Hydrocortisone abrogates proliferation of T cells in autologous mixed lymphocyte reaction by rendering the interleukin-2 Producer T cells unresponsive to interleukin-1 and unable to synthesize the T-cell growth factor.
Hydrocortisone (HC-A) inhibited the proliferative response in the autologous mixed lymphocyte reaction (AMLR). The inhibitory activity became apparent 48 h after initiation of the cultures and was maintained throughout the culture period. T cells from cultures treated with HC-A showed a proliferative response to interleukin-2 (IL-2) of a similar degree as T cells from cultures not exposed to this drug. Hydrocortisone abrogated the production of IL-2 in AMLR. The addition of interleukin-1 (IL-1) to HC-A-treated cultures did not restore or increase the synthesis of IL-2, whereas IL-1 added to non HC-A treated cultures significantly enhanced the synthesis of IL-2, Finally, IL-2 but not IL-1 could overcome the abrogatory effect of hydrocortisone on proliferation of T cells induced by AMLR. These results indicate that HC-A inhibits proliferation of T cells in AMLR by causing the IL-2 producer T cells to become unresponsive to IL-1 and unable to synthesize IL-2. This drug does not, however, interfere with the process by which resting T cells acquire responsiveness to IL-2.
D006801:Humans; D006854:Hydrocortisone / Q000494:pharmacology*; D007166:Immunosuppressive Agents / Q000494:pharmacology; D007375:Interleukin-1; D007376:Interleukin-2 / Q000096:biosynthesis*; D008213:Lymphocyte Activation / Q000187:drug effects*; D007959:Lymphocyte Culture Test, Mixed; D008222:Lymphokines / Q000096:biosynthesis*; D011506:Proteins / Q000494:pharmacology; D013601:T-Lymphocytes / Q000276:immunology* / Q000378:metabolism
D007166:Immunosuppressive Agents; D007375:Interleukin-1; D007376:Interleukin-2; D008222:Lymphokines; D011506:Proteins; D006854:Hydrocortisone