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)

Overnight treatment of murine leukocytes with corticotropin-releasing hormone (CRH) and arginine vasopressin enhances natural killer cell activity. Moreover, the opioid receptor antagonist, naloxone, as well as the delta-class opioid receptor antagonist, naltrindole, can block this effect. The responsivity of murine leukocytes to CRH is both dose- and time-dependent. The effector cells are both MAC-1 and Thy-1.2 antigen-positive. Whereas beta-endorphin is also shown to enhance natural killer cell activity in a naloxone-reversible manner, adrenocorticotropic hormone (ACTH) has a negligible effect. Macrophage depletion prior to incubation with CRH blocks the CRH-induced natural killer cell augmentation. These results suggest hypothalamic-releasing hormones such as CRH may have a biologically relevant role in the modulation of immune cells either directly or indirectly through the induction of neuropeptide hormones known to have immunomodulatory capabilities.
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PMID:Corticotropin-releasing hormone augments natural killer cell activity through a naloxone-sensitive pathway. 216 Apr 75

Intracellular calcium mobilization is an important early event involved in T cell activation. The endogenous opioid peptide beta-endorphin is known to modulate immune functions that depend on T cell activation, therefore its effect on intracellular calcium mobilization was investigated. The intracellular calcium concentration ([Ca2+]i) of T cell-enriched splenocytes was measured by flow cytofluorometric analysis using the calcium-sensitive dye, Fluo-3. By gating on the T cell marker, Thy-1, a 95%-pure population of T cells was identified for study. Cells preincubated with beta-endorphin showed significantly enhanced [Ca2+]i responses to the mitogen, Concanavalin A (Con A). This was detectable with concentrations of beta-endorphin as low as 10(-13) M; maximal enhancement required 10(-10) to 10(-9) M doses. The efficacy of beta-endorphin was dependent on the duration of pretreatment. beta-Endorphin amplified the Con A-induced increase in [Ca2+]i by reducing the lag time for the response to Con A and by increasing the mean [Ca2+]i of the cells. N-Ac-beta-endorphin, which shows minimal potency at neuronal opiate receptors, was unable to substitute for beta-endorphin. Naltrindole, a highly selective delta opiate receptor antagonist, inhibited the action of beta-endorphin, whereas a selective mu opiate receptor antagonist was ineffective. Although less potent than beta-endorphin, the delta opiate receptor agonist D-Ala2-D-Leu5-enkephalin also significantly enhanced [Ca2+]i responses. In summary, concentrations of beta-endorphin, within the physiological range found in the systemic circulation, modulate the increase in T cell [Ca2+]i induced by Con A. Both the efficacy of D-Ala2-D-Leu5-enkephalin alone and the antagonism of beta-endorphin by naltrindole suggest that a delta-type opiate receptor may mediate these effects.
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PMID:Beta-endorphin enhances Concanavalin-A-stimulated calcium mobilization by murine splenic T cells. 875 65

Acute low-dose ultraviolet B (UVB) radiation impairs the induction of contact hypersensitivity (CH) and induces tolerance in UVB-susceptible strains of mice when dinitrofluorobenzene (DNFB) is applied to an irradiated skin surface. We are interested in learning the cellular and molecular bases for the existence of UVB susceptibility in certain strains of mice. CH was induced by subcutaneous injections into naive syngeneic C57BL/6 and BALB/c mice of dinitrophenyl (DNP)-derivatized Thy-1(+)-depleted epidermal cells enriched for Ia+ cells (LC/DNP, 2 x 10(4) cells per mouse). Tolerance was detected by applying 185 microg of DNFB epicutaneously to mice treated 2 wk earlier with a putative tolerating regimen and testing CH expression. We found that LC/DNP obtained from C57BL/6 skin 2 h after UVB irradiation (400 J per m2) failed to induce CH and induced DNP-specific tolerance instead; by contrast, similar cells obtained from same or even higher dose (400 J per m2 and 1200 J per m2) UVB-exposed BALB/c skin induced vigorous CH, and no tolerance was detected. In both C57BL/6 and BALB/c mice, Ia+-depleted EC/DNP neither sensitized naive syngeneic mice nor induced tolerance. LC/DNP prepared from unirradiated trunk skin of either C57BL/6 or BALB/c mice and pre-incubated in vitro for 2 h with cis-UCA, TNF-alpha, or IL-10 failed to induce intense CH; instead, all induced DNP-specific tolerance. Pre-incubation of similar LCs with alpha-MSH in vitro for 2 h also failed to induce CH but did not cause tolerance. Thus, single low-dose UVB irradiation alters the immunogenic and tolerogenic potentials of LCs only in UVB-susceptible mice; by contrast, pre-treatment of LCs with UVB-dependent soluble factors can achieve effects similar to UVB irradiation in both UVB-susceptible and -resistant strains of mice. These findings demonstrate that UVB susceptibility in mice may be determined by the production of UVB-dependent soluble factors within UVB-irradiated skin.
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PMID:Ultraviolet B-exposed and soluble factor-pre-incubated epidermal Langerhans cells fail to induce contact hypersensitivity and promote DNP-specific tolerance. 912 22