Titre
MHC-II-independent CD4+ T cells induce colitis in immunodeficient RAG-/- hosts.
Type
article
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Périodique
Auteur(s)
Trobonjaca, Z.
Auteure/Auteur
Leithäuser, F.
Auteure/Auteur
Möller, P.
Auteure/Auteur
Bluethmann, H.
Auteure/Auteur
Koezuka, Y.
Auteure/Auteur
MacDonald, H.R.
Auteure/Auteur
Reimann, J.
Auteure/Auteur
Liens vers les personnes
Liens vers les unités
ISSN
0022-1767
Statut éditorial
Publié
Date de publication
2001
Volume
166
Numéro
6
Première page
3804
Dernière page/numéro d’article
3812
Peer-reviewed
Oui
Langue
anglais
Résumé
CD4(+) alpha beta T cells from either normal C57BL/6 (B6) or MHC-II-deficient (A alpha(-/-) or A beta(-/-)) B6 donor mice engrafted into congenic immunodeficient RAG1(-/-) B6 hosts induced an aggressive inflammatory bowel disease (IBD). Furthermore, CD4(+) T cells from CD1d(-/-) knockout (KO) B6 donor mice but not those from MHC-I(-/-) (homozygous transgenic mice deficient for beta(2)-microglobulin) KO B6 mice induced a colitis in RAG(-/-) hosts. Abundant numbers of in vivo activated (CD69(high)CD44(high)CD28(high)) NK1(+) and NK1(-) CD4(+) T cells were isolated from the inflamed colonic lamina propria (cLP) of transplanted mice with IBD that produced large amounts of TNF-alpha and IFN-gamma but low amounts of IL-4 and IL-10. IBD-associated cLP Th1 CD4(+) T cell populations were polyclonal and MHC-II-restricted when derived from normal B6 donor mice, but oligoclonal and apparently MHC-I-restricted when derived from MHC-II-deficient (A alpha(-/-) or A beta(-/-)) B6 donor mice. cLP CD4(+) T cell populations from homozygous transgenic mice deficient for beta(2)-microglobulin KO B6 donor mice engrafted into RAG(-/-) hosts were Th2 and MHC-II restricted. These data indicate that MHC-II-dependent as well as MHC-II-independent CD4(+) T cells can induce a severe and lethal IBD in congenic, immunodeficient hosts, but that the former need the latter to express its IBD-inducing potential.
Sujets
PID Serval
serval:BIB_18264
PMID
Date de création
2007-11-19T11:12:16.633Z
Date de création dans IRIS
2025-05-20T13:42:42Z