PLoS Pathogens | |
Antibody-Independent Control of γ-Herpesvirus Latency via B Cell Induction of Anti-Viral T Cell Responses | |
Herbert W. Virgin IV1  Kelly B McClellan1  Samuel H Speck2  Shivaprakash Gangappa3  | |
[1] Department of Pathology and Immunology, Washington University School of Medicine, Saint Louis, Missouri, United States of America;Division of Microbiology and Immunology, Yerkes Regional Primate Research Center, Emory University, Atlanta, Georgia, United States of America;Emory Transplant Center, Emory University School of Medicine, Atlanta, Georgia, United States of America | |
关键词: B cells; T cells; Viral persistence; latency; Cytotoxic T cells; Antibodies; Viral replication; Enzyme-linked immunoassays; Viral genome; | |
DOI : 10.1371/journal.ppat.0020058 | |
学科分类:生物科学(综合) | |
来源: Public Library of Science | |
【 摘 要 】
B cells can use antibody-dependent mechanisms to control latent viral infections. It is unknown whether this represents the sole function of B cells during chronic viral infection. We report here that hen egg lysozyme (HEL)-specific B cells can contribute to the control of murine γ-herpesvirus 68 (γHV68) latency without producing anti-viral antibody. HEL-specific B cells normalized defects in T cell numbers and proliferation observed in B cell−/− mice during the early phase of γHV68 latency. HEL-specific B cells also reversed defects in CD8 and CD4 T cell cytokine production observed in B cell−/− mice, generating CD8 and CD4 T cells necessary for control of latency. Furthermore, HEL-specific B cells were able to present virally encoded antigen to CD8 T cells. Therefore, B cells have antibody independent functions, including antigen presentation, that are important for control of γ-herpesvirus latency. Exploitation of this property of B cells may allow enhanced vaccine responses to chronic virus infection.
【 授权许可】
CC BY
【 预 览 】
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