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)

The Bcl-2 proto-oncogene regulates cell survival by antagonizing events that lead to apoptotic cell death and has been reported to be expressed in situ in lymphoid tissues, glandular epithelium, neurons, and basal epidermal cells. When we performed immunostaining on cryostat sections of normal skin, anti-Bcl-2 reactivity was confined to scattered dendritic cells in the basal epidermal layer. Double-staining experiments showed that the Bcl-2+ cells were positive for vimentin but negative for cytokeratins, CD1a, and CD45 antigens, excluding keratinocytes and Langerhans cells as possible candidates for constitutive Bcl-2 expression. Bcl-2+ epidermal cells also reacted with the monoclonal anti-melanocyte antibody NKI/beteb, and were absent from lesional skin in vitiligo, confirming that they represented epidermal melanocytes. Western blot analysis of cultured melanocytes and melanoma cell lines revealed a 26-kd protein specifically reacting with the anti-Bcl-2 monoclonal antibody. Immunostaining of pigmented lesions revealed strong expression of Bcl-2 by five of five nevocellular nevi and seven of seven melanomas. Our observations demonstrate that, within normal human epidermis, melanocytes are the only cells that express Bcl-2 constitutively and that Bcl-2 is expressed in benign and malignant pigmented tumors of the skin in situ.
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PMID:Human melanocytes and melanoma cells constitutively express the Bcl-2 proto-oncogene in situ and in cell culture. 788 47

Evidence for the involvement of cellular immunity in the etiopathogenesis of the hypopigmentary disorder vitiligo is provided by rare cases of inflammatory vitiligo. Nonlesional, perilesional, and lesional skin biopsies from three inflammatory vitiligo patients were immunohistochemically analyzed. The composition of inflammatory infiltrates present in perilesional skin was analyzed by antibodies to T cells (CD2, CD3, CD4, and CD8), Langerhans cells (CD1a), and macrophages (CD36 and CD68). The presence of activation markers on inflammatory cells was evaluated by analysis of HLA-DR, interleukin-2 receptor, and HECA452 expression. The presence or absence of melanocytes was determined by the antibody NKI-beteb. Moreover, the abundance of matrix molecule tenascin was semi-quantified using T2H5. Results indicate that within perilesional skin, epidermis-infiltrating T cells exhibit an increased CD8/CD4 ratio and increased cutaneous lymphocyte antigen and interleukin-2 receptor expression. These cells are frequently juxtapositionally apposed to remaining melanocytes. In perilesional dermis, CD68+OKM5- macrophages were more numerous than in lesional or nonlesional skin. Keratinocytes as well as melanocytes consistently express major histocompatibility complex class II antigens along stretches of basal and suprabasal layers in perilesional epidermis. Moreover, inflammation is accompanied by increased tenascin content. Although these observations do not permit differentiation between the immune infiltrates being a result as opposed to the cause of the disease process, results presented in this study are very suggestive of involvement of local immune reactivity in melanocyte destruction.
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PMID:Presence of T cells and macrophages in inflammatory vitiligo skin parallels melanocyte disappearance. 864 62

Sunburn, immune suppression, photoaging, and skin cancers result from uncontrolled overexposure of human skin to solar ultraviolet radiation (UVR). Preventive measures, including photoprotection, are helpful and can be achieved by topical sunscreening agents. Polypodium leucotomos (PL) has been used for the treatment of inflammatory diseases and has shown some in vitro and in vivo inmunomodulating properties. Its beneficial photoprotective effects in the treatment of vitiligo and its antioxidant properties encouraged us to evaluate in vivo the potentially useful photoprotective property of natural extract of PL after topical application or oral ingestion. Twenty-one healthy volunteers [either untreated or treated with oral psoralens (8-MOP or 5-MOP)] were enrolled in this study and exposed to solar radiation for evaluation of the following clinical parameters: immediate pigment darkening (IPD), minimal erythema dose (MED), minimal melanogenic dose (MMD), and minimal phototoxic dose (MPD) before and after topical or oral administration of PL. Immunohistochemical assessment of CD1a-expressing epidermal cells were also performed. PL was found to be photoprotective after topical application as well as oral administration. PL increased UV dose required for IPD (P < 0.01), MED (P < 0.001) and MPD (P < 0.001). After oral administration of PL, MED increased 2.8 +/- 0.59 times and MPD increased 2.75 +/- 0.5 and 6.8 +/- 1.3 times depending upon the type of psoralen used. Immunohistochemical study revealed photoprotection of Langherhans cells by oral as well as topical PL. The observed photoprotective activities of oral or topical PL reveal a new avenue in examining the potentially useful field of systemic photoprotection and suggests that PL can be used as adjunct treatment and can make photochemotherapy and phototherapy possibly safe and effective when the control of cutaneous phototoxicity to PUVA or UVB is a limiting factor in such phototherapies.
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PMID:Topical or oral administration with an extract of Polypodium leucotomos prevents acute sunburn and psoralen-induced phototoxic reactions as well as depletion of Langerhans cells in human skin. 936 Nov 29

The pathogenesis of vitiligo is still controversial. The purpose of this study was to gain insight into the nature of lymphoid cells infiltrating depigmented areas of skin in vitiligo. Immunochemical procedures were carried out in biopsies from 20 patients with active lesions to search for cells expressing CD1a, CD2, CD3, CD4, CD5, CD8, CD20, CD25, CD30, CD56, CD68 and CD79a. Results indicate that early lesions are infiltrated mainly by dendritic cells, whereas older lesions display significantly lower proportions of these cells and increased percentages of mature T cells. This finding might suggest that the autoimmune reactivity towards melanocyte antigens might be T cell-dependent and antigen-driven. It is possible that a non-immune offence of melanocytes is responsible for the exposure of intracellular antigens, while autoreactivity might be a secondary, self-perpetuating mechanism.
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PMID:Immunophenotypic characterization of lymphoid cell infiltrates in vitiligo. 2360 58