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Mechanisms regulating expansion of CD 8+ T cells during HIV ‐1 infection
Author(s) -
Nasi A.,
Chiodi F.
Publication year - 2018
Publication title -
journal of internal medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.625
H-Index - 160
eISSN - 1365-2796
pISSN - 0954-6820
DOI - 10.1111/joim.12722
Subject(s) - inflammation , immune system , immunology , homing (biology) , t cell , cytokine , medicine , biology , cytotoxic t cell , lymphatic system , in vitro , ecology , biochemistry
Abstract Abnormal immune activation and expansion of CD 8+ T cells, especially of memory and effector phenotypes, take place during HIV ‐1 infection, and these abnormal features persist during administration of antiretroviral therapy ( ART ) to infected patients. The molecular mechanisms for CD 8+ T‐cell expansion remain poorly characterized. In this article, we review the literature addressing features of CD 8+ T‐cell immune pathology and present an integrated view on the mechanisms leading to abnormal CD 8+ T‐cell expansion during HIV ‐1 infection. The expression of molecules important for directing the homing of CD 8+ T cells between the circulation and lymphoid tissues, in particular CCR 5 and CXCR 3, is increased in CD 8+ T cells in circulation and in inflamed tissues during HIV ‐1 infection; these disturbances in the homing capacity of CD 8+ T cells have been linked to increased CD 8+ T‐cell proliferation. The production of IL ‐15, a cytokine responsible for physiological proliferation of CD 8+ T cells, is increased in lymphoid tissues during HIV ‐1 infection as result of microbial translocation and severe inflammation. IL ‐15, and additional inflammatory cytokines, may lead to deregulated proliferation of CD 8+ T cells and explain the accumulation of CD 8+ T cells in circulation. The decreased capacity of CD 8+ T cells to localize to gut‐associated lymphoid tissue also contributes to the accumulation of these cells in blood. Control of inflammation, through ART administration during primary HIV ‐1 infection or therapies aimed at controlling inflammation during HIV ‐1 infection, is pivotal to prevent abnormal expansion of CD 8+ T cells during HIV ‐1 infection.