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)

Scleroderma is a chronic autoimmune connective tissue disorder of unknown etiology that affects the microvasculature and loose connective tissue. Langerhans cells play an important role in the immune system of the skin. By immunohistochemistry we investigated the phenotypical characteristics of epidermal and dermal Langerhans cells and their spatial relationship with infiltrating lymphocytes in systemic scleroderma (SSc) and localized scleroderma. Skin samples were obtained from patients by 6 mm punch biopsy. Samples were stained with antibodies against CD1a and CD86. The number of cells stained with both antibodies in the dermal and epidermal infiltration was calculated. In contrast to normal skin, both types of scleroderma skin showed a marked increase in CD1a+ dermal Langerhans cells, whereas the number of CD1a+ cells in localized scleroderma was much higher than that in SSc (p < 0.05) either in the dermis or in the epidermis. The expression of CD86 was increased in the dermis of localized scleroderma compared with that in SSc or normal skin (p < 0.05). This study revealed that Langerhans cells may play an important role in the pathogenesis of scleroderma, especially in localized scleroderma. CD86 is predominantly expressed on dermal Langerhans cells in the lesional skin of localized scleroderma. Therefore, it might play an important role in the pathogenesis of localized scleroderma.
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PMID:Expression of CD1a and CD86 on scleroderma Langerhans cells. 1808 89

Discoid lupus erythematosus (DLE) is a chronic connective tissue disease of unknown etiology, but immunologic factors may play an important role in the pathogenesis. We investigated the features of immunohistochemical characterization of the cellular infiltrate in DLE. Skin samples were obtained from 5 patients using a 6 mm punch biopsy. Samples were stained with monoclonal antibodies against CD1a, CD3, CD4, CD8, CD20, CD25, CD30, and CD57. The number of cells stained with each monoclonal antibody was calculated. The number of cells stained with each monoclonal antibody in the dermis infiltration in DLE was calculated and all were higher than those in the normal control. The numbers of CD3(+), CD4(+), CD8(+), CD20(+), CD25(+), or CD57(+) cells in DLE were statistically higher than those in normal skin (p < 0.05). The numbers of CD1a(+) and CD30(+) cells in DLE were appreciably increased but had no statistical significance compared with normal skin. In conclusion, this study revealed that T lymphocytes, B lymphocytes, and natural killer cells may play some roles in the pathogenesis of DLE.
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PMID:Immunohistochemical characterization of the cellular infiltrate in discoid lupus erythematosus. 2157 52