Regulation of Interleukin 2 Receptor Expression by Interleukin 2 |
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Authors: | A. B. RESKE-KUNZ,D. VON,STELDERN E. RÜ DE,T. DIAMANTSTEIN |
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Affiliation: | Institute of Immunology, University of Mainz, Mainz, Department of Medical Microbiology and Immunology, University of Ulm, Ulm, and Immunology Research Unit, Free University of Berlin, Berlin, FRG |
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Abstract: | ![]() The regulatory influence of Interleukin 2 (IL-2) on the expression of IL-2 receptors (IL-2R) was studied using long-term cultured T-cell lines and recombinant IL-2 (r-IL-2). Three T-cell lines with different growth requirements were used as model systems: insulin-specific BK-BI-1.2 cells express IL-2R transiently after antigenic restimulation, ovalbumin-reactive BK-OVA-1R cells express IL-2R permanently, and BK-BI-2.6.C6 cells bear IL-2R constitutively but do not exhibit antigen reactivity. All three T-cell lines exhibited the property of increased IL-2R expression in the presence of r-IL-2, as tested by cytofluorometry employing monoclonal antibody AMT-13 directed at the murine IL-2R. IL-2R density was influenced selectively by r-IL-2, because the level of Thy-1.2 molecules was similar in the presence and absence of r-IL-2. With BK-BI-2.6.C6 cells, r-IL-2 was shown to upregulate high-affinity receptors. Since BK-BI-2.6.C6 and BK-OVA-1R cells were grown in the absence of feeder cells, these data show that r-IL-2 can regulate the expression of its own receptor without the participation of monokines. Results obtained with the T-cell line BK-BI-1.2, representing insulin-specific T cells with transient IL-2R expression, show that the presence of r-IL-2 did not prevent a decline in IL-2R density occurring on day 5 after antigenic stimulus. This indicates that additional mechanisms besides antigen- and IL-2-induced IL-2R upregulation are operative in controlling IL-2R density on the cell surface. |
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