![]() ![]() 6, 7 It was reported that lymphocytes infiltrating inflamed tissues released β-endorphin, which produced analgesia by acting on opioid receptors (7-transmembrane segment, Gi/o-protein–coupled receptors) expressed on peripheral afferent nerves. 4, 5 The interactions between the nervous and immune systems are indicated by the ability of immune cells and neurons to synthesize cytokines, neuropeptides, and hormones. 3 These communication pathways have been highlighted by the characterization on immune and nervous cells of common receptors for cytokines, hormones, and neuropeptides. 2 In turn, cytokines produced mainly by immune cells modify the neuronal activity, as exemplified by the effect of interleukin 1 (IL-1) on the central nervous system. Within an integrated organization, the immune system accommodates a variety of signals originating from the neuroendocrine system 1 the immunomodulatory potency of hormones and neuropeptides has been described extensively. Together, our data show that anti-MOR autoantibodies are commonly expressed in healthy humans and could participate in the control of lymphocyte homeostasis by promoting Fas-mediated apoptosis. ![]() Similar sensitization to Fas-mediated apoptosis was observed in splenocytes from mice undergoing passive transfer either with IgG from mice previously immunized against CHO cells expressing MOR or with IgG directed against the first and third extracellular loops of the receptor. ![]() Splenocytes from mice injected with Chinese hamster ovary (CHO) cells expressing MOR were sensitized to Fas-mediated apoptosis, whereas those from mice injected with CHO cells or phosphate-buffered saline were not. We took advantage of the high sequence homology between murine MOR and hMOR extracellular loops to estimate the effect on murine splenocytes of anti-hMOR antibodies raised by immunizing mice. In analogy to studies of the effects of morphine, we investigated the ability of antibodies to sensitize splenocytes to Fas (CD95)-mediated apoptosis. Because of the inability of IgG to cross the blood-brain barrier, we investigated the effects of the expression of anti-hMOR autoantibodies on immune cells. In this study, we found that each healthy donor's serum contained anti-hMOR IgG autoantibodies with a specific activity against both the first and the third extracellular loops of the receptor. These autoantibodies behaved agonistically because of their ability to bind to the first and third extracellular loops of the receptor. We previously observed the presence of anti-human μ-opioid-receptor (anti-hMOR) autoantibodies in IgG pools prepared from several thousand healthy blood donors. ![]()
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