Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This experiment pursued the time course of contact hypersensitivity to 2,4-dinitro-1-fluorobenzene (DNFB) and histologic changes of the cutaneous reaction in mice. The contact hypersensitivity reached a maximum 4 days after sensitization (96.9 +/- 6.7% vs. 22.7 +/- 1.3% in control) and persisted for 3 weeks. The cutaneous hypersensitivity reaction showed peak reactivity at 24 hr after challenge (96.2 +/- 4.7% vs. 11.5 +/- 1.7% in control), and persisted up to 96 hr (13.2 +/- 2.1%). Prime histologic changes observed in this experiment were the exocytosis of lymphoid cells and epidermal thickening which appeared at 20 hr after challenge. Edema, vasodilatation and increased mast cells were observed within the dermis at 4-8 hr. However, edema and vasodilatation disappeared gradually, but numbers of mast cell increased up to 96 hr. The dermal infiltrates were maximum at the 28-72 hr after challenge.
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PMID:Time course of contact hypersensitivity to DNFB and histologic findings in mice. 326 35

Calcitonin gene-related peptide has been shown to modulate inflammatory and immune responses in various systems. Recent studies in our laboratory and colleagues have shown that intracutaneously injected calcitonin gene-related peptide impairs the induction of contact hypersensitivity in mice, and participates in the pathogenesis of failed contact hypersensitivity induction after acute, low-dose ultraviolet B radiation. In this study we investigated the ability of calcitonin gene-related peptide to induce tolerance in normal and mast cell deficient mice and we examined the extent to which calcitonin gene-related peptide contributes to the tolerance induced by acute, low-dose ultraviolet B radiation. Calcitonin gene-related peptide was injected intradermally followed by application of 2,4-dinitro-1-fluorobenzene to the injected skin surface. Tolerance was assessed by re-exposing the mice 2 wk later to a second, sensitizing dose of 2, 4-dinitro-1-fluorobenzene on uninjected skin. We found that calcitonin gene-related peptide induced tolerance to 2, 4-dinitro-1-fluorobenzene in both normal and mast cell deficient mice. Calcitonin gene-related peptide-induced tolerance was blocked by intradermal injection of a calcitonin gene-related peptide antagonist [CGRP-(8-37)] that selectively blocks the calcitonin gene-related peptide receptor. Tolerance was also abolished by intraperitoneally injected anti-interleukin-10, but not anti-tumor necrosis factor alpha, antibodies. When 2,4-dinitro-1-fluorobenzene was painted on skin into which splenic dendritic cells pretreated with calcitonin gene-related peptide had been injected, tolerance was observed. Calcitonin gene-related peptide- treated dendritic cells mixed with anti-interleukin-10 antibody prior to intradermal injection failed to promote tolerance. Finally, injection of CGRP-(8-37) into skin that was subsequently exposed to acute, low-dose ultraviolet B radiation partially prevented tolerance induced by local application of 2,4-dinitro-1-fluorobenzene. These results indicate that calcitonin gene-related peptide has the capacity to promote cutaneous tolerance through an interleukin-10-dependent mechanism. This mechanism, which does not require the participation of mast cells, contributes to the tolerance promoted by acute, low-dose ultraviolet B radiation. Thus, calcitonin gene-related peptide from cutaneous nerve endings plays a key role in the local immune aberrations caused by ultraviolet B radiation.
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PMID:Hapten-specific tolerance promoted by calcitonin gene-related peptide. 1112 Nov 23