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Effect of Synthetic beta-Endorphin-Like Peptide Immunorphin on Human T Lymphocytes

E. V. Navolotskaya*, N. V. Malkova, T. A. Zargarova, T. N. Lepikhova, S. B. Krasnova, and V. M. Lipkin

Branch of the Shemyakin and Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Sciences, pr. Nauki 6, Pushchino, Moscow Region, 142290 Russia; fax: (0967) 79-0527; E-mail: navolots@fibkh.serpukhov.su

* To whom correspondence should be addressed.

Received March 22, 2001; Revision received June 8, 2001
beta-Endorphin and the synthetic beta-endorphin-like decapeptide Ser-Leu-Thr-Cys-Leu-Val-Lys-Gly-Phe-Tyr (referred to as immunorphin), corresponding to the sequence 364-373 of the CH3 domain of human immunoglobulin G heavy chain, were shown to stimulate concanavalin A-induced proliferation of T lymphocytes from the blood of healthy donors. [Met5]Enkephalin and the antagonist of opioid receptors naloxone examined in parallel were inactive. The stimulating effect of beta-endorphin and immunorphin on T lymphocyte proliferation is not inhibited by naloxone. Studies on receptor binding of 125I-labeled immunorphin to T lymphocytes revealed that it binds with high affinity to naloxone-insensitive receptors (Kd = 7.0 ± 0.3 nM). Unlabeled immunorphin completely inhibits 125I-labeled beta-endorphin specific binding to naloxone-insensitive receptors on T lymphocytes (Ki = 0.6 ± 0.1 nM). Thus, beta-endorphin and immunorphin interact with common naloxone-insensitive receptors on T lymphocytes.
KEY WORDS: beta-endorphin, naloxone, immunoglobulin G (IgG), peptides, receptors, T lymphocytes