcr/rxad036] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/21/2023] [Revised: 06/05/2023] [Accepted: 06/13/2023] [Indexed: 06/24/2023]
Abstract
Systemic lupus erythematosus (SLE) is an autoimmune disease that causes damage to multiple organs. Various factors, including vaccination, have been associated with SLE development. Vaccination for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) began in 2020, and there are a few reports on the exacerbation of SLE after SARS-CoV-2 vaccination. The influence of SARS-CoV-2 vaccination on SLE development remains unclear. We present the case of a 53-year-old man who developed peritonitis and was subsequently diagnosed with SLE on Day 9 after receiving a third dose of the messenger ribonucleic acid-1273 SARS-CoV-2 vaccine. This case and previous reports have shown that patients who developed SLE after SARS-CoV-2 vaccination are more likely to develop it within 2 weeks of vaccination, especially when they have a higher rate of immunological abnormalities or a family history of autoimmune diseases. Furthermore, these features suggest that type I interferon is involved in the pathogenesis of SLE after SARS-CoV-2 vaccination.
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Affiliation(s)
- Masayori Moriyama
- Division of Rheumatology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan
| | - Kentaro Noda
- Division of Rheumatology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan
| | - Haruyasu Ito
- Division of Rheumatology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan
| | - Takayuki Matsushita
- Division of Rheumatology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan
| | - Daitaro Kurosaka
- Division of Rheumatology, Department of Internal Medicine, The Jikei University School of Medicine, Tokyo, Japan
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Omersel J, Karas Kuželički N. Vaccinomics and Adversomics in the Era of Precision Medicine: A Review Based on HBV, MMR, HPV, and COVID-19 Vaccines. J Clin Med 2020; 9:E3561. [PMID: 33167413 PMCID: PMC7694388 DOI: 10.3390/jcm9113561] [Citation(s) in RCA: 18] [Impact Index Per Article: 3.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/25/2020] [Revised: 10/31/2020] [Accepted: 11/02/2020] [Indexed: 02/06/2023] Open
Abstract
Precision medicine approaches based on pharmacogenomics are now being successfully implemented to enable physicians to predict more efficient treatments and prevention strategies for a given disease based on the genetic background of the patient. This approach has already been proposed for vaccines, but research is lagging behind the needs of society, and precision medicine is far from being implemented here. While vaccinomics concerns the effectiveness of vaccines, adversomics concerns their side effects. This area has great potential to address public concerns about vaccine safety and to promote increased public confidence, higher vaccination rates, and fewer serious adverse events in genetically predisposed individuals. The aim here is to explore the contemporary scientific literature related to the vaccinomic and adversomic aspects of the three most-controversial vaccines: those against hepatitis B, against measles, mumps, and rubella, and against human Papilloma virus. We provide detailed information on the genes that encode human leukocyte antigen, cytokines and their receptors, and transcription factors and regulators associated with the efficacy and safety of the Hepatitis B and Measles, Mumps and Rubella virus vaccines. We also investigate the future prospects of vaccinomics and adversomics of a COVID-19 vaccine, which might represent the fastest development of a vaccine ever.
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Affiliation(s)
| | - Nataša Karas Kuželički
- Faculty of Pharmacy, University of Ljubljana, Aškerčeva cesta 7, 1000 Ljubljana, Slovenia;
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Kaminski ZJ, Relich I, Konieczna I, Kaca W, Kolesinska B. Cross-Reactivity of Polyclonal Antibodies againstCanavalia ensiformis(Jack Bean) Urease andHelicobacter pyloriUrease Subunit A Fragments. Chem Biodivers 2017; 15. [DOI: 10.1002/cbdv.201700444] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/25/2017] [Accepted: 11/16/2017] [Indexed: 12/28/2022]
Affiliation(s)
- Zbigniew Jerzy Kaminski
- Institute of Organic Chemistry; Lodz University of Technology; Zeromskiego 116 94-050 Lodz Poland
| | - Inga Relich
- Institute of Organic Chemistry; Lodz University of Technology; Zeromskiego 116 94-050 Lodz Poland
| | - Iwona Konieczna
- Department of Microbiology; Jan Kochanowski University; Swietokrzyska 11 25-406 Kielce Poland
| | - Wieslaw Kaca
- Department of Microbiology; Jan Kochanowski University; Swietokrzyska 11 25-406 Kielce Poland
| | - Beata Kolesinska
- Institute of Organic Chemistry; Lodz University of Technology; Zeromskiego 116 94-050 Lodz Poland
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Vaccinations and risk of systemic lupus erythematosus and rheumatoid arthritis: A systematic review and meta-analysis. Autoimmun Rev 2017; 16:756-765. [PMID: 28483543 DOI: 10.1016/j.autrev.2017.05.012] [Citation(s) in RCA: 27] [Impact Index Per Article: 3.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/19/2017] [Accepted: 04/23/2017] [Indexed: 12/21/2022]
Abstract
BACKGROUND In the past several years, more and more studies proposed some concerns on the possibly increased risk of autoimmune diseases in individuals receiving vaccinations, but published studies on the associations of vaccinations with risks of systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) reported conflicting findings. A systematic review and meta-analysis was carried out to comprehensively evaluate the relationship between vaccinations and risk of SLE and RA. METHODS Pubmed, Web of Science and Embase were searched for observational studies assessing the associations of vaccinations with risks of RA and SLE. Two authors independently extracted data from those eligible studies. The quality of eligible studies was assessed by using the Newcastle-Ottawa Scale (NOS). The pooled relative risk (RR) with 95% confidence intervals (CIs) was used to measure the risk of RA and SLE associated with vaccinations, and was calculated through random-effect meta-analysis. RESULTS Sixteen observational studies were finally considered eligible, including 12 studies on the association between vaccinations and SLE risk and 13 studies on the association between vaccinations and RA risk. The pooled findings suggested that vaccinations significantly increased risk of SLE (RR=1.50; 95%CI 1.05-2.12, P=0.02). In addition, there was an obvious association between vaccinations and increased risk of RA (RR=1.32; 95%CI 1.09-1.60, P=0.004). Meta-analysis of studies reporting outcomes of short vaccinated time also suggested that vaccinations could significantly increase risk of SLE (RR=1.93; 95%CI 1.07-3.48, P=0.028) and RA (RR=1.48; 95%CI 1.08-2.03, P=0.015). Sensitivity analyses in studies with low risk of bias also found obvious associations of vaccinations with increased risk of RA and SLE. CONCLUSION This study suggests that vaccinations are related to increased risks of SLE and RA. More and larger observational studies are needed to further verify the findings above and to assess the associations of vaccinations with other rheumatic diseases.
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Batista-Duharte A, Portuondo D, Pérez O, Carlos IZ. Systemic immunotoxicity reactions induced by adjuvanted vaccines. Int Immunopharmacol 2014; 20:170-80. [DOI: 10.1016/j.intimp.2014.02.033] [Citation(s) in RCA: 23] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/06/2013] [Revised: 02/04/2014] [Accepted: 02/21/2014] [Indexed: 02/08/2023]
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Abstract
We recently introduced the concept of the infectome as a means of studying all infectious factors which contribute to the development of autoimmune disease. It forms the infectious part of the exposome, which collates all environmental factors contributing to the development of disease and studies the sum total of burden which leads to the loss of adaptive mechanisms in the body. These studies complement genome-wide association studies, which establish the genetic predisposition to disease. The infectome is a component which spans the whole life and may begin at the earliest stages right up to the time when the first symptoms manifest, and may thus contribute to the understanding of the pathogenesis of autoimmunity at the prodromal/asymptomatic stages. We provide practical examples and research tools as to how we can investigate disease-specific infectomes, using laboratory approaches employed from projects studying the “immunome” and “microbiome”. It is envisioned that an understanding of the infectome and the environmental factors that affect it will allow for earlier patient-specific intervention by clinicians, through the possible treatment of infectious agents as well as other compounding factors, and hence slowing or preventing disease development.
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Smyk DS, Koutsoumpas AL, Mytilinaiou MG, Rigopoulou EI, Sakkas LI, Bogdanos DP. Helicobacter pylori and autoimmune disease: Cause or bystander. World J Gastroenterol 2014; 20:613-629. [PMID: 24574735 PMCID: PMC3921471 DOI: 10.3748/wjg.v20.i3.613] [Citation(s) in RCA: 109] [Impact Index Per Article: 9.9] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/30/2013] [Revised: 11/26/2013] [Accepted: 12/06/2013] [Indexed: 02/06/2023] Open
Abstract
Helicobacter pylori (H. pylori) is the main cause of chronic gastritis and a major risk factor for gastric cancer. This pathogen has also been considered a potential trigger of gastric autoimmunity, and in particular of autoimmune gastritis. However, a considerable number of reports have attempted to link H. pylori infection with the development of extra-gastrointestinal autoimmune disorders, affecting organs not immediately relevant to the stomach. This review discusses the current evidence in support or against the role of H. pylori as a potential trigger of autoimmune rheumatic and skin diseases, as well as organ specific autoimmune diseases. We discuss epidemiological, serological, immunological and experimental evidence associating this pathogen with autoimmune diseases. Although over one hundred autoimmune diseases have been investigated in relation to H. pylori, we discuss a select number of papers with a larger literature base, and include Sjögrens syndrome, rheumatoid arthritis, systemic lupus erythematosus, vasculitides, autoimmune skin conditions, idiopathic thrombocytopenic purpura, autoimmune thyroid disease, multiple sclerosis, neuromyelitis optica and autoimmune liver diseases. Specific mention is given to those studies reporting an association of anti-H. pylori antibodies with the presence of autoimmune disease-specific clinical parameters, as well as those failing to find such associations. We also provide helpful hints for future research.
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Abstract
New vaccines in infants are generally well tolerated and serious adverse events are rare. We present a patient who developed severe sensorimotor polyneuropathy 2 weeks after the first immunization with hexavalent routine vaccine (INFANRIX hexa). Through intense physiotherapy the infant made a complete recovery.
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Affiliation(s)
- Daiva Gorczyca
- From the Third Department and Clinic of Paediatrics, Immunology and Rheumatology of Developmental Age, Wroclaw Medical University , Poland
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11
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Bogdanos DP, Smyk DS, Invernizzi P, Rigopoulou EI, Blank M, Pouria S, Shoenfeld Y. Infectome: a platform to trace infectious triggers of autoimmunity. Autoimmun Rev 2012; 12:726-40. [PMID: 23266520 PMCID: PMC7105216 DOI: 10.1016/j.autrev.2012.12.005] [Citation(s) in RCA: 67] [Impact Index Per Article: 5.2] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/25/2012] [Accepted: 12/12/2012] [Indexed: 02/06/2023]
Abstract
The "exposome" is a term recently used to describe all environmental factors, both exogenous and endogenous, which we are exposed to in a lifetime. It represents an important tool in the study of autoimmunity, complementing classical immunological research tools and cutting-edge genome wide association studies (GWAS). Recently, environmental wide association studies (EWAS) investigated the effect of environment in the development of diseases. Environmental triggers are largely subdivided into infectious and non-infectious agents. In this review, we introduce the concept of the "infectome", which is the part of the exposome referring to the collection of an individual's exposures to infectious agents. The infectome directly relates to geoepidemiological, serological and molecular evidence of the co-occurrence of several infectious agents associated with autoimmune diseases that may provide hints for the triggering factors responsible for the pathogenesis of autoimmunity. We discuss the implications that the investigation of the infectome may have for the understanding of microbial/host interactions in autoimmune diseases with long, pre-clinical phases. It may also contribute to the concept of the human body as a superorganism where the microbiome is part of the whole organism, as can be seen with mitochondria which existed as microbes prior to becoming organelles in eukaryotic cells of multicellular organisms over time. A similar argument can now be made in regard to normal intestinal flora, living in symbiosis within the host. We also provide practical examples as to how we can characterise and measure the totality of a disease-specific infectome, based on the experimental approaches employed from the "immunome" and "microbiome" projects.
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Affiliation(s)
- Dimitrios P Bogdanos
- Institute of Liver Studies, King's College London School of Medicine at King's College Hospital, Denmark Hill Campus, London, UK.
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12
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Sagi L, Baum S, Agmon-Levin N, Sherer Y, Katz BSP, Barzilai O, Ram M, Bizzaro N, SanMarco M, Trau H, Shoenfeld Y. Autoimmune bullous diseases the spectrum of infectious agent antibodies and review of the literature. Autoimmun Rev 2011; 10:527-35. [PMID: 21527361 DOI: 10.1016/j.autrev.2011.04.003] [Citation(s) in RCA: 57] [Impact Index Per Article: 4.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/29/2011] [Accepted: 04/05/2011] [Indexed: 12/14/2022]
Abstract
Pemphigus and bullous pemphigoid are two autoimmune diseases that have a similar pathogenesis. Both have a genetic predisposition which promotes the production of auto-antibodies targeted against different components of the epidermal desmosome and hemidesmosome. Environmental factors play an important role in the pathogenesis of this autoimmune disease. Among these, the role of infectious agents was debated as a causative factor. We sought to determine a possible connection between various infectious agents and autoimmune bullous disease (ABD). A cohort of 148 serum samples of patients with pemphigus, bullous pemphigoid and controls was screened for evidence of a prior infection with HBV, HCV, EBV, CMV, Helicobacter pylori, Toxoplasma gondii and Treponema pallidum, utilizing the Bio-Rad BioPlex 2200 system as well as ELISA assays to complete the panel. HBV, HCV, H. pylori, T. gondii and CMV were demonstrated to have significantly higher prevalence of antibodies in patients with pemphigus and bullous pemphigoid in comparison to controls. Among them, we found a novel association between H. pylori and ABD. Our study suggests a contributing role for HBV, HCV, H. pylori, T. gondii and CMV in inducing ABD in the genetically susceptible host.
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Affiliation(s)
- Lior Sagi
- Department of Dermatology, Sheba Medical Center, Tel Hashomer, Israel
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Koenig HC, Sutherland A, Izurieta HS, McGonagle D. Application of the immunological disease continuum to study autoimmune and other inflammatory events after vaccination. Vaccine 2010; 29:913-9. [PMID: 21036134 DOI: 10.1016/j.vaccine.2010.10.044] [Citation(s) in RCA: 16] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/23/2010] [Revised: 10/05/2010] [Accepted: 10/18/2010] [Indexed: 11/29/2022]
Abstract
In vaccine safety monitoring, the evaluation of possible autoimmune events is challenging. Developing grouping systems based on pathophysiology, instead of organ systems, may enhance our ability to identify or verify associations between vaccines and adverse immunologically mediated events in clinical trials and post-licensure surveillance. Emerging data suggest that self-directed tissue inflammation occurs along a continuum from innate immune-driven diseases to adaptive immune-driven diseases. Herein, we develop this proposed classification for the vaccination setting in which inflammatory diseases are placed along a continuum according to the two major arms of the immune system, the innate immune arm (mediated by cells including neutrophils, macrophages and complement) and the adaptive immune arm (cell-mediated and humoral response). We incorporate hypersensitivity reactions and molecular mimicry vaccine-related reactions into this mechanistic scheme. We show how this could have important implications to assess mechanisms of potential immune-mediated adverse events following vaccination.
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Affiliation(s)
- Helen C Koenig
- Center for Biologics Evaluation and Research, Food and Drug Administration, Rockville, MD, USA
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Abstract
The etiology and pathogenesis of autoimmune diseases have long been an enigmatic subject that have involved genetic and environmental factors. Recent intriguing data has contributed to the mechanisms involved, including the relationship of infectious agents and loss of tolerance. This loss of tolerance is illustrated by the data on the immune response to Hepatitis B virus such as the molecular mimicry between HBV antigens and self proteins, the generation of immune complexes between HBV antigens and antibodies, and apoptosis/tissue damage resulting in the exposure of intracellular antigens to the immune system. In this paper, we review the current database related to HBV infection and a variety of autoimmune conditions, including autoimmune hepatitis, systemic lupus erythematosus, aplastic anemia, antiphospholipid syndrome, polyarteritis nodosa, rheumatoid arthritis, type 1 diabetes, multiple sclerosis, thyroid disease and uveitis.
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Development of autoimmune process in rats immunized with influenza vaccine. Acta Med Litu 2009. [DOI: 10.2478/v10140-009-0004-x] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/21/2022] Open
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Anam K, Amare M, Naik S, Szabo KA, Davis TA. Severe tissue trauma triggers the autoimmune state systemic lupus erythematosus in the MRL/++ lupus-prone mouse. Lupus 2009; 18:318-31. [DOI: 10.1177/0961203308097479] [Citation(s) in RCA: 17] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/05/2023]
Abstract
Tissue damage associated with a severe injury can result in profound inflammatory responses that may trigger autoimmune development in lupus-prone individuals. In this study, we investigated the role of a large full-thickness cutaneous burn injury on the early onset of autoimmune disease in lupus-prone MRL/++ mice. MRL/++ mice (chronic model) exhibit autoimmune symptoms at >70 weeks of age, whereas MRL/-Faslpr mice (acute model) develop autoimmune disease in 17–22 weeks due to a lymphoproliferative mutation. Autoimmune disease developed in MRL/++ mice (4–15 weeks post injury) is manifested by skin lesions, vasculitis, epidermal ulcers, cellular infiltration, splenomegaly, lymphadenopathy, hypergammaglobulinemia, elevated autoantibodies and renal pathologies including proteinuria, glomerulonephritis and immune complex deposition; complications that contribute to reduced survival. Transcription studies of wound margin tissue show a correlation between the pathogenic effects of dysregulated IL-1β, IL-6, TNF-α and PGE2 synthesis during early wound healing and early onset of autoimmune disease. Interestingly, MRL/++ mice with healed wounds (30–40 days post burn) strongly rejected skin isografts. Conversely, skin isografts transplanted onto naive age-matched MRL/++ littermates achieved long-term survival. Collectively, these findings suggest that traumatic injury exacerbates inflammatory skin disease and severe multi-organ pathogenesis in lupus-prone mice.
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Affiliation(s)
- K Anam
- Regenerative Medicine Department, Naval Medical Research Center, Silver Spring, Maryland, USA
| | - M Amare
- Regenerative Medicine Department, Naval Medical Research Center, Silver Spring, Maryland, USA
| | - S Naik
- Regenerative Medicine Department, Naval Medical Research Center, Silver Spring, Maryland, USA
| | - KA Szabo
- Department of Diagnostic Pathology, Walter Reed Army Institute of Research, Silver Spring, Maryland, USA
| | - TA Davis
- Regenerative Medicine Department, Naval Medical Research Center, Silver Spring, Maryland, USA
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Zonneveld-Huijssoon E, Ronaghy A, Van Rossum MAJ, Rijkers GT, van der Klis FRM, Sanders EAM, Vermeer-De Bondt PE, Hoes AW, van der Net JJ, Engels C, Kuis W, Prakken BJ, Van Tol MJD, Wulffraat NM. Safety and efficacy of meningococcal c vaccination in juvenile idiopathic arthritis. ACTA ACUST UNITED AC 2007; 56:639-46. [PMID: 17265499 DOI: 10.1002/art.22399] [Citation(s) in RCA: 51] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/11/2022]
Abstract
OBJECTIVE To determine whether vaccinations aggravate the course of autoimmune diseases such as juvenile idiopathic arthritis (JIA) and whether the immune response to vaccinations may be hampered by immunosuppressive therapy for the underlying disease. METHODS In this multicenter cohort study, 234 patients with JIA (ages 1-19 years) were vaccinated with meningococcal serogroup C (MenC) conjugate to protect against serogroup C disease (caused by Neisseria meningitidis). Patients were followed up for disease activity for 1 year, from 6 months before until 6 months after vaccination. IgG antibody titers against MenC polysaccharide and the tetanus carrier protein were determined by enzyme-linked immunosorbent assay and toxin binding inhibition assay, respectively. A serum bactericidal assay was performed to determine the function of the anti-MenC antibodies. RESULTS No change in values for any of the 6 components of the core set criteria for juvenile arthritis disease activity was seen after MenC vaccination. Moreover, no increase in the frequency of disease relapse was detected. Mean anti-MenC IgG concentrations in JIA patients rose significantly within 6-12 weeks after vaccination. Of 157 patients tested, 153 were able to mount anti-MenC IgG serum levels >2 micro g/ml, including patients receiving highly immunosuppressive medication. The 4 patients with a lower anti-MenC antibody response displayed sufficient bactericidal activity despite receiving highly immunosuppressive medication. CONCLUSION The MenC conjugate vaccine does not aggravate JIA disease activity or increase relapse frequency and results in adequate antibody levels, even in patients receiving highly immunosuppressive medication. Therefore, patients with JIA can be vaccinated safely and effectively with the MenC conjugate.
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Bogdanos DP, Smith H, Ma Y, Baum H, Mieli-Vergani G, Vergani D. A study of molecular mimicry and immunological cross-reactivity between hepatitis B surface antigen and myelin mimics. Clin Dev Immunol 2005; 12:217-24. [PMID: 16295528 PMCID: PMC2275415 DOI: 10.1080/17402520500285247] [Citation(s) in RCA: 51] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/03/2022]
Abstract
On the basis of the reported association between hepatitis B vaccination
(HBvacc) and autoimmune demyelinating complications such as multiple sclerosis
(MS), we have looked for aminoacid similarities between the small hepatitis
B virus surface antigen (SHBsAg), and the MS-autoantigens myelin basic protein
(MBP) and myelin oligodendrocyte glycoprotein (MOG) that could serve as targets
of immunological cross-reactivity. Twenty-mer peptides spanning 4 SHBsAg/MOG
and 1 SHBsAg/MBP mimicking pairs, were constructed and tested by ELISA as
targets of cross-reactive responses. A total of 147 samples from 58 adults were
collected before HBvacc (58/58), and post-HBvacc (48/58 before the second and
41/58 before the third boost). Eighty-seven sera from anti-SHBsAg antibody
negative patients with various diseases were tested as pathological controls.
Reactivity to at least one of the SHBsAg peptides was found in 8 (14%)
pre-HBvacc subjects; amongst the remaining 50, reactivity to at least one of the
SHBsAg peptides appeared in 47 (94%) post-HBvacc. Reactivity to at least one
of the MOG mimics was present in 4 (8%) pre-HBvacc and in 30 (60%)
post-HBvacc (p < 0.001). Overall 30/50 (60%) vaccinees had SHBsAg/MOG
double reactivity on at least one occasion compared to none before-vaccination
and in 2 (2%) of the pathological controls (p < 0.001 for both). SHBsAg/MOG
double reactivity was cross-reactive as confirmed by inhibition studies. At 6 months
post-vaccination, 3 of the 4 anti-MOG reactive cases before vaccination and 7
of the 24 (29%) of the anti-MOG reactive cases at 3 months post-vaccination had
lost their reactivity to MOG5-24. There was no reactivity to the SHBsAg/MBP
mimics. None of the vaccinees reported symptoms of demyelinating disorders. In
view of the observed SHBsAg/MOG cross-reactivity, the vaccine's possible role as
an immunomodulator of viral/self cross-reactivity must be further investigated.
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Geier DA, Geier MR. A case-control study of serious autoimmune adverse events following hepatitis B immunization. Autoimmunity 2005; 38:295-301. [PMID: 16206512 DOI: 10.1080/08916930500144484] [Citation(s) in RCA: 95] [Impact Index Per Article: 4.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/25/2022]
Abstract
Hepatitis B infection is one of the most important causes of acute and chronic liver disease. During the 1980s, genetically engineered hepatitis B vaccines (HBVs) were introduced in the United States. A large-series of serious autoimmune conditions have been reported following HBVs, despite the fact that HBVs have been reported to be "generally well-tolerated." A case-control epidemiological study was conducted to evaluate serious autoimmune adverse events prospectively reported to the vaccine adverse events reporting system (VAERS) database following HBVs, in comparison to an age, sex, and vaccine year matched unexposed tetanus-containing vaccine (TCV) group for conditions that have been previously identified on an a priori basis from case-reports. Adults receiving HBV had significantly increased odds ratios (OR) for multiple sclerosis (OR = 5.2, p < 0.0003, 95% Confidence Interval (CI) = 1.9 - 20), optic neuritis (OR = 14, p < 0.0002, 95% CI = 2.3 - 560), vasculitis (OR = 2.6, p < 0.04, 95% CI = 1.03 - 8.7), arthritis (OR = 2.01, p < 0.0003, 95% CI = 1.3 - 3.1), alopecia (OR = 7.2, p < 0.0001, 95% CI = 3.2 - 20), lupus erythematosus (OR = 9.1, p < 0.0001, 95% CI = 2.3 - 76), rheumatoid arthritis (OR = 18, p < 0.0001, 95% CI = 3.1 - 740), and thrombocytopenia (OR = 2.3, p < 0.04, 95% CI = 1.02 - 6.2) in comparison to the TCV group. Minimal confounding or systematic error was observed. Despite the negative findings of the present study regarding the rare serious adverse effects of HBVs, it is clear that HBV does, indeed, offer significant benefits, but it is also clear that chances of exposure to hepatitis B virus in adults is largely life-style dependent. Adults should make an informed consent decision, weighing the risks and benefits of HBV, as to whether or not to be immunized.
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Abstract
The etiology of autoimmune diseases is still not clear but genetic, immunological, hormonal and environmental factors are considered to be important triggers. Most often autoimmunity is not followed by clinical symptoms unless an additional event such as an environmental factor favors an overt expression. Many environmental factors are known to affect the immune system and may play a role as triggers of the autoimmune mosaic.Infections: bacterial, viral and parasitic infections are known to induce and exacerbate autoimmune diseases, mainly by the mechanism of molecular mimicry. This was studied for some syndromes as for the association between SLE and EBV infection, pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection and more. Vaccines, in several reports were found to be temporally followed by a new onset of autoimmune diseases. The same mechanisms that act in infectious invasion of the host, apply equally to the host response to vaccination. It has been accepted for diphtheria and tetanus toxoid, polio and measles vaccines and GBS. Also this theory has been accepted for MMR vaccination and development of autoimmune thrombocytopenia, MS has been associated with HBV vaccination. Occupational and other chemical exposures are considered as triggers for autoimmunity. A debate still exists about the role of silicone implants in induction of scleroderma like disease.Not only foreign chemicals and agents have been associated with induction of autoimmunity, but also an intrinsic hormonal exposure, such as estrogens. This might explain the sexual dimorphism in autoimmunity.Better understanding of these environmental risk factors will likely lead to explanation of the mechanisms of onset and progression of autoimmune diseases and may lead to effective preventive involvement in specific high-risk groups. So by diagnosing a new patient with autoimmune disease a wide anamnesis work should be done.
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Affiliation(s)
- Vered Molina
- Department of Medicine B and The Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, Israel
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N/A. N/A. Shijie Huaren Xiaohua Zazhi 2004; 12:2400-2402. [DOI: 10.11569/wcjd.v12.i10.2400] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 02/06/2023] Open
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Burnett R, Ravel G, Descotes J. Clinical and histopathological progression of lesions in lupus-prone (NZB×NZW) F1 mice. ACTA ACUST UNITED AC 2004; 56:37-44. [PMID: 15581273 DOI: 10.1016/j.etp.2004.04.010] [Citation(s) in RCA: 21] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/28/2022]
Abstract
This study was conducted to review the progression with age of renal and other changes in (NZB x NZW) F1 females obtained from a commercial colony, housed under SPF conditions. Sixty-two mice were given food and water ad libitum and sacrificed at intervals up to 47 weeks of age. Routine haematology and urinalysis were performed at regular intervals. The serum levels of IgA, IgG, IgM and antinuclear antibody levels were monitored along with urinary protein. Major organs and tissues from all animals were preserved and examined. Special attention was paid to the kidneys: in addition to routine 4-microm paraffin sections, 1-microm resin sections were prepared and examined. Positive levels of urinary protein (> 1 g/L) were only found in 50% of the animals, even at 32 weeks of age. Histopathologically, the expected type of glomerular damage was present; but the incidence and severity of the change were low, with only 33% of the mice affected at 32 weeks of age. Most mice had fatty vacuolation in the liver. At 24 weeks of age, 50% of the mice sacrificed had haemorrhagic degeneration of the liver. This was not seen at later time points. Only two mice survived until 47 weeks of age. In summary, these findings were of the expected type, but at a much lower incidence and severity than formerly reported. The background of the strain and the experimental conditions are of great importance in the progress of these renal lesions. The lack of homogeneity of the renal changes would make it difficult to determine any influence of xenobiotics on the progress of autoimmune diseases.
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Affiliation(s)
- Roger Burnett
- MDS Pharma Services, Les Oncins, 69210 St Germain sur l'Arbresle, France.
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