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)

It is remarkable to uncover a new aspect of congenital epibulbar solid dermoids and lipodermoids. We describe a dramatic central epicorneal polypoidal lipodermoid coloboma accompanied by an upper eyelid coloboma that was not associated with Goldenhar syndrome. Histopathologically the excised lesion displayed superficial layers of epidermis and a thin dermis with eccrine glands, vestigial hair structures, and bundles of arrector pili smooth muscle that extended from the undersurface of the epidermis to the bulge area of the primitive hairs. This last feature is not present in normal eyelid skin nor in the conjunctiva, and has not been previously documented to occur in epibulbar dermoids and lipodermoids. S-100-positive dendritic melanocytes and CD1a-positive Langerhans cells were both observed intraepidermally, indicating a complete complement of normal cells in this layer. Beneath the dermis was a massive collection of lobules of mature adipose tissue that fused with the corneal stroma. A virtually identical pedunculated limbal tumor has been previously reported that was associated with Goldenhar syndrome. Review of earlier published cases of epibulbar dermoids and lipodermoids establishes that central corneal lesions are not a stigma of Goldenhar syndrome, in contrast to limbal masses. Other epibulbar choristomas that can be confused with lipodermoids are described.
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PMID:Epicorneal polypoidal lipodermoid: lack of association of central corneal lesions with goldenhar syndrome verified with a review of the literature. 1978 22

Mucosal Leishmaniasis (ML) may occur in both nasal and oral mucosa. However, despite the impressive tissue destruction, little is known about the oral involvement. To compare some changes underlying inflammation in oral and nasal ML, we performed immunohistochemistry on mucosal tissue of 20 patients with ML (nasal [n = 12]; oral [n = 8] lesions) and 20 healthy donors using antibodies that recognize inflammatory markers (CD3, CD4, CD8, CD22, CD68, neutrophil elastase, CD1a, CLA, Ki67, Bcl-2, NOS2, CD62E, Fas and FasL). A significantly larger number of cells, mainly T cells and macrophages, were observed in lesions than in healthy tissue. In addition, high nitric oxide synthase 2 (NOS2) expression was associated with a reduced detection of parasites, highlighting the importance of NOS2 for parasite elimination. Oral lesions had higher numbers of neutrophils, parasites, proliferating cells and NOS2 than nasal lesions. These findings, together with the shorter duration of oral lesions and more intense symptoms, suggest a more recent inflammatory process. It could be explained by lesion-induced oral cavity changes that lead to eating difficulties and social stigma. In addition, the frequent poor tooth conservation and gingival inflammation tend to amplify tissue destruction and symptoms and may impair and confuse the correct diagnosis, thus delaying the onset of specific treatment.
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PMID:Comparative study of the in situ immune response in oral and nasal mucosal leishmaniasis. 2209 33