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Related Experiment Videos

Delayed-type hypersensitivity to elastase-soluble lung peptides in the tight-skin (Tsk) mouse.

F A DeLustro, A M Mackel, E C LeRoy

    Cellular Immunology
    |October 1, 1983
    PubMed
    Summary

    Aging impacts the immune response to connective tissue antigens in tight-skin (Tsk) mice. Tsk/+ mice develop delayed-type hypersensitivity (DTH) to lung peptides, suggesting an autoimmune component in this aging mouse model.

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    Area of Science:

    • Immunology
    • Connective Tissue Diseases
    • Aging Research

    Background:

    • The tight-skin (Tsk) mouse mutant exhibits connective tissue abnormalities.
    • Understanding immune responses in aging Tsk mice is crucial for disease modeling.

    Purpose of the Study:

    • To investigate the development of immunity to homologous connective tissue antigens in aging Tsk/+ mice.
    • To characterize the nature of the immune response, including delayed-type hypersensitivity (DTH).

    Main Methods:

    • Assessing DTH responses to elastase-solubilized lung peptides and collagens in Tsk/+ and normal (+/+) mice of various ages.
    • Adoptive transfer of spleen cells from Tsk/+ mice to normal recipients.
    • Inhibition of DTH transfer using anti-Thy 1.2 antibodies and complement.

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  • Serological analysis for antibody activity against tested antigens.

    • Main Results:

    • Tsk/+ mice showed a developing DTH response to lung peptides from 10 to 22 weeks of age.
    • No significant DTH response was observed against type I or IV collagen in Tsk/+ mice.
    • Normal littermates did not respond to any tested antigens.
    • DTH reactivity was adoptively transferable with Tsk/+ spleen cells and T-cell dependent (reduced by anti-Thy 1.2 treatment).
    • No detectable antibody activity was found in Tsk/+ or +/+ mice.

    Conclusions:

    • Aging Tsk/+ mice develop a T-cell mediated delayed-type hypersensitivity to connective tissue antigens, specifically lung peptides.
    • This immune response is distinct from antibody-mediated autoimmunity.
    • The findings correlate with pathological manifestations in the Tsk/+ mutant mouse, suggesting an autoimmune component in its aging phenotype.