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Regulation of Interleukin 2 Receptor Expression by Interleukin 2
Author(s) -
RESKEKUNZ A. B.,
STELDERN D.,
RÜDE E.,
DIAMANTSTEIN T.
Publication year - 1986
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1986.tb02006.x
Subject(s) - interleukin 2 , receptor , microbiology and biotechnology , biology , cell culture , t cell , interleukin 4 , chemistry , cytokine , immune system , immunology , biochemistry , genetics
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 constilutively 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 cyto‐fluoromelry 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‐IR 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.