Abstract
The production of high-affinity and broadly neutralizing antibodies plays a key role in the defense against pathogens. These antibody responses require effective germinal center (GC) reaction within anatomical niches of GCs, where follicular helper T (Tfh) cells provide cognate help to B cells for T cell-dependent antibody responses. Emerging evidences indicate that GC reaction in normal state and perhaps establishment of latent Tfh cell reservoir in HIV/SIV infection are tightly regulated by epigenetic histone modifications, which are responsible for activating or silencing chromatin. A better understanding of the mechanisms behind GC responses at cellular and molecular levels thus provides necessary knowledge for vaccination and immunotherapy. In this review, we discussed the epigenetic regulation of GC responses, especially for GC B and Tfh cell under normal state or HIV/SIV infection.
Highlights
B-cell lineage commitment develops in primary lymphoid tissues such as fetal liver and bone marrow, and enters circulation [1]
Germinal center (GC) reaction is the critical checkpoint in the development of T-dependent B-cell responses against foreign pathogens
Emerging studies have shown germinal center (GC) responses are strictly regulated by epigenetic modifications, which cooperate with timely expression of transcriptional factors for follicular B/T helper cell differentiation, thereby modulating antibody responses to foreign- and self-antigens [4]
Summary
Tulane National Primate Research Center, Tulane University School of Medicine, Covington, LA, United States. The production of high-affinity and broadly neutralizing antibodies plays a key role in the defense against pathogens. These antibody responses require effective germinal center (GC) reaction within anatomical niches of GCs, where follicular helper T (Tfh) cells provide cognate help to B cells for T cell-dependent antibody responses. Emerging evidences indicate that GC reaction in normal state and perhaps establishment of latent Tfh cell reservoir in HIV/SIV infection are tightly regulated by epigenetic histone modifications, which are responsible for activating or silencing chromatin. We discussed the epigenetic regulation of GC responses, especially for GC B and Tfh cell under normal state or HIV/SIV infection
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