par Dubey, C;Kuhn, Josée 
;Wissing, Karl Martin ;Nisol, F;Chavez, Marcella;Bazin, H;Goldman, Michel ;Druet, P;Bellon, B
Référence Journal of autoimmunity, 5, 5, page (629-640)
Publication Publié, 1992-10
;Wissing, Karl Martin ;Nisol, F;Chavez, Marcella;Bazin, H;Goldman, Michel ;Druet, P;Bellon, BRéférence Journal of autoimmunity, 5, 5, page (629-640)
Publication Publié, 1992-10
Article révisé par les pairs
| Résumé : | A model of neonatal allotolerance was developed in rats. Brown-Norway (BN) neonates injected with semi-allogeneic (BN x Lewis) F1 hybrid spleen cells express a long-lasting chimerism and exhibit polyclonal B cell activation demonstrated by hyperimmunoglobulinemia affecting mainly IgE and IgG1, anti-laminin and anti-DNA autoantibodies as well as glomerulonephritis and anti-hapten antibodies. These abnormalities are autoregulated although the chimerism persists. In contrast, Lewis (LEW) neonates injected with semi-allogeneic (BN x LEW) F1 hybrid spleen cells exhibit a very short-lasting chimerism and transient activation of B cells, as reflected by increased allo-class II antigen expression, but do not develop an autoimmune disease. The autoimmune syndrome observed in BN rats is similar to that reported in mice during host-versus-graft reaction. Similarities between the drug-induced models of autoimmunity and allogeneic reactions in BN rats are also striking. The susceptibility of BN rats and the resistance of LEW rats to these autoimmune diseases might respectively reflect the involvement of TH2-like or of TH1-like subsets. |
