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Med Hypotheses. 2016 Mar;88:53-6. doi: 10.1016/j.mehy.2016.01.009. Epub 2016 Jan 23.

Systemic activation of the immune system in HIV infection: The role of the immune complexes (hypothesis).

Author information

1
Institute of Ecology and Genetics of Microorganisms UB RAS, Perm, Russia; Perm State University, Perm, Russia. Electronic address: bioqueen@mail.ru.
2
Institute of Ecology and Genetics of Microorganisms UB RAS, Perm, Russia; Perm State University, Perm, Russia.
3
Perm Regional Centre for Protection against AIDS and Infectious Diseases, Perm, Russia; Perm State University, Perm, Russia.

Abstract

Currently, immune activation is proven to be the basis for the HIV infection pathogenesis and a strong predictor of the disease progression. Among the causes of systemic immune activation the virus and its products, related infectious agents, pro-inflammatory cytokines, and regulatory CD4+ T cells' decrease are considered. Recently microbial translocation (bacterial products yield into the bloodstream as a result of the gastrointestinal tract mucosal barrier integrity damage) became the most popular hypothesis. Previously, we have found an association between immune complexes present in the bloodstream of HIV infected patients and the T cell activation. On this basis, we propose a significantly modified hypothesis of immune activation in HIV infection. It is based on the immune complexes' participation in the immunocompetent cells' activation. Immune complexes are continuously formed in the chronic phase of the infection. Together with TLR-ligands (viral antigens, bacterial products coming from the damaged gut) present in the bloodstream they interact with macrophages. As a result macrophages are transformed into the type II activated forms. These macrophages block IL-12 production and start synthesizing IL-10. High level of this cytokine slows down the development of the full-scale Th1-response. The anti-viral reactions are shifted towards the serogenesis. Newly synthesized antibodies' binding to viral antigens leads to continuous formation of the immune complexes capable of interacting with antigen-presenting cells.

PMID:
26880638
DOI:
10.1016/j.mehy.2016.01.009
[Indexed for MEDLINE]

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