par Slaoui, Moncef;Urbain, Jacques 
;Lowy, A.;Monroe, J. G.;Willems, Fabienne ;Benacerraf, B.;Greene, M.
Référence The Journal of immunology, 136, 6, page (1968-1973)
Publication Publié, 1986-03
;Lowy, A.;Monroe, J. G.;Willems, Fabienne ;Benacerraf, B.;Greene, M.Référence The Journal of immunology, 136, 6, page (1968-1973)
Publication Publié, 1986-03
Article révisé par les pairs
| Résumé : | The ABA-specific antibody response of A/J mice (Igh Ie) is dominated by the CRIa idiotype. In contrast, BALB/c mice (Igh Ia) do not produce CRIa-bearing anti-ABA antibodies after antigenic challenge. We have shown previously that treatment with rabbit anti-CRIa (R-anti-CRIa) induces the expression of "CRIa-like" anti-arsonate antibodies in BALB/c mice. In the present report, we demonstrate that R-anti-CRIa treatment enables BALB/c mice to respond to A/J ABA-specific first-order suppressor molecules (TsF1). Manipulated BALB/c also produced CRIa bearing ABA-specific immune response. Thus, R-anti-CRIa treatment induces a change in the characteristic Igh restriction pattern typically seen in this system. These data suggest that Igh restriction in the ABA-specific T suppressor cell pathway is the result of CRIa+ dominance in the T suppressor cell response of A/J mice. The effectiveness of idiotypic manipulation in inducing the expression of a given idiotype at both the B cell and T suppressor cell levels is discussed. |
