Microbial TLR Agonists and Humoral Immunopathogenesis in HIV Disease
Kilby, J Michael
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CitationYu, Xiaocong, Zihai Li, Zhenxian Zhou, J Michael Kilby, and Wei Jiang. 2013. “Microbial TLR Agonists and Humoral Immunopathogenesis in HIV Disease.” Epidemiology (Sunnyvale, Calif.) 3 (1): 120. doi:10.4172/2161-1165.1000120. http://dx.doi.org/10.4172/2161-1165.1000120.
AbstractAlthough T cells are the primary and most-studied targets of the Human Immunodeficiency Virus (HIV), B cells, especially memory B lymphocytes, are also chronically depleted in the course of HIV disease. Although the lack of CD4+ T cell help may explain these deficiencies, intrinsic defects in B lymphocytes appear to contribute to B cell depletion and reduced antibody (Ab) production in the setting of HIV, especially of some antigens eliciting T cell-independent responses. The gut mucosal barrier is disrupted in HIV disease, resulting in increased systemic exposure to microbial products such as Toll-Like Receptor (TLR) agonists. The association of enhanced systemic levels of TLR agonists and B cell dysfunction in HIV disease is not understood. This review discusses the potential role of microbial TLR agonists in the B cell depletion, enhanced autoantibody production and impaired responses to vaccination observed in HIV-infected hosts. Increased microbial translocation in HIV infection may drive B cells to produce autoantibodies and increase susceptibilities of B cells to apoptosis through activation-induced cell death. Determining the mechanisms of B cell perturbations in HIV disease will inform the design of novel strategies of improve immune responses to vaccines, reduce opportunistic infections and slow disease progression.
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