You are here:
| Reference : Autoimmunity following neonatal tolerance to alloantigens: role of donor I-A and I-E mol... |
| Scientific journals : Article | |||
| Life sciences : Biochemistry, biophysics & molecular biology Life sciences : Genetics & genetic processes | |||
| http://hdl.handle.net/2268/4856 | |||
| Autoimmunity following neonatal tolerance to alloantigens: role of donor I-A and I-E molecules | |
| English | |
| Kramar, G. [World Health Organization-Immunology Research and Training Center, Department of Pathology, CMU, 1211 Geneva 4, > > > >] | |
Schurmans, Stéphane  [Université Libre de Bruxelles - ULB > Institut de Recherche Interdisciplinaire en Biologie Humaine et Nucléaire, Institut de Biologie et de Médecine Moléculaire > > >] | |
| Berney, M. [World Health Organization-Immunology Research and Training Center, Department of Pathology, CMU, 1211 Geneva 4, > > > >] | |
| Izui, S. [World Health Organization-Immunology Research and Training Center, Department of Pathology, CMU, 1211 Geneva 4, > > > >] | |
| del Giudice, G. [Institute of Biochemistry, University of Lausanne, 1066 Epalinges, Switzerland > > > >] | |
| Lambert, P. H. [> >] | |
| 1995 | |
| Journal of Autoimmunity | |
| Academic Press | |
| 8 | |
| 177-192 | |
| International | |
| 0896-8411 | |
| London | |
| United Kingdom | |
| [en] Autoimmunity ; neonatal tolerance ; alloantigens ; molecules | |
| [en] The injection of semi-allogeneic F1 spleen cells into newborn mice of a parental strain induces a state of immune tolerance characterized by anti-donor CTL unresponsiveness and the appearance of a transient SLE-like autoimmune syndrome associating autoantibody production, hypergammaglobulinemia, splenomegaly and glomerulonephritis. Our previous experiments have demonstrated that host Th2-like CD4+ T lymphocytes activate donor F1 B cells persisting in the host to produce autoantibodies, and that this cellular interaction relies on the presence of alloMHC class II molecules on donor B cells. In order to investigate the role and the involvement of MHC alloantigens in the cellular T(host)-B(donor) interaction, newborn C57BL/6 (B6) mice were injected with F1 spleen cells differing from the host at the level of defined portions of the MHC class I (K) or class II (I-A and I-E) molecules. B6 mice injected at birth with spleen cells from different F1 strains were tolerant to each alloantigen (alloAg) tested, as assessed by specific anti-donor CTL unresponsiveness. However, the SLE-like autoimmune syndrome only developed in B6 mice injected at birth with F1 spleen cells differing at the level of MHC class II I-A or I-E molecules. Autoantibodies appeared later in B6 mice neonatally tolerized to I-E alloAg than those detected in B6 mice neonatally tolerized to I-A alloAg. These results show that the SLE-like autoimmune disease that develops concomitantly to neonatally-induced tolerance to alloAg is the consequence of cognate T host-B donor cellular interactions triggered by even minute differences in the MHC class II I-A or MHC class II I-E molecules | |
| Researchers ; Professionals | |
| http://hdl.handle.net/2268/4856 | |
| 10.1006/jaut.1995.0014 |
| File(s) associated to this reference | ||||||||||||||
|
Fulltext file(s):
| ||||||||||||||
All documents in ORBi are protected by a user license.
