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The Journal of Immunology, Vol 140, Issue 11 3844-3850, Copyright © 1988 by American Association of Immunologists
ARTICLES |
H Zaghouani, J Pene, V Rousseau and M Stanislawski
Immunology Laboratory, Institut de Recherches Scientifiques sur le Cancer, Villejuif, France.
We obtained a mAb, B5, defining a major crossreactive Id, the B5 Id, having an in vivo regulatory function. BALB/c mice immunized against the bacterial dextran Ag B1355S produce lambda 1-bearing anti-alpha (1- 3) glucosidic linkage of dextran B1355S (DEX) antibodies. Of these antibodies 30% expressed the B5 Id determinant. As was observed for the IdX-Id, B5 idiotope expression was also linked to the BALB/c H chain allotype. The antibody family expressing the B5 Id included IdX+ as well as IdX- defined monoclonal anti-alpha (1-3) DEX antibodies. Injection into BALB/c mice of mAb B5 conjugated to keyhole limpet hemocyanin led to enhancement of serum anti-alpha (1-3) DEX antibody synthesis, and to a strong increase in B5+ Ig lacking dextran-binding activity. IdX+ serum Ig were also increased in these mice. Injection of this mAb into allotype congenic nonresponder C.B20 mice induced a significant serum lambda 1-bearing anti-alpha (1-3) dextran antibody response (5 to 50 micrograms/ml). However, in A/J nonresponder mice, a similar treatment induced only the dextran-nonbinding component, which reached high levels (approximately 7 mg/ml) in the sera of these mice. In the majority of these A/J mice, we detected a specific anti-(4- hydroxy-5-iodo-3-nitrophenyl)acetyl antibody response characterized by B5 Id-positive antibodies. This observation can be explained by an in vivo regulatory idiotope-mediated cross-regulation.
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