
IL-7-induced proliferation of peripheral Th17 cells is impaired in HAART-controlled HIV infection
Author(s) -
Sandra Côté,
Alana Stilla,
Stephanie C. Burke Schinkel,
Tamara Berthoud,
Jonathan B. Angel
Publication year - 2019
Publication title -
aids
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.195
H-Index - 216
eISSN - 1473-5571
pISSN - 0269-9370
DOI - 10.1097/qad.0000000000002164
Subject(s) - human immunodeficiency virus (hiv) , immunology , virology , medicine , immunopathology , sida , lentivirus , peripheral , viral disease
Th17 cells are key regulators of functional immunity in mucosal tissues, including the gut-associated lymphoid tissue (GALT), an important site of immune impairment in HIV infection. During HIV infection, Th17 cells are lost in large numbers from the GALT. Despite the recovery of peripheral CD4 T cells that accompanies suppression of viral replication with HAART, Th17 cells in GALT are not completely restored. IL-7 is essential for the survival and proliferation of T cells, but its signaling through its receptor IL-7Rα (CD127), is impaired in CD8 T cells and thymocytes during HIV infection. We set out to determine if decreased CD127 expression or impaired CD127 signaling may be the cause of Th17 impairment in HAART-controlled HIV infection.