The impact of inflammation and immune activation on B cell differentiation during HIV-1 infection.

Frontiers in Immunology
Nicolas RuffinFrancesca Chiodi

Abstract

One important pathogenic feature of human immunodeficiency virus (HIV)-1 infection is chronic immune activation and impaired survival of T and B cells. A decline of resting memory B cells was reported to occur in both children and adults infected with HIV-1; these cells are responsible for maintaining an adequate serological response to antigens previously encountered in life through natural infection or vaccination. Further understanding of the mechanisms leading to impaired B cell differentiation and germinal center reaction might be essential to design new HIV vaccines and therapies that could improve humoral immune responses in HIV-1 infected individuals. In the present article we summarize the literature and present our view on critical mechanisms of B cell development impaired during HIV-1 infection. We also discuss the impact of microbial translocation, a driving force for persistent inflammation during HIV-1 infection, on survival of terminally differentiated B cells and how the altered expression of cytokines/chemokines pivotal for communication between T and B cells in lymphoid tissues may impair formation of memory B cells.

Citations

Oct 12, 2014·The Journal of the Association of Nurses in AIDS Care : JANAC·Natalie L WilsonMirjam-Colette Kempf
Sep 16, 2016·Frontiers in Immunology·Bahaa Abu-RayaArnaud Marchant
Jan 1, 2017·The Journal of Immunology : Official Journal of the American Association of Immunologists·Ramla F TankoWendy A Burgers
Nov 23, 2017·Frontiers in Immunology·Gwenoline BorhisYolande Richard
Aug 9, 2020·Frontiers in Cellular and Infection Microbiology·Robert BaduraAna E Sousa

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