Journal
PLOS ONE
Volume 7, Issue 3, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0032964
Keywords
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Categories
Funding
- Canadian Institutes of Health [MOP-82849, HBF-82849]
- Fondation du CHUM
- Fonds de la Recherche en Sante Que bec (FRSQ)
- French Institut National de la Sante et de la Recherche Medicale (INSERM)
- Agence Nationale de Recherche sur le SIDA (ANRS)
- Fondation de France
- Universite de Montreal
- CIHR [HOP-103230, MOP-93770]
- ANRS/FRSQ
- FRSQ
- INSERM
- FRSQ-SIDA Infectious Diseases Network
- Canadian HIV Trials Network-CIHR [CTN 257]
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CD4(+) T-cells from gut-associated lymphoid tissues (GALT) are major targets for HIV-1 infection. Recruitment of excess effector CD8(+) T-cells in the proximity of target cells is critical for the control of viral replication. Here, we investigated the colocalization potential of HIV-specific CD8(+) and CD4(+) T-cells into the GALT and explored the role of retinoic acid (RA) in regulating this process in a cohort of HIV-infected subjects with slow disease progression. The expression of the gut-homing molecules integrin beta 7, CCR6, and CXCR3 was identified as a signature for HIV-specific but not CMV-specific CD4(+) T-cells thus providing a new explanation for their enhanced permissiveness to infection in vivo. HIV-specific CD8(+) T-cells also expressed high levels of integrin b7 and CXCR3; however CCR6 was detected at superior levels on HIV-specific CD4(+) versus CD8(+) T-cells. All trans RA (ATRA) upregulated the expression of integrin beta 7 but not CCR6 on HIV-specific T-cells. Together, these results suggest that HIV-specific CD8(+) T-cells may colocalize in excess with CD4+ T-cells into the GALT via integrin beta 7 and CXCR3, but not via CCR6. Considering our previous findings that CCR6(+)CD4(+) T-cells are major cellular targets for HIV-DNA integration in vivo, a limited ability of CD8(+) T-cells to migrate in the vicinity of CCR6(+)CD4(+) T-cells may facilitate HIV replication and dissemination at mucosal sites.
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