THE EXPRESSION OF H‐2K, H‐2D AND Ia ANTIGENS IN VARIOUS TISSUES AS ASSESSED IN Fc RECEPTOR INHIBITION SYSTEMS
Open Access
- 1 October 1975
- journal article
- Published by Wiley in International Journal of Immunogenetics
- Vol. 2 (5-6) , 389-401
- https://doi.org/10.1111/j.1744-313x.1975.tb00547.x
Abstract
SUMMARY: The ability of mouse alloantibody to inhibit EA rosette formation and antibody‐dependent cell‐mediated cytotoxicity (ADCC) was used to study the expression of H‐2K, Ia and H‐2D antigens in various tissues. As previously reported antisera against each of these groups of antigens inhibited B lymphocyte EA rosette formation. Continuing studies confirmed these observations but established that quantitative differences may exist in the ease with which antibody against antigens in each region can inhibit EA rosettes: anti H‐2D and anti‐Ia seemed stronger relative to their cytotoxic titres than anti H‐2K. Possible reasons for this are discussed. When rosette forming cells from other tissues were studied, (bone marrow cells, peritoneal macrophages and tumour cells), they were inhibited by anti H‐2K and anti H‐2D sera but not by anti Ia sera, presumably reflecting the restricted distribution of Ia antigens in those tissues.Inhibition of ADCC by various antisera reflected qualitatively and quantitatively the expression of H‐2 antigens in various tissues: whereas effector cell activity in spleen, bone marrow, or peritoneal cell populations was inhibited by anti H‐2 or anti‐Ia sera, the amount of inhibition observed with anti‐Ia was much less when the tissue expressed little Ia antigen (bone marrow) than when it expressed abundant Ia antigen (spleen). The ability of cytotoxicity inhibition to detect antibody coated cells was used to assess the relative amount of Ia antigen on thymus and on lymph node cells, showing significant amounts of Ia antigen on thymus cells. Fc receptor inhibition studies may thus be useful as new approaches to the study of the expression of the antigens of the major histocompatibility complex.Keywords
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