Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06126 (CD1a)
 2,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study was undertaken to characterize further the structure and function of cutaneous nerves which we have previously shown to associate with skin immune cells (Hosoi et al., Nature 1993: 363:159). Ultrastructurally, axons were prominent within the superficial dermis and epidermis in neonatal murine skin, but they were inconspicuous in adult murine and primate skin. Immunohistochemical and immunoultrastuctural evaluation of normal adult human and simian skin for neural cell adhesion molecule (N-CAM), however, defined a plexus of axons surrounding superficial dermal mast cells and extending as delicate, vertical branches into the overlying epidermal layer. Antibodies to neuropeptides substance P, calcitonin gene-related peptide, and to nerve cell-specific clathrin (LCb subunit) also reacted with this neural plexus. Double labeling disclosed intimate associations of N-CAM-positive axons with dermal chymase-positive mast cells as well as with epidermal CD1a-positive Langerhans' cells by confocal scanning laser microscopy. Functionally, capsaicin applied to forearm skin revealed by 6 h discharge of mast cell chymase and induction of E-selectin in adjacent microvascular endothelium, events consistent with release of substance P from axons and subsequent stimulation of cytokine-mediated mast cell-endothelial interaction. Identical application of capsaicin to human skin xenografted to immunodeficient mice, and thus experimentally lacking in unmyelinated axons, failed to show similar findings. These results provide additional support to the concept that an elaborate network of cutaneous axons may play a functional role in regulation of skin inflammation and immunity.
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PMID:Characterization of unmyelinated axons uniting epidermal and dermal immune cells in primate and murine skin. 950 40

Psychological stress is believed to exacerbate inflammatory skin disease but the underlying mechanisms are poorly understood. We investigated the impact of acute social stress--Trier public speaking test--on: epidermal Langerhans' cell (LC) frequency; and cutaneous nerve fiber expression of protein gene product (PGP) 9.5 and calcitonin gene-related peptide (CGRP). Thirty-six healthy volunteers each had a pair of baseline 6 mm biopsies taken from sun-protected buttock skin. A second pair of biopsies was taken from contralateral buttock 4 hours (n=5) or 24 hours (n=15) after the Trier stressor. Controls (n=16) did not perform the Trier and had biopsies 24 hours apart. One of each pair of biopsies (baseline; 4 or 24 hours) was processed for counts of epidermal CD1a(+) LC; the other examined for PGP 9.5 and CGRP expression. We observed a significant (P<0.01) 16.4% reduction in epidermal LC frequency 24 hours post-stressor as compared with baseline; there was no significant change from baseline in non-stressed controls. At 24 hours, PGP 9.5 and CGRP were increased (P=0.025) and reduced (P=0.03), respectively, from baseline in the stressed group compared with controls. These data suggest that acute social stress reduces epidermal LC frequency and modulates cutaneous neuropeptide expression thereby supporting the concept of a "brain-skin" axis.
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PMID:The effects of acute social stress on epidermal Langerhans' cell frequency and expression of cutaneous neuropeptides. 1798 31