Ia-positive stimulator cells are required in primary, but not in secondary, mixed leukocyte reactions against H-2K and H-2D differences.
Open Access
- 1 May 1981
- journal article
- research article
- Published by Oxford University Press (OUP) in The Journal of Immunology
- Vol. 126 (5) , 1774-1779
- https://doi.org/10.4049/jimmunol.126.5.1774
Abstract
The expression of I region gene products on stimulator cells in primary and secondary MLR directed against differences determined by the K or D regions of the H-2 gene complex was examined in B10-congenic mice. Treatment of the stimulator cells with anti-Ia antisera and complement (C) eliminates stimulation in primary MLR against K or D region gene products, indicating that the stimulator cells must express Ia antigens on their membranes. Further, stimulation in primary MLR against D region antigens is abolished by treatment of the stimulator cells with C and antisera against either I-A or I-E subregion products, but not by treatment of stimulator cells with C and antisera against I-J subregion products. Therefore, these stimulator cells express on their membranes both I-A and I-E subregion gene products, but not I-J subregion gene products. In contrast, in secondary MLR against K or D region gene products, treatment of stimulator cells with anti-Ia antisera and C does not abolish stimulation, indicating that Ia-negative cells can stimulate primed responder cells. These results indicate that the mechanisms of cell-cell recognition necessary in secondary MLR against K or D region gene products are different from those in primary MLR to the same products.This publication has 2 references indexed in Scilit:
- Cellular and genetic control of antibody responses in vitro. III. Immune response gene regulation of accessory cell functionThe Journal of Experimental Medicine, 1978
- Properties of the antigen-specific suppressive T-cell factor in the regulation of antibody response of the mouse. IV. Special subregion assignment of the gene(s) that codes for the suppressive T-cell factor in the H-2 histocompatibility complex.The Journal of Experimental Medicine, 1976