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Related Experiment Videos

Responsiveness to HY antigen Ir gene complementation and target cell specificity

E Simpson, R D Gordon

    Immunological Reviews
    |January 1, 1977
    PubMed
    Summary

    Cytotoxic T cell responses to HY antigen in mice are restricted by H-2 genes. Immune response (Ir) gene complementation suggests multiple genes influence anti-HY immunity beyond H-2 K/D associations.

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    Area of Science:

    • Immunology
    • Genetics
    • T cell immunology

    Background:

    • Cytotoxic T lymphocyte (CTL) responses are crucial for adaptive immunity.
    • The HY antigen system involves T cell recognition of male-specific antigens.
    • H-2 restriction dictates T cell recognition of antigens presented by Major Histocompatibility Complex (MHC) molecules.

    Purpose of the Study:

    • To review H-2 restricted cytotoxic T cell responses to the HY antigen in mice.
    • To analyze mapping data associating H-2 K and/or D haplotypes with responses to male cells.
    • To investigate the role of Ir genes in HY antigen recognition.

    Main Methods:

    • Review of existing literature and mapping data.
    • Analysis of H-2 haplotypes (H-2b, H-2d, H-2k, H-2s) and their association with anti-HY responses.
    • Examination of Ir gene complementation in F1 mice and recombinant strains.

    Main Results:

    • H-2 restriction is a key feature of anti-HY cytotoxic T cell responses in mice.
    • Mapping data reveals associations between H-2 K/D genes and responses to male cells across various haplotypes.
    • Ir gene complementation is observed in F1 hybrids from non-responder parents and in a recombinant strain, indicating complex genetic control.

    Conclusions:

    • Anti-HY immunity involves H-2 K/D gene products and at least two, possibly more, Ir genes.
    • These Ir genes contribute to the overall immune response to HY antigen, acting in conjunction with MHC-restricted recognition.
    • The findings highlight the complex genetic architecture underlying T cell-mediated responses to self-minor antigens.

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