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)

Recent evidence has established that non-MHC-encoded molecules of the CD1 family mediate MHC-independent pathways for antigen presentation and T cell activation. Human group 1 CD1 molecules (CD1a, CD1b, CD1c) are expressed mainly on professional antigen-presenting cells, and mediate presentation of microbial lipid and glycolipid antigens to T cells. These group 1 CD1 molecules differentially sample distinct endocytic compartments that may contain different sets of lipid antigens derived from intracellular microbes, and activate antigen-specific T cells. These T cells lyse infected antigen-presenting cells and secrete Th1 cytokines, such as interferon- gamma, and granulysin, a potent antimicrobial protein, and thus can control microbial infection. Reactivity to CD1a, b, and c molecules in the absence of foreign antigen has also been detected in T cells bearing alphabeta and gammadelta TCRs. These T cells may recognize self-lipid antigens and are considered to be autoreactive. In particular, the main tissue subset of gammadelta T cells (V delta 1(+)subset) show prominent reactivity to CD1c, and produce interferon- gamma and granulysin. These CD1c directly reactive T cells may mediate immunity against microbial infection even before antigen-specific T cells differentiate and expand. Together, human CD1a, b and c molecules elicit T cell-dependent immunity to the universe of foreign and self-lipid antigens in both innate and acquired immunity settings.
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PMID:T lymphocyte recognition of human group 1 CD1 molecules: implications for innate and acquired immunity. 1114 56

The early clinical presentations of Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are similar to that of erythema multiforme major (EMM). Cytotoxic molecules, especially granulysin, are expressed in the skin lesions of SJS/TEN and cause extensive keratinocyte death. It is postulated that the function of regulatory T cells (Treg) in SJS/TEN is inadequate. This study examined whether an immunohistological examination of cytotoxic molecules and the immunophenotype of Treg is useful for discriminating SJS from EMM in the early period. Over the past 9 years, the lesional skin of 14 patients with SJS/TEN and 16 patients with EMM was biopsied. Double immunofluorescence labeling of CD8 and granulysin, perforin, or granzyme B was performed, and immunohistochemical analyses of granulysin, perforin, granzyme B, CD1a, CD3, CD4, CD8, CD68 and Foxp3 were conducted using a highly sensitive indirect immunoperoxidase technique. The number of cells positive for each antibody per five high-power fields was counted. The proportions of granulysin(+) cells/CD8(+) cells (P = 0.012) and perforin(+) cells/CD8(+) cells (P = 0.037) in SJS/TEN were significantly higher than in EMM. The number of Foxp3(+) cells/five high-power fields in SJS/TEN was significantly lower than in EMM (P = 0.004). Similarly, the number of CD4(+) cells/five high-power fields in SJS/TEN was significantly lower than in EMM (P = 0.0017). These data suggest that these panels of antibodies for labeling cytotoxic molecules, CD4 and Treg are useful for discriminating early SJS/TEN and EMM with a skin biopsy.
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PMID:Distinguishing between erythema multiforme major and Stevens-Johnson syndrome/toxic epidermal necrolysis immunopathologically. 2245 64