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

When screening skin cryosections with a panel of monoclonal antibodies (MoAb), we found that the anti-CD69 MoAb Leu-23 reacted with a subpopulation of epidermal dendritic cells, presumably Langerhans cells (LC). The staining intensity was enhanced by gentle trypsin pretreatment of the sections. Flow cytometric analysis of LC-enriched epidermal cells (EC) revealed that nearly all CD1a-bearing LC display anti-CD69 reactivity when tested briefly after termination of the enrichment procedure. Immunoprecipitation experiments showed that isolated LC specifically express a disulphide-linked dimer composed of 26/30kDa subunits that therefore slightly differs from the 28/32kDa CD69 complex described on activated T or natural killer (NK) cells. This difference is probably due to a different post-translational glycosylation pattern as evidenced by Endoglycosidase-F treatment of the immunoprecipitate disclosing the 24-kDa core protein of CD69. When freshly isolated LC-enriched EC were kept in culture, anti-CD69 reactivity gradually decreased but the addition of IFN-gamma to the culture medium sustained the CD69 expression on LC in vitro. These results strongly suggest that resident but not LC recovered from EC cultures bear CD69 moieties. It remains to be seen whether the expression of this antigen can be linked to (a) particular functional property (ies) of intraepidermal LC.
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PMID:CD69, an early activation antigen on lymphocytes, is constitutively expressed by human epidermal Langerhans cells. 156 26

The mechanism underlying a transition of the oral cavity mucosal epithelium towards susceptibility to opportunistic infections in HIV-seropositive patients was investigated. Phenotypic markers CD1a, HLA-DR, and CD86 of oral mucosal Langerhans' cells (LCs), p17 core protein of human immunodeficiency virus (HIV), and CD45RO of memory T cells were labeled on oral hairy leukoplakia lesional biopsies and clinically normal autologous tissue of HIV-infected patients. HIV p17 protein was detected in association with mucosal LCs, mainly within the lesional epithelium. There were significant correlations between the detection of HIV p17 and the depletion of LCs, and between the depletion of LCs and the presence of hairy leukoplakia lesions. Conjugates of activated LCs and memory T cells were also evident in the submucosal area of lesional biopsies. The findings from this study support the hypothesis that oral mucosal LCs are also the target of HIV infection. Cytopathic changes of LCs caused by productive HIV infection may contribute to selective depletion of LCs, which may impair the mucosal immunologic protection against colonization by microorganisms causing HIV-associated oral mucosal lesions.
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PMID:Oral mucosal Langerhans' cells as target, effector and vector in HIV infection. 1097 48