Genetic control of allogeneic interactions in the guinea pig. I. Evidence from mixed leukocyte culture and normal lymphocyte transfer reactions

Geczy, C.L.; Geczy, A.F.

European Journal of Immunology 8(4): 236-243


ISSN/ISBN: 0014-2980
PMID: 149667
DOI: 10.1002/eji.1830080404
Accession: 068522300

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The role of gene products of the B region of the guinea pig major histocompatibility complex (MHC) in the production of mixed leukocyte culture mitogenic factor (MLC-MF) was investigated. Lymphoid cells of partially inbred and outbred guinea pigs which bear the serologically defined B.2 alloantigen, respond poorly or not at all in the guinea pig MLC. Since MLC culture supernatants from B.2+ 3rd party lymphoid cells, it is possible that either B.2+ lymphoid cells do not elaborate MLC-MF or they produce a suppressor factor. Genetic studies demonstrated that genes closely linked to or identical with the gene(s) coding for the B.2 alloantigen, regulate MLC unresponsiveness. By contrast to their unresponsiveness in the MLC, B.2+ lymphoid cells produce migration inhibition factor at least as well as cells bearing the B.1 and B.3 specificities, and they respond in vitro to antigens which are under the control of specific immune response genes. The genetic restrictions for responsiveness in the MLC are supported by in vivo studies which strongly suggest that the degree of interaction between allogeneic lymphoid cells (normal lymphocyte transfer, immune lymphocyte transfer and direct reactions) are also under the control of genes which map in or near the B region of the guinea pig MHC. Preliminary evidence suggests that the B.2+ donor cells rather than B.2+ host cells are responsible for initiating the unresponsiveness associated with the normal lymphocyte transfer reaction. These studies should provide a basis for the reproducible production of MLC-MF and a system for the study of some molecular aspects of allogeneic interactions in vitro and in vivo.