CD101 genetic variants modify regulatory and conventional T cell phenotypes and functions.
Details
Serval ID
serval:BIB_A95D49E87527
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
CD101 genetic variants modify regulatory and conventional T cell phenotypes and functions.
Journal
Cell reports. Medicine
Working group(s)
Partners in Prevention HSV/HIV Transmission Study, and the Partners PrEP Study Teams
Contributor(s)
Celum C., Wald A., Lingappa J.R., Baeten J.M., Campbell M.S., Corey L., Coombs R.W., Hughes J.P., Magaret A., McElrath M.J., Morrow R., Mullins J.I., Coetzee D., Fife K., Were E., Essex M., Makhema J., Katabira E., Ronald A., Bukusi E., Cohen C., Kapiga S., Manongi R., Farquhar C., John-Stewart G., Kiarie J., Delany-Moretlwe S., Rees H., de Bruyn G., Gray G., McIntyre J., Mugo N.R., Celum C., Baeten J.M., Donnell D., Coombs R.W., Frenkel L., Hendrix C.W., Lingappa J.R., McElrath M.J., Fife K., Were E., Tumwesigye E., Ndase P., Katabira E., Ronald A., Bukusi E., Cohen C., Wangisi J., Campbell J., Tappero J., Kiarie J., Farquhar C., John-Stewart G., Mugo N.R.
ISSN
2666-3791 (Electronic)
ISSN-L
2666-3791
Publication state
Published
Issued date
15/06/2021
Peer-reviewed
Oui
Volume
2
Number
6
Pages
100322
Language
english
Notes
Publication types: Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
Publication Status: epublish
Publication Status: epublish
Abstract
We recently reported that the risk of sexually acquired HIV-1 infection is increased significantly by variants in the gene encoding CD101, a protein thought to modify inflammatory responses. Using blood samples from individuals with and without these variants, we demonstrate that CD101 variants modify the prevalence of circulating inflammatory cell types and show that CD101 variants are associated with increased proinflammatory cytokine production by circulating T cells. One category of CD101 variants is associated with a reduced capacity of regulatory T cells to suppress T cell cytokine production, resulting in a reduction in the baseline level of immune quiescence. These data are supported by transcriptomics data revealing alterations in the intrinsic regulation of antiviral pathways and HIV resistance genes in individuals with CD101 variants. Our data support the hypothesis that CD101 contributes to homeostatic regulation of bystander inflammation, with CD101 variants altering heterosexual HIV-1 acquisition by facilitating increased prevalence and altered function of T cell subsets.
Keywords
Adult, Antigens, CD/genetics, Antigens, CD/immunology, B-Lymphocytes/immunology, B-Lymphocytes/virology, Cell Lineage/immunology, Dendritic Cells/immunology, Dendritic Cells/virology, Female, Gene Expression Profiling, Gene Expression Regulation, Genetic Predisposition to Disease, HIV Infections/immunology, HIV Infections/transmission, HIV Infections/virology, HIV-1/immunology, Humans, Immunity, Innate, Immunophenotyping, Male, Monocytes/immunology, Monocytes/virology, Mutation, Phenotype, Receptors, CCR5/genetics, Receptors, CCR5/immunology, Receptors, CXCR4/genetics, Receptors, CXCR4/immunology, T-Lymphocytes, Regulatory/immunology, T-Lymphocytes, Regulatory/virology, CD101, HIV acquisition, T cell, host genetic variation, immune quiescence, inflammation, inflammatory homeostasis
Pubmed
Web of science
Open Access
Yes
Create date
28/02/2022 11:45
Last modification date
23/03/2024 7:24