In:
The Journal of Immunology, The American Association of Immunologists, Vol. 190, No. 1_Supplement ( 2013-05-01), p. 136.26-136.26
Kurzfassung:
Glucocorticoid-Induced TNF Receptor family-related protein Ligand (GITR-L) is expressed on antigen presenting cells. Surprisingly, GITR-L−/−Rag−/− mice develop a markedly milder colitis than Rag−/− mice upon transferring CD4+CD45RBhi T cells or by administering agonistic anti-CD40 antibody. In both colitis models as well as in a peritonitis model a reduced number of Ly6C+CD11b+MHCII+ macrophages was found in the inflamed sites of GITR-L−/− mice. By contrast, the number of non-differentiated monocytes was approximately three-fold higher in the spleen of inflamed GITR-L−/−Rag−/− mice than in Rag−/− mice. The formation of an active dimer of the angiotensin II type 1 receptor (AT-1) by splenic monocytes, which regulates their egress, was dynamically affected by the GITR-L deficiency. Infusion of Angiotensin II caused retention of splenic monocytes in GITR-L−/− but not wt mice. We conclude that upon induction of inflammation GITR-L regulates egress of monocytes from the spleen, thus impacting intestinal homeostasis in mice.
Materialart:
Online-Ressource
ISSN:
0022-1767
,
1550-6606
DOI:
10.4049/jimmunol.190.Supp.136.26
Sprache:
Englisch
Verlag:
The American Association of Immunologists
Publikationsdatum:
2013
ZDB Id:
1475085-5