In vivo and in vitro assessment of B-B cell interactions: inhibition of proliferation and antibody production of the CRIA B cells mediated by the surface immunoglobulins of anti-CRIA B cells

✍ Scribed by Jamila Ismaili

• Publisher: John Wiley and Sons
• Year: 1998
• Tongue: English
• Weight: 202 KB
• Volume: 28
• Category: Article
• ISSN: 0014-2980
• DOI: 10.1002/(sici)1521-4141(199804)28:04<1358::aid-immu1358>3.0.co;2-d

✦ Synopsis

In this work we have assessed the effect of cell surface anti-immunoglobulin (Ig) of anti-idiotypic B cells on their idiotypic counterparts in vivo and in vitro, as a surrogate for soluble anti-surface Ig, using the well-characterized anti-arsonate system. The response of A/J mice against the hapten arsonate coupled to keyhole limpet hemocyanin (ARS-KLH) is dominated by a closely related family of antibodies sharing the same determinant, named the CRIA idiotype. We show herein that a massive induction of anti-CRIA B cells, subsequent to immunization with the mAb 3665 (CRIA + , arsonate binding) coupled to KLH, mediated a strong and long-lasting inhibition of this dominant oligoclonal response to arsonate. The titer of antiarsonate antibodies remained, however, unchanged. Adoptive transfers to x-irradiated syngeneic mice showed that anti-CRIA-producing B cells have a direct effect on induction of inhibition. This was supported by the in vitro data where irradiated anti-CRIA B cells could induce inhibition of both antibody production and mitogenesis of their counterparts, CRIA B cells. This inhibitory effect could be decreased when the surface anti-surface Ig were hidden by the 3665 Fab fragments but not by anti-MHC class II antibodies. These interactions between CRIA and anti-CRIA B cells were solely Igh restricted and the inhibition was likely initiated by hyperaggregation of surface Ig. The presence of ARS-KLH-primed T cells in vitro could prevent the growth inhibition but not the suppression of antibody production. A similar profile was noticed in vitro for soluble polyclonal rabbit anti-CRIA Ab. All together, our data suggest that a negative signaling in B cells may be initiated by surface Ig of their idiotypic partners subsequent to a strong cross-linking of their surface Ig receptors.