Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27851927
&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215
Aire Inhibits the Generation of a Perinatal Population of
Interleukin-17A-Producing ?? T Cells to Promote Immunologic Tolerance
#MMPMID27851927
Fujikado N
; Mann AO
; Bansal K
; Romito KR
; Ferre EMN
; Rosenzweig SD
; Lionakis MS
; Benoist C
; Mathis D
Immunity
2016[Nov]; 45
(5
): 999-1012
PMID27851927
show ga
Aire's primary mechanism of action is to regulate transcription of a battery of
genes in medullary thymic epithelial cells (mTECs) and, consequently, negative
selection of effector T cells and positive selection of regulatory T cells. We
found that Aire-deficient mice had expanded thymic and peripheral populations of
perinatally generated IL-17A(+)V?6(+)V?1(+) T cells, considered to be "early
responders" to tissue stress and drivers of inflammatory reactions.
Aire-dependent control of Il7 expression in mTECs regulated the size of thymic
IL-17A(+)V?6(+)V?1(+) compartments. In mice lacking Aire and ?? T cells, certain
tissues typically targeted in the "Aire-less" disease, notably the retina, were
only minimally infiltrated. IL-17A(+)V?6(+)V?1(+) cells were present in the
retina of wild-type mice and expanded very early in Aire-deficient mice. A
putatively parallel population of IL-17A(+)V?9(+)V?2(+) T cells was increased in
humans lacking Aire. Thus, Aire exerts multi-faceted autoimmune control that
extends to a population of innate-like T cells.
free
free
free
