Copyright
©The Author(s) 2022.
World J Gastroenterol. Oct 28, 2022; 28(40): 5784-5800
Published online Oct 28, 2022. doi: 10.3748/wjg.v28.i40.5784
Published online Oct 28, 2022. doi: 10.3748/wjg.v28.i40.5784
Immune cells | Released cytokines |
NK cells | IFN-γ, TNF-α, IL-10 |
NKT cells | IFN-γ, IL-4, IL-13 |
Monocytes | IFN-γ, TNF-α, IL-10 |
Macrophages | IFN-γ, IL-6, MCP-1, IL-1β, TNF-α, CXCL10 |
γδT cells | IL-17, TNF-α |
HSCs | IL-1β, IL-6, TGF-β |
Kupffer cells | IL-10, TGF-β, IL-12, IL-6, TNF-α |
CD8+ T cells | IFN-γ, TNF-α, IL-2, IL-10, IL-17, IL-21 |
CD4+ T cells | IFN-γ, IL-21,IL-17 |
Regulatory T cells | IL-10, TGF-β, IL-35 |
Regulatory B cells | IL-10 |
Gene ontology | Gene | Genetic determinants (SNP/Hap/CNVs) |
HLA | HLA-A | *33:03:01 |
HLA-B | *13:01:01 | |
HLA-B | *07, *58 | |
HLA-C | Leu-15, rs2853953, rs3130542 | |
HLA-DOA | rs378352 | |
HLA-DP | rs9366816 | |
HLA-DPA1 | rs3077, rs2301220, rs2395309, rs9277341 | |
HLA-DPB1 | G-A-G-A-T-T1, G-G-G-G-T-C2, rs2281388, rs9277535, rs9277542, rs9277534, *0201, *0401, *0901, positions 84–87, *0402, *0501, *0201-*0401, *0201-*0402, *0201-*0501, *0401-*0402, *0401-*0501, *0402-*0402, *0402-*0501, *0501-*0501, *0501- *0901, *0501*others, rs9277378, rs10484569, rs3117222, rs9380343, rs3135021 | |
HLA-DQ | rs9275319, rs9275572, A1*0101-B1*0501, A1*0102-B1*0303, A1*0102-B1*0604, A1*0301-B1*0601, A1*0102-B1*0602, A1*0102-B1*0602, A1*0301-B1*0302, A1*0301-B1*0303, A1*0301-B1*0401, A1*0501-B1*0301 | |
HLA-DPA1/ DPB1 | A-A3, A-A4, T-A-T5,C-A-T6, A-A-C-T7, A-A-C-C//A-G-T-G-C-C8, A-A-C-T//A-G-T-G-C-C9, G-G-T-C//A-G-T-G-C-C10, A1*0103-B1*0401, A1*0103-B1*0402, A1*0202-B1*0301, A1*0202-B1*0501 | |
HLA-DQA2 | rs9276370 | |
HLA-DQB1 | *0201, *0301, *0303, *0502, *0604, rs2856718, *0401-*0501, *0402-*0402, *0402-*0501, *0501-*0501 | |
HLA-DQB2 | rs7453920, rs7756516 | |
HLA-DRB1 | *13 | |
HLA-DP/DQ | T-T-G-A-T11, T-T-G-G-T12, carrying 4–6 variant alleles, G-A13, A-G14, A-A15 | |
HLA-J | rs400488 | |
Cytokines | IL-10 | −592 |
IL-10RB | rs2834167 | |
IL-12B | rs3212227 | |
IL-16 | rs11556218 | |
IL-21 | rs2221903 | |
IL-12B | rs3212227 | |
IL-18 | −137 | |
IFN-γ | +874 | |
IFN-α2 | p.Ala120Thr | |
IFN-αR2 | rs1051393, rs12233338 | |
IFNLR1 | rs4649203, rs7525481 | |
IFN-γR1 | rs3799488 | |
IFN-γR2 | rs1059293 | |
TNF-α | T-C-C-G-G-G16, C-A-C-G-G-G17 ,−238, −308, −857, −863 | |
TGF-α | +106151, +103461, A-T-G-T-T-T-T-C-T18 | |
Chemokines | CCR5 | Δ32 |
TLRs | TLR-3 | rs3775291, rs1879026 |
TLR-9 | rs352140 | |
MicroRNAs | miR-30a | rs1358379 |
miR-101-2 | T-C19, rs12375841 | |
miR-106b-25 | rs999885 | |
miR-122 | rs3783553, rs4309483 | |
miR-196a-2 | rs11614913 | |
miR-let-7c | rs6147150 | |
miR-219-1 | rs107822, rs213210, rs421446, C-A-C20, T-G-T21 | |
miR-323b | rs56103835 | |
miR-423 | rs6505162 | |
miR-492 | rs2289030 | |
Others | C2 | p.Glu318Asp, rs7746553, rs9267673, rs9267665, rs9267677, rs9279450, rs10947223 |
CD40 | rs1883832 | |
CFB | rs12614 | |
CTLA-4 | C-A-C-C-G22, T/C-A-C-C-G23, T-A-C-C-A24, rs231775,rs3087243, rs5742909 | |
EHMT2 | rs7887, rs652888, rs35875104, rs41267090 | |
ESR1 | +29 | |
IFN4/HLA-DQ | rs12971396-rs9275319, rs12971396-rs12979860-rs9275319 | |
INST10 | rs7000921 | |
KIF1B | A-T-A25 | |
MCP1 | −2518, −2518/−2076(−/ht2), −2518/−2076(ht2/ht2) | |
MIF | rs755622 | |
MxA | −123 | |
MX1 | rs467960 | |
NF-κB | rs2233406, rs3138053 | |
NLRX1 | p.Arg707Cys | |
NOTCH4 | rs422951 | |
NTCP | rs2296651, rs943277, rs4646285 | |
OCT4 | rs13409, rs885952, rs879882, rs1265163, rs2394882, rs3094193, rs3130501, rs3130503, rs3130931, rs3132526, rs3757349, rs9263800, rs117265349 | |
PAPL | rs423058 | |
SOCS3 | C-C26, T-T-C-T-A27, rs111033850, rs12953258, | |
SPP1 | −1800 | |
STAT4 | C-T-C-T-T28, rs7574865,rs8179673, rs10168266, rs11889341, | |
TCF19 | rs1419881 | |
TMEM2 | p.Ser1254Asn | |
TMEM2/IFNA2/ NLRX1/C2 | p.Ser1254-Asn/p.Ala120Thr/p.Arg707Cys/p.Glu318Asp | |
UBE2L3 | rs2266959, rs4821116 | |
VARS2 | rs1043483, rs1264295, rs2249464, rs2517459, rs2532932, rs9394021, | |
VDR | FokI | |
ZNRD1 | G-G-A29, rs3757328 |
Gene ontology | Gene | Genetic determinants (SNP/Hap/CNVs) |
HLA | HLA-DP | rs3077, rs9277535 |
HLA-DQA1-DQB1-DRB1 | *0302-*0303-*09 | |
HLA-DQB1 | *0303 | |
HLA-DRB1 | *08 | |
HLA-A, B, C | *1101-*4601-*0102 | |
Cytokines | IL-28B | A-C1,rs8099917, rs12979860, rs12980275 |
Others | CYP24A1 | rs2248359 |
CYP27B1 | rs10877012, rs4646536 | |
G3BP2 | rs3821977 | |
OAS | G-T-G-A2, C-C-T-A3, C-C-C-A4, A-C-T-A5 | |
OAS3 | rs2072136 | |
PRELID2 | rs371991 | |
STAT4 | rs7574865 | |
TRAPPC9 | rs78900671 | |
VDBP | rs7041 | |
VDR | rs1544410, rs731236, rs11568820, rs10735810 |
Ref. | Year | The regimens of INF-α retreatment |
van Zonneveld et al[10] | 2004 | One hundred and sixty-five patients received their first IFN-α treatment. Of them, 48 non-responders received 2-3 courses of IFN-α |
Manesis and Hadziyannis[11] | 2001 | Two hundred and sixteen patients received IFN-α therapy, of whom 51 received a second IFN-α treatment and 9 were treated with three courses of IFN-α |
Niederau et al[12] | 1996 | One hundred and three cases were treated IFN-α. Of them, 29 received a second course of therapy, and 17 received a third course of IFN-α |
Carreño et al[13] | 1999 | Fifty-seven patients underwent a course of IFN-α therapy. Of them, 27 received a second course of IFN-α; and 30 others who did not receive IFN-α retreatment served as controls. IFN-α retreatment was found to enhance the antiviral effects against HBV |
Ballauff et al[14] | 1998 | After all the children received the first course of IFN-α treatment, 15 were given the second course of IFN-α (study group), while the other 19 did not receive the second course of IFN-α, serving as the control group. HBV DNA clearance and anti-HBe seroconversion occurred in 5 of 15 children (33%) in the study group and 5 of 19 children (26%) in the control group |
Yin and Zhong[15] | 2016 | Inappropriate therapies induced HBV resistance, multi-drug resistance and failure of combination therapy with nucleoside plus nucleotide in China. An IFN-α regimen, i.e. (1) Switch from nucleoside plus nucleotide to IFN-α therapy; and (2) subsequent IFN-α retreatment, was used to treat these patients. IFN-α switching therapy leaded to safe cessation of nucleoside plus nucleotide combination therapy, and IFN-α retreatment induced sustained response of IFN-α |
Sarin et al[16] | 2016 | Asian-Pacific clinical practice guidelines 2015 recommended IFN-α retreatment to treat chronic HBV infection |
Liaw et al[17] | 2012 | Asian-Pacific clinical practice guidelines 2012 recommended IFN-α retreatment to treat chronic HBV infection |
Liaw et al[18] | 2008 | Asian-Pacific clinical practice guidelines 2008 recommended IFN-α retreatment to treat chronic HBV infection |
Yin et al[64] | 2021 | IFN-α retreatment was recommended for patients on entecavir or tenofovir monotherapy with persistent low-level viremia |
- Citation: Yin GQ, Chen KP, Gu XC. Heterogeneity of immune control in chronic hepatitis B virus infection: Clinical implications on immunity with interferon-α treatment and retreatment. World J Gastroenterol 2022; 28(40): 5784-5800
- URL: https://www.wjgnet.com/1007-9327/full/v28/i40/5784.htm
- DOI: https://dx.doi.org/10.3748/wjg.v28.i40.5784