Microbial TLR Agonists and Humoral Immunopathogenesis in HIV DiseaseXiaocong Yu1, Zihai Li2, Zhenxian Zhou3, J Michael Kilby2 and Wei Jiang2
1Department of Medicine, Harvard Medical School, Boston, MA 02215, USA
2Department of Microbiology and Immunology, Department of Medicine, Division of Infectious Diseases, Medical University of South Carolina, BSB214E, Charleston, SC, 29425, USA
3NanJing Second Hospital, Infectious Diseases, NanJing, China
- *Corresponding Author:
- Wei Jiang
Department of Microbiology and Immunology
Department of Medicine, Division of Infectious Diseases
Medical University of South Carolina
BSB214E, Charleston, SC, 29425, USA
E-mail: [email protected]
Received date: December 20, 2012; Accepted date: January 29, 2013; Published date: February 02, 2013
Citation: Yu X, Jiang W, Li Z, Kilby JM, Zhou Z (2013) Microbial TLR Agonists and Humoral Immunopathogenesis in HIV Disease. Epidemiol 3:120. doi: 10.4172/2161-1165.1000120
Copyright: © 2013 Yu X, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Although 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.