Titre
Nuclear myxovirus-resistance protein Mx is a minor histocompatibility antigen
Type
article
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Auteur(s)
Speiser, D. E.
Auteure/Auteur
Zurcher, T.
Auteure/Auteur
Ramseier, H.
Auteure/Auteur
Hengartner, H.
Auteure/Auteur
Staeheli, P.
Auteure/Auteur
Haller, O.
Auteure/Auteur
Zinkernagel, R. M.
Auteure/Auteur
Liens vers les personnes
Liens vers les unités
ISSN
0027-8424
Statut éditorial
Publié
Date de publication
1990-03
Volume
87
Numéro
5
Première page
2021
Dernière page/numéro d’article
5
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Mar
Research Support, Non-U.S. Gov't --- Old month value: Mar
Résumé
Minor histocompatibility antigens (MiHAgs) cause slow-to-rapid organ transplant rejection by immunocompetent hosts and mild-to-severe graft-versus-host reactions in immunosuppressed hosts. MiHAgs are allelic forms of major histocompatibility complex (MHC) class I-restricted self-antigens recognized by cytotoxic T cells and usually are defined immunogenetically. Although structurally not identified as yet, it is assumed that MiHAgs are internal cell antigens that are processed and then presented by MHC class I proteins similar to viral antigens. To define a MiHAg both molecularly and functionally, we took advantage of the allelic difference of the structurally characterized intracellular myxovirus-resistance protein (Mx) and investigated its antigenicity. Skin grafts from congenic Mx+ mice carrying the functional Mx1 gene were rejected by mice lacking a functional Mx1 gene (Mx- mice). In parallel, cytotoxic MHC class I-restricted effector T cells specific for Mx protein and the H-2Kk antigen (but not for several other allelic H-2 antigens) were strongly induced in Mx- mice immunized with spleen cells from interferon-treated Mx+ mice. These data show that allelic forms of cell internal proteins presented by MHC class I may act as MiHAgs.
Sujets
PID Serval
serval:BIB_3A5E30D4D470
PMID
Date de création
2008-01-28T10:33:02.271Z
Date de création dans IRIS
2025-05-20T20:18:03Z