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Role of T-cell trafficking in the pathogenesis of HIV disease

Cicala, Claudia; Arthos, James; Fauci, Anthony S.

Current Opinion in HIV and AIDS: March 2019 - Volume 14 - Issue 2 - p 115–120
doi: 10.1097/COH.0000000000000529
T-CELLS IN HIV INFECTION: Edited by Mathias Lichterfeld and Tony Kelleher
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Purpose of review Trafficking of lymphocytes into and between gut inductive and effector sites of the gut tissues is regulated by integrin α4β7. Recent findings that describe the central role of α4β7hi CD4+ T cells in HIV pathogenesis, and the possibility of targeting these cells to prevent or treat HIV infection will be reviewed.

Recent findings Recent reports indicate that the frequency of α4β7hi CD4+ T cells is directly correlated with the risk of HIV acquisition and CD4+ T-cell decline post infection. MAdCAM -mediated signaling through α4β7, in the presence of retinoic acid, supports viral replication in recently activated naïve CD4+ T cells. Treatment of HIV-infected patients with vedolizumab, an α4β7 antagonist, is well tolerated, and reduces the size and number of lymphoid aggregates in gut associated lymphoid tissues.

Summary Integrin α4β7 underlies one of the principal mechanisms that CD4+ T cells employ to traffic to the gut. It also defines a subset of cells that play a significant role in HIV transmission and pathogenesis. Understanding how α4β7 facilitates gut homing may provide insight into key aspects of HIV transmission, pathogenesis, and the formation of viral reservoirs. Targeting α4β7 may have utility in the prevention and treatment of HIV infection.

Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland, USA

Correspondence to James Arthos, Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA. Tel: +1 301 761 6684; fax: +1 301 4024122; e-mail: jarthos@niaid.nih.gov

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