Idiotypic and anti-idiotypic B-B cell interaction is controlled by major histocompatibility complex-restricted regulation.

Abstract:

:We have previously reported that the immunization of BALB/c mice with MOPC-104E myeloma protein (M104E) induced idiotype-specific Ly 1-negative B lymphocytes that had an ability to enhance idiotype-positive anti-dextran antibody production. It was also shown that the cell interaction between idiotypic and anti-idiotypic B lymphocytes was observed in a class II-restricted manner. The effect of monoclonal anti-class II antibody on the B-B cell interaction is investigated in this report. The addition of anti-I-A or anti-I-E monoclonal antibody into the B-B cell interaction system, from both BALB/c (H-2d) and BALB.K (H-2k), inhibited the enhanced antibody production mediated by idiotype-immune B lymphocytes. Interestingly, however, it was revealed that the anti-I-A and anti-I-E antibodies acted differently on each B-lymphocyte population. Pretreatment of an anti-idiotypic (idiotype-immune) enhancing B-lymphocyte population with anti-I-A antibody diminished its enhancing activity, while anti-I-E did not. On the other hand, pretreatment of dextran-immune antibody producing B cells with anti-I-A antibody showed no effect, while anti-I-E inhibited anti-dextran antibody production. When the enhancing B-lymphocyte population of F1 mice was treated with anti-I-A antibody specific for one of their parents' haplotypes, co-operation with the respective haplotype B cells was inhibited, but the other haplotype was not. The inhibitory effect of anti-class II antibodies could only be seen at the early phase of culture period. Taken together, the results of these experiments suggest that the class II antigens are concerned with the self-recognitive cell interaction among B lymphocytes in the frame of idiotype network systems.

journal_name

Immunology

journal_title

Immunology

authors

Bitoh S,Fujimoto S,Yamamoto H

subject

Has Abstract

pub_date

1989-04-01 00:00:00

pages

479-84

issue

4

eissn

0019-2805

issn

1365-2567

journal_volume

66

pub_type

杂志文章