Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Purified CD8+ T cells from influenza A/WSN-immune BALB/c (H-2d) mice respond with the generation of secondary A/WSN-specific Tc cells in vitro when stimulated with a synthetic peptide (NPP) with a sequence derived from influenza A virus nucleoprotein with high affinity for Kd class I MHC molecules. The process of the conversion of NPP-Kd-responding Tc cell precursors into effector Tc cells in a population of CD8+ T cells occurs with no demonstrable requirements for accessory cells or their lymphokine products. The addition of culture supernatants from several mouse and human B cell lymphomas and LPS-activated normal mouse B cells to the culture of NPP-stimulated immune CD8+ T cells enhanced the induction of secondary Ag-specific Tc cells. None of the tested supernatants in the absence of Ag (NPP) induced cytolytic Tc cells, indicating that B cell-derived secretory factors can exert their activity only on Ag-exposed CD8+ T cells. The augmentatory effect of these supernatants on Ag-specific activation of memory CD8+ T cells was attributed to the synergism between B cell-derived factors and IL-2 which is produced endogenously in cultures of NPP-stimulated D8+ T cells. The possible role of B cell-derived helper factors is discussed.
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PMID:Enhancement of antigen-specific activation of CD8+ memory cytotoxic T cells by B cell-derived factors. 128 80

The expression of the beta-endorphin receptor on both activated and unstimulated mouse spleen cells was studied. Results showed that unstimulated cells have only one type of beta-endorphin receptor with a specific low affinity (Kd = 1.034 +/- 0.0237 x 10(-7) M, 25,000 sites/cell). After Con A stimulation, cells express two types of receptors, one with a low affinity (Kd = 1.034 +/- 0.024 x 10(-7) M, 320,000 sites/cell) and the other with a high affinity (Kd = 1.052 +/- 0.033 x 10(-9) M, 49,000 sites/cell). The kinetic experiments during 4 days after Con A activation indicated that the receptor of high affinity emerged from 24 to 72 h, while the low affinity one increased in number after stimulation. The receptor numbers of both high and low affinity ones reached a maximum peak at 72 h, then began to decline. The addition of exogenous rIL-2 depressed the Con A-induced increment of the receptor numbers of both the high and low affinity ones, but enhanced the proliferative response of the cells. It is suggested that the degree of the expression of the receptors does not simply depend on the mitogenic degree of the cells. In addition, our experiment demonstrated that splenocytes cultured in medium with or without Con A or Con A + rIL-2 for 96 h did not secrete any detectable amount of beta-endorphin with use of the RIA assay, which is sensitive enough to detect the much lower levels of beta-endorphin than that necessary for biological effects. We suggest that the expression of the high affinity beta-endorphin receptor on the activated T-lymphocytes may have to precede the production of IL-2 to potentiate the T-cell proliferative response. The mechanisms and modes of interaction between the neuroendocrine system and the immune system were discussed.
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PMID:Regulation of beta-endorphin receptor expression in mouse spleen cells with Con A and rIL-2. 132 92

The production of IL-1 and IL-6 by pituitary cells has recently been demonstrated. In this study we investigated the expression of IL-2 and its receptor (IL-2R) by pituitary cells of different species. In Northern blots, a single hybridizing band of 1 kb, identical to that in normal stimulated lymphocytes, was obtained with specific IL-2 probes. In the mouse AT-20 pituitary tumor cell line, IL-2 mRNA expression was detected after stimulation with corticotropin-releasing hormone or phorbol myristate acetate. In human corticotrophic adenoma cells, basal IL-2 mRNA expression as well as IL-2 secretion were further stimulated by phorbol myristate acetate. Both adenoma and AtT-20 cells showed detectable amounts of IL-2R mRNA and by immunofluorescence, IL-2R membrane expression. In addition, dual immunofluorescence studies in rat anterior pituitary cells demonstrated colocalization of IL-2R with ACTH-positive cells and other cell types expressing the receptor. In addition to the action of lymphocyte-produced IL-2, this cytokine may have a paracrine or autocrine regulatory role within the pituitary. It remains to be established whether IL-2 production occurs in the normal pituitary or is intrinsic to the process of tumor development of these cells. IL-2 may be involved in the growth control of pituitary cells.
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PMID:Interleukin-2 and interleukin-2 receptor expression in human corticotrophic adenoma and murine pituitary cell cultures. 133 Nov 77

The pattern of expression of at least four neuropeptides contained in adrenomedullary chromaffin cells is altered by exposure to the cytokines interleukin-1 alpha (IL-1 alpha) and tumor necrosis factor-alpha (TNF alpha), alone or in combination with stimulation of other second messenger pathways. Vasoactive intestinal polypeptide (VIP) was elevated 2- to 3-fold by 1 nM IL-1 alpha within 48 h of exposure, while neurotensin and substance P synthesis were unaffected, and met-enkephalin levels were decreased 25-35%. Stimulation of VIP and substance P biosynthesis by forskolin was markedly enhanced by IL-1 alpha, while forskolin stimulation of enkephalin and neurotensin biosynthesis was unaffected. IL-1 alpha amplified the effect of phorbol myristate acetate to increase the VIP content of chromaffin cells, but antagonized phorbol ester-induced elevation of neurotensin levels. TNF alpha also demonstrated a neuropeptide-specific pattern of modulation of second-messenger effects on chromaffin cell neuropeptide levels similar to those seen with IL-1 alpha. The neuroendocrine actions of IL-1 alpha described above, unlike IL-1 action in the immune system, do not appear to be mediated through IL-2 as this cytokine did not affect VIP or enkephalin expression in the presence or absence of protein kinase stimulation. Neither IL-1 alpha nor TNF alpha affected the calcium-coupled stimulation of neuropeptide secretion and biosynthesis that occurs in response to cell depolarization in these and other neuroendocrine cells in vitro and in vivo. These data provide a functional demonstration of IL-1 and TNF receptors in chromaffin cell cultures and suggest a physiological role for cytokine production in the adrenal medulla. Since both the magnitude and direction of neuropeptide synthesis modulation by IL-1 alpha and TNF alpha are highly peptide-specific, it appears that these cytokines do not merely augment second messenger pathways that affect neuropeptide synthesis, but potentially regulate the activity of factors controlling the pattern of neuropeptide gene expression in chromaffin cells.
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PMID:Interleukin-1 alpha and tumor necrosis factor-alpha differentially regulate enkephalin, vasoactive intestinal polypeptide, neurotensin, and substance P biosynthesis in chromaffin cells. 137 39

The present study investigated whether a short synthetic peptide NPP, with a modified sequence (147-158 R156-) derived from influenza A virus nucleoprotein with high affinity for Kd major histocompatibility complex class I molecules, could induce primary influenza virus-specific cytotoxic T (Tc) cells in vitro. Naive BALB/c (H-2d) splenocytes did not respond to the stimulation with only NPP with the generation of effector Tc cells specific for influenza A virus-infected target cells in vitro. However, they were able to do so if cultured with NPP in the presence of IL-7. IL-7 activity in this system differed significantly from IL-2 activity in the specificity of the effect. The use of exogenous IL-2, instead of IL-7, with NPP resulted in the induction of lytic cells that lysed both influenza virus-infected and uninfected syngeneic target cells. These results suggest that IL-7 is a potent regulatory cytokine in the antigen-specific activation of resting naive Tc cell precursors and may provide the necessary conditions for the induction of human primary Tc cells in vitro.
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PMID:Induction of primary anti-viral cytotoxic T cells by in vitro stimulation with short synthetic peptide and interleukin-7. 144 9

Opioid peptides appear to be dynamic signaling molecules that are produced within the immune system and are active regulators of an immune response. Furthermore, the receptors for these peptides occurring on immunocyte membranes share characteristics with neuronal opioid receptors, including molecular size, immunogenicity, and the use of specific intracellular signaling pathways. Recent studies of the interaction of opioids with cytokines have indicated that opioid peptides are intimately involved within the immune system. Specifically, opioids, including 2-n-pentyloxy-2-phenyl-4-methyl-morpholine, naloxone, and beta-endorphin, have been shown to interact with IL-2 receptors (134) and regulate production of IL-1 and IL-2 (48-50, 135). Conversely, IL-1 has been shown to up-regulate opioid peptide binding in brain tissue (136). Furthermore, the induction of IL-1 by opioids has also been identified in the invertebrate Mytilus, indicating the evolutionary conservation of this relationship (137). These results seem to typify the intricate association between the immune and neuroendocrine systems through opioid pathways. It is predicted that future endeavors will use this relationship to diagnose and treat specific diseases that have at their basis neuroendocrine and immunologic imbalances.
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PMID:The role of endogenous opioids and their receptors in the immune system. 165 70

Human peripheral blood mononuclear cells are analyzed for preproenkephalin gene expression and peptide processing. Met-enkephalin immunoreactivity as detected with a specific antiserum is found in the cytoplasm of monocytes but not in T lymphocytes. Secretion of met-enkephalin was analyzed with an RIA that is specific for the met-enkephalin pentapeptide. Unfractionated PBMC spontaneously released 40 pg/ml met-enkephalin and this increased two- to fourfold after stimulation with PHA. Lower levels (less than 100 pg/ml) of met-enkephalin were detected in supernatants from purified T cells that were activated with PHA and IL-2. In contrast, stimulation of purified monocytes with LPS or PMA resulted in the release of up to 600 pg/ml of the processed peptide. To examine whether T cells can produce met-enkephalin precursor peptides, T cell conditioned media were treated with trypsin and carboxypeptidase-B, which is known to release met-enkephalin from the propeptide. This increased levels of met-enkephalin to 400 pg/ml, indicating that lymphocytes secrete the propeptide but do not process it to met-enkephalin. The 1.4-kb preproenkephalin mRNA is detected in activated blood mononuclear cells and in purified monocytes and T cells. To determine whether monocytes or lymphocytes express met-enkephalin in vivo, lymphoid tissues were analyzed by immunohistochemistry. In human spleen tissue, positive cells were found in the red pulp but not in the follicles, which is also consistent with met-enkephalin expression in monocytes. In summary, these results show that human peripheral blood mononuclear cells express preproenkephalin mRNA and that monocytes, but not T cells, process the propeptide to metenkephalin.
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PMID:Differential processing of proenkephalin-A by human peripheral blood monocytes and T lymphocytes. 188 71

In recent years there has been considerable discussion of possible cross-regulatory mechanisms involving the immune system and the neuroendocrine system. Certainly, evidence of hormonal communication between these two systems would provide at least a partial explanation for the many anecdotal observations of physical and mental stress affecting disease course. In previous studies of a neoplastic lymphokine-responsive B cell clone, BCL1-3B3, we noted that these cells produced a lymphokine which could affect normal B cell growth and viability. Physical characterization of this lymphokine indicated that its molecular weight was identical to that of the neuroendocrine hormone adrenocorticotropin (ACTH). Since Blalock and colleagues had reported the production of ACTH by virally-infected B cells, we have investigated whether ACTH can functionally mimic the BCL1-3B3-derived lymphokine. The neuroendocrine hormone adrenocorticotropin (ACTH) can increase in vitro murine B lymphocyte proliferation when added at physiologically relevant concentrations between 10(-9) to 10(-11) M. ACTH does not mimic the action of any lymphokine known to be required for B cell proliferation such as IL-2, IL-4, or IL-5. ACTH requires the presence of one or more of these known B cell stimulatory factors for its action and the most marked increase in B cell proliferation were noted in assays for IL-5 activity where 10(-10) M ACTH increased thymidine incorporation up to five-fold. Using two-stage assays, we determined that ACTH acts during the latter stages of B cell activation (i.e., 3-4 days after initial stimulation with either the combination of IL-4, GAMIg-Sepharose, and IL-1 or the combination of DxS and IL-5). These data indicate a direct role for a stress-induced neuroendocrine hormone in modulating the course of a humoral immune response.
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PMID:Adrenocorticotropin (ACTH) functions as a late-acting B cell growth factor and synergizes with interleukin 5. 196 84

Several experiments have demonstrated that there is a relationship between neuroendocrine and immune systems. Despite these interesting findings, only few studies have been performed up to now to evaluate the possible importance of neuroimmune interactions in influencing the biological efficacy and toxicity of cancer immunotherapy with IL-2. To analyze the effects of IL-2 on endocrine secretions, we have measured by RIA serum levels of cortisol, beta-endorphin, GH, PRL and of the pineal hormone melatonin in metastatic renal cancer patients, treated with 5-day courses of IL-2 at a daily dose of 3 x 10(6) U/m2, given through a 24-hour intravenous infusion. Six IL-2 courses were evaluated, by collecting blood samples at 4-hour intervals for 24 hours and by comparing the hormonal values with those observed in baseline conditions. Both cortisol and beta-endorphin mean values significantly increased during IL-2 infusion. GH and PRL also increased, but not in a significant manner. Finally, melatonin mean levels significantly decreased during the infusion. The IL-2-induced effects on cortisol, beta-endorphin and melatonin resulted in a complete abolition of their physiological circadian rhythm. These results show that IL-2 infusion induces important changes in endocrine secretions. Because of the immunosuppressive effect of cortisol and the stimulatory one of melatonin, their changes during IL-2 infusion might influence the biological activity of immunotherapy itself. Further studies will be required to define better the clinical importance of IL-2 induced hormonal changes.
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PMID:Endocrine effects of a 24-hour intravenous infusion of interleukin-2 in the immunotherapy of cancer. 214 95

To assess the chronic effects of interleukin-1 (IL-1) and IL-2 on the hypothalamo-pituitary-adrenal axis in vivo, we administered recombinant human (rh) IL-1 alpha, rhIL-1 beta or rhIL-2 (2.0 micrograms/day) repetitively to adult male rats for 10 days. In rhIL-1 beta-treated rats, adrenocorticotropic hormone-like immunoreactivity (ACTH-LI) of the anterior pituitary appeared to increase first on day 3 followed by an increase of corticotropin-releasing hormone (CRH)-LI both in the hypothalamus and in the adrenal gland after day 7. At the end of the 10-day treatment, wet weights of the adrenal glands of rhIL-1 beta-treated rats increased significantly compared with those of control rats. Plasma ACTH levels in rhIL-1 beta-treated rats at the sampling time continued to be elevated throughout the experimental period. Under the same experimental design, rhIL-1 alpha increased plasma ACTH levels at the sampling time without changes in adrenal weight or in the peptide contents investigated. The same amount of rhIL-2 had no effect on these measured variables during the 10-day treatment. These data indicate that the repetitive administration of IL-1 beta resulted in chronic effects in the hypothalamo pituitary-adrenal axis to increase the activities in these organs during the treatment and, moreover, IL-1 possibly has a positive direct effect on the CRH-containing cells in the adrenal glands.
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PMID:Chronic effects of interleukin-1 on hypothalamus, pituitary and adrenal glands in rat. 216 96


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