• Humans
• Tumor Microenvironment/immunology
• Uterine Cervical Neoplasms/immunology
• Uterine Cervical Neoplasms/therapy
• Uterine Cervical Neoplasms/pathology
• Uterine Cervical Neoplasms/virology
• Female
• Papillomavirus Infections/immunology
• Papillomavirus Infections/complications
• Prognosis

• HPV
• Latin America
• cervical cancer
• epidemiology
• immunological aspects
• vaccines

• Humans
• Female
• Uterine Cervical Neoplasms/epidemiology
• Uterine Cervical Neoplasms/prevention & control
• Uterine Cervical Neoplasms/pathology
• Human Papillomavirus Viruses
• Papillomavirus Infections/epidemiology
• Papillomavirus Infections/prevention & control
• Latin America/epidemiology
• Papillomaviridae/genetics
• Vaccination
• Papillomavirus Vaccines

• 10209-2022 Jalisco Scientific Development Fund to Address Social Challenges "FODECIJAL 2022"

• HIV
• Human papillomavirus
• IFN-I
• IL17
• Immunohistochemistry
• Plasmacytoid dendritic cells

• CAPES

• Cervical cancer
• Cytokine
• Diagnosis
• Immunotherapy
• Inflammation
• Soluble HLA-G

• Humans
• Female
• HLA-G Antigens
• Cytokines
• Interleukin-10
• Interleukin-17
• Uterine Cervical Neoplasms/therapy
• Interleukin-6
• Interleukin-8
• Immunotherapy
• Tumor Microenvironment

• 81901625 National Natural Science Foundation of China
• LY20H100004 National Natural Science Foundation of Zhejiang province
• 20ywa04 Taizhou Municipal Science and Technology Bureau
• 1901ky19 Taizhou Municipal Science and Technology Bureau

• CAR-Ts
• TCR-Ts
• TILs
• cervical cancer
• engineered T cells
• immune checkpoint

• Female
• Humans
• Uterine Cervical Neoplasms/therapy
• CD8-Positive T-Lymphocytes
• Immunotherapy

Numerous case-control studies have reported associations between interleukin-17 (IL-17) polymorphisms and colorectal cancer; however, the results were inconsistent. The aim of this meta-analysis was to further clarify the effects of IL-17 polymorphisms on colorectal cancer susceptibility.

Relevant studies were extracted from the electronic databases PubMed, Embase, Web of Science, China National Knowledge Infrastructure (CNKI), and the Chinese Biomedical Literature Database (CMB) up to April 2021. The odds ratio and 95% confidence interval were used to estimate the strength of the associations.

Ten articles including 2599 cases and 2845 controls were enrolled in our research after strict literature screening. Highly significant associations between the IL-17A rs2275913 polymorphism and increased colorectal cancer susceptibility were observed in all five gene models (allelic, dominant, recessive, homozygous, and heterozygous models), and subgroup analysis based on ethnicity revealed that these associations existed not only in the Asian population but also in the Caucasian population. However, the results showed no significantly elevated colorectal cancer risk correlated with the IL-17F rs763780 polymorphism, and a slightly lower colorectal cancer susceptibility for the Caucasian population was discovered in the recessive and homozygous models of this mutation.

The IL-17A rs2275913 polymorphism may be an independent risk factor contributing to colorectal cancer susceptibility, while the IL-17F rs763780 polymorphism may decrease susceptibility to colorectal cancer. Future studies with large-scale samples are warranted to identify these associations.

The online version contains supplementary material available at 10.1186/s12957-022-02586-2.

• Colorectal cancer
• IL-17
• Meta-analysis
• Polymorphism
• Susceptibility

• Cervical cancer
• Cytokines
• Inflammation
• Purinergic signaling

Diverse evidence revealed that CD4⁺ T cells play an important role in antitumor immunity by promoting or suppressing cytotoxic T cell responses. This review outlines the role of CD4⁺ T subsets within the tumor microenvironment and summarizes the latest progress regarding their potentials in cancer immunotherapy and methods for improving outcomes in cancer strategies by modulating CD4⁺ T responses.

Over the past decades, CD4⁺ T cells have been considered as a supporting actor in the fields of cancer immunotherapy. Until recently, accumulating evidence has demonstrated the critical role of CD4⁺ T cells during antitumor immunity. CD4⁺ T cells can either suppress or promote the antitumor cytotoxic CD8⁺ T cell responses, either in secondary lymphoid organs or in the tumor. In this review, we provide an overview of the multifaceted role of different CD4⁺ T cell subsets in cancer immune response and their contribution during cancer therapies. Specifically, we focus on the latest progress regarding the impact of CD4⁺ T cell modulation on immunotherapies and other cancer therapies and discuss the prospect for harnessing CD4⁺ T cells to control tumor progression and prevent recurrence in patients.

• CD4+ T cells
• adoptive cell transfer
• cancer immunotherapy
• cancer vaccine
• immune checkpoint inhibitors

• HPV
• cervical cancer
• host-pathogen interaction
• immune evasion
• innate immunity
• vaccines

• cancer immunity
• immunotherapy
• targeted therapy
• γδ T cells
• γδ T-cell lymphoma
• γδ T-cell transformation

• I 4157 Austrian Science Fund FWF
• I 4218 Austrian Science Fund FWF

Various immune cells are involved in host immune responses to cancer. T-helper (Th) 1 cells, cytotoxic CD8⁺ T cells, and natural killer cells are the major effector cells in anti-tumor immunity, whereas cells such as regulatory T cells and myeloid-derived suppressor cells are negatively involved in anti-tumor immunity. Th2 cells and Th17 cells have been shown to have both pro-tumor and anti-tumor activities. The migratory properties of various immune cells are essential for their function and critically regulated by the chemokine superfamily. In this review, we summarize the roles of various immune cells in tumor immunity and their migratory regulation by the chemokine superfamily. We also assess the therapeutic possibilities of targeting chemokines and chemokine receptors in cancer immunotherapy.

Various immune cells are involved in host tumor immune responses. In particular, there are many T cell subsets with different roles in tumor immunity. T-helper (Th) 1 cells are involved in cellular immunity and thus play the major role in host anti-tumor immunity by inducing and activating cytotoxic T lymphocytes (CTLs). On the other hand, Th2 cells are involved in humoral immunity and suppressive to Th1 responses. Regulatory T (Treg) cells negatively regulate immune responses and contribute to immune evasion of tumor cells. Th17 cells are involved in inflammatory responses and may play a role in tumor progression. However, recent studies have also shown that Th17 cells are capable of directly inducting CTLs and thus may promote anti-tumor immunity. Besides these T cell subsets, there are many other innate immune cells such as dendritic cells (DCs), natural killer (NK) cells, and myeloid-derived suppressor cells (MDSCs) that are involved in host immune responses to cancer. The migratory properties of various immune cells are critical for their functions and largely regulated by the chemokine superfamily. Thus, chemokines and chemokine receptors play vital roles in the orchestration of host immune responses to cancer. In this review, we overview the various immune cells involved in host responses to cancer and their migratory properties regulated by the chemokine superfamily. Understanding the roles of chemokines and chemokine receptors in host immune responses to cancer may provide new therapeutic opportunities for cancer immunotherapy.

• Th1
• Th17
• Th2
• chemokine
• chemokine receptor
• dendritic cell
• macrophage
• neutrophil
• regulatory T
• tumor microenvironment

• Echinocooccosis
• Interleukin17
• Iraq
• Echinococccus granuulosus

• Animals
• Female
• Humans
• Male
• Echinococcosis/blood
• Echinococcosis/epidemiology
• Echinococcosis/immunology
• Echinococcus
• Interleukin-17/blood
• Iraq/epidemiology
• Zoonoses
• Echinococcus granulosus
• Adult
• Middle Aged
• Aged

• Cancer
• Immune response
• Interleukin-17
• Pathophysiology
• Th17 cells
• Tumor microenvironment

Interleukin (IL)-17 has been regarded as a significant factor in inflammation. In addition, IL-17 is known to be involved in the progression of cancers; however, the function of IL-17 in cervical cancer remains unclear. In the present study, cell viability was detected by Cell Counting Kit-8 assay. Quantitative PCR and western blotting were performed to detect gene and protein expression levels, respectively, in cancer cells or tissues. Ki-67 staining was used to evaluate cell proliferation. Wound-healing assay was used to detect cell migration. Moreover, Transwell assay was performed to investigate the invasion of cervical cancer cells. The results revealed that IL-17 significantly promoted the proliferation of cervical cancer cells. Additionally, IL-17 notably enhanced the migration and invasion of cervical cancer cells in vitro. IL-17 promoted the progression of cervical cancer via the activation of JAK2/STAT3 and PI3K/Akt/NF-κB signaling. In conclusion, IL-17 was a key regulator during the progression of cervical cancer through the JAK2/STAT3 and PI3K/Akt/nuclear factor-κB signaling pathway, which may serve as a novel target for the treatment of cervical cancer.

• JAK2/STAT3
• PI3K/Akt
• cervical cancer
• interleukin-17
• nuclear factor-κB

Introduction: Lung cancer is the second most frequent malignancy worldwide, but its aetiology is still unclear. Inflammatory cytokines and Th cells, including Th17, are now emerging as being involved in NSCLC pathways, thus postulating a role of IL-17 in tumour angiogenesis by stimulating the vascular endothelial growth factor and the release of nitric oxide. Despite the fact that many biomarkers are used for chest malignancy diagnosis, data on FeNO levels and inflammatory cytokines in NSCLC are still few. Our study aimed to evaluate the relationship between pulmonary nitric oxide production and VEGF and Th17-related cytokines in the EBC of patients affected by early-stage NSCLC. Methods: FeNO measurement and lung function tests were performed in both patients affected by NCSLC and controls; EBC samples were also taken, and Th1 (IL-1, IL-6, IL-12, IFN-g, TNF-a), Th17 (IL-17, IL-23) and Th2 (IL-4, IL-5, IL-13) related cytokines were measured. Results: Th1 and Th17-related cytokines in EBC, except for IFN-gamma and TNF-alpha, were significantly higher in patients than in healthy controls, whereas no differences were seen for Th2-related cytokines. FeNO at the flow rate of 50 mL/s, JawNO and CalvNO levels were significantly higher in patients affected by NSCLC compared to controls. Significant correlations were found between FeNO 50 mL/s and IL-17, IL-1 and VEGF. JawNO levels positively correlated with IL-6, IL-17 and VEGF. No correlations were found between FeNO and Th2-related cytokines. Conclusion: This is the first report assessing a relationship between FeNO levels and Th17-related cytokines in the EBC of patients affected by early-stage NSCLC. IL-17, which could promote angiogenesis through the VEGF pathway, might be indirectly responsible for the increased lung production of NO in patients with NSCLC.

• CalvNO
• EBC
• FeNO
• IL-17
• IL-23
• JawNO
• NSCLC
• Th-17 cells
• VEGF
• exhaled breath condensate
• lung malignancy
• non-small-cell lung cancer

Cervical cancer is a top lethal cancer for women worldwide. Although screening and vaccination programs are available in many countries, resulting in the decline of new cases, this is not true for developing countries where there are many new cases and related deaths. Cancer immunotherapy through adaptive cell therapy (ACT) has been applied in clinics, but now much attention is focused on autogenic tumor-infiltrating lymphocyte (TIL)-based therapy, which has shown more specificity and better ability to inhibit tumor growth. Data from melanoma and cervical cancers confirm that tumor-specific T cells in TILs can be expanded for more specific and effective ACT. Moreover, TILs are derived from individual patients and are ready to home back to kill tumor cells after patient infusion, aligning well with personalized and precision medicine. In addition to therapy, TIL cell types and numbers are good indicators of host immune response to the tumor, and thus they have significant values in prognosis. Because of the special relationship with human papillomavirus (HPV) infection, cervical cancer has some specialties in TIL-based prognosis and therapy. In this review, we summarize the recent advances in the prognostic significance of TILs and TIL-based therapy for cervical cancer and discuss related perspectives.

• CD4+ T cells
• CD8+ T cells
• TILs
• adaptive cell therapy
• cancer immunotherapy
• cervical cancer
• human papillomavirus
• regulatory T cells
• tumor prognosis
• tumor-infiltrating lymphocytes

Evidences highlight the role of various CD4⁺ helper T cells (CD4⁺ Th) subpopulations in orchestrating the immune responses against cancers. Epigenetics takes an important part in the regulation of CD4⁺ Th polarization and plasticity. In this review, we described the epigenetic factors that govern CD4⁺ T cells differentiation and recruitment in the tumor microenvironment and their subsequent involvement in the antitumor immunity. Finally, we discussed how to manipulate tumor reactive CD4⁺ Th responses by epigenetic drugs to improve anticancer immunotherapy.

• CD4+ helper T cells
• epigenetics
• immunotherapy
• plasticity
• tumor microenvironment

• cervical cancer
• human papillomavirus
• immunoevasion
• immunomodulation
• nuclear factor – kappa B
• signal transducer activator of transcription 3

• Cervical cancer
• human papilloma virus
• immune response
• vaccines

Th17 cells represent a subset of CD4+ T cells characterized by the master transcription factor RORγt and the production of IL-17. Epigenetic modifications such as post-translational histone modifications and DNA methylation play a key role in Th17 cell differentiation and high plasticity. Th17 cells are highly recruited in many types of cancer and can be associated with good or bad prognosis. Here, we will review the remodeling of the epigenome induced by the tumor microenvironment, which may explain Th17 cell predominance. We will also discuss the promising treatment perspectives of molecules targeting epigenetic enzymes to remodel a Th17-enriched tumor microenvironment.

• TIL
• Th17 cells
• epigenetic modifications
• tumor microenvironment

• Angiogenesis
• CXCR2 ligands
• IL17
• Metastasis
• NETs
• NLR
• Neutrophil
• Neutrophil-released proteases
• Pro-tumor chemokines
• Pro-tumor cytokines
• Tumor microenvironment

• Humans
• Neoplasms/pathology
• Neovascularization, Pathologic
• Neutrophils/pathology
• Tumor Microenvironment

• R01 CA228524 NCI NIH HHS
• U54 CA163120 NCI NIH HHS

IL-17 is produced by RAR-related orphan receptor gamma t (RORγt)-expressing cells including Th17 cells, subsets of γδT cells and innate lymphoid cells (ILCs). The biological significance of IL-17-producing cells is well-studied in contexts of inflammation, autoimmunity and host defense against infection. While most of available studies in tumor immunity mainly focused on the role of T-bet-expressing cells, including cytotoxic CD8⁺ T cells and NK cells, and their exhaustion status, the role of IL-17-producing cells remains poorly understood. While IL-17-producing T-cells were shown to be anti-tumorigenic in adoptive T-cell therapy settings, mice deficient in type 17 genes suggest a protumorigenic potential of IL-17-producing cells. This review discusses the features of IL-17-producing cells, of both lymphocytic and myeloid origins, as well as their suggested pro- and/or anti-tumorigenic functions in an organ-dependent context. Potential therapeutic approaches targeting these cells in the tumor microenvironment will also be discussed.

• Interleukin-17
• T-lymphocytes
• Th17 cells
• Tumor microenvironment

• Animals
• Biological Coevolution
• Host-Pathogen Interactions
• Inflammation/immunology
• Neoplasms/immunology
• Neoplasms/microbiology
• Neoplasms/parasitology
• Neoplasms/pathology
• Parasites/physiology
• Risk Factors
• Selection, Genetic

• R01 AI079085 NIAID NIH HHS
• R01 CA164719 NCI NIH HHS
• R56 AI091889 NIAID NIH HHS
• RC1 AI086788 NIAID NIH HHS

The progression of cancer is not only about the tumor cell itself, but also about other involved players including cancer cell recruited immune cells, their released pro-inflammatory factors, and the extracellular matrix. These players constitute the tumor microenvironment and play vital roles in the cancer progression. Neutrophils—the most abundant white blood cells in the circulation system—constitute a significant part of the tumor microenvironment. Neutrophils play major roles linking inflammation and cancer and are actively involved in progression and metastasis. Additionally, recent data suggest that neutrophils could be considered one of the emerging targets for multiple cancer types. This review summarizes the most recent updates regarding neutrophil recruitments and functions in the tumor microenvironment as well as potential development of neutrophils-targeted putative therapeutic strategies.

• cancer metastasis
• neutrophil extracellular traps
• neutrophil polarization
• neutrophils