EXPRESSION OF Ia-LIKE ANTIGENS IN NORMAL HUMAN NONLYMPHOID TISSUES

Pg, Natali; C, De Martino; Quaranta,; Mr, Nicotra; Frezza, F; Ma, Pellegrino; Ferrone, Soldano

doi:10.1097/00007890-198101000-00017

Cited by 252 publications

(113 citation statements)

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“…Other investigators (18)(19)(20) have suggested that these DR+ cells were IDC, of the type seen in T cell areas of lymph nodes, which might function as antigen-presenting cells in the synovium. However, these cells have not been previously examined in the EM, and their structural characteristics have remained uncertain, particularly since they have been identified mainly by immunofluorescent staining (1 [8][9][10][11][12][13][14][15][16][17][18][19][20].…”

Section: Discussionmentioning

confidence: 99%

Electron microscopic study of HLA‐DR and monocyte/macrophage staining cells in the rheumatoid synovial membrane

Iguchi

Kurosaka

Ziff

1986

Arthritis & Rheumatism

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We examined synovial membrane samples from 6 rheumatoid arthritis (RA) and 3 osteoarthritis patients and from 1 normal subject, by an immunoelectron microscopic technique using anti-HLA-DR (anti-Ia) and anti-monocyte/macrophage (63D3) monoclonal antibodies. In the lining layer, the type A macrophage-like cells were strongly DR+ and 63D3+, whereas the type B fibroblast-like cells were almost completely negative. Lymphocyte-rich areas (containing more than 90% densely packed lymphocytes) showed weak and patchy DR staining of the lymphocytes. In these areas, 3 4 % of the cells were macrophage-like cells which were 63D3-, a type of staining compatible with that of the interdigitating cell (IDC). In the plasma cell-containing (transitional) areas, many strongly DR+ macrophage-like cells were observed in close contact with lymphocytes and plasma cells. Ten to twenty percent of these cells were 63D3-, which suggests that they were IDC. Cells with the structural appearance of IDC were most frequently seen in those transitional areas which contained elevated concentrations (50-70%) of lymphocytes. In uninfiltratFrom the Harold C.

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Section: Discussionmentioning

confidence: 99%

Electron microscopic study of HLA‐DR and monocyte/macrophage staining cells in the rheumatoid synovial membrane

Iguchi

Kurosaka

Ziff

1986

Arthritis & Rheumatism

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“…Until recently, data suggested that c-Kit might act as a tumor-suppressor gene in melanoma. Indeed, c-Kit is expressed in melanocytes, benign melanocytic nevi and in situ malignant melanoma, but tends to be reduced or lost with tumor progression to invasive and metastatic melanoma (Natali et al, 1992). Furthermore, c-Kit expression is lost in most melanoma cell lines (Lassam and Bickford, 1992).…”

Section: Introductionmentioning

confidence: 99%

c-Kit mutants require hypoxia-inducible factor 1α to transform melanocytes

et al. 2009

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Many studies have highlighted the critical role of c-Kit in normal melanocyte development but its role in melanoma development remains unclear. Although c-Kit expression is often lost during melanoma progression, a subset of melanoma has been found to overexpress c-Kit and mutations activating c-Kit have recently been identified in some acral and mucosal melanoma. To address the role of these c-Kit mutants in the transformation of melanocytes, we characterized the physiological responses of melanocytes expressing the most frequent c-Kit mutants found in melanoma (K642E and L576P) and a novel mutant we identified in an acral melanoma. We analysed signaling pathways activated downstream of c-Kit and showed that all three mutants led to a strong activation of the phosphatidyl-inositol-3 kinase (PI3K) pathway but only weak activation of the Ras/Raf/Mek/Erk pathway, which was not sufficient to promote uncontrolled melanocyte proliferation and transformation. However, in hypoxic conditions or coexpressed with a constitutively active form of hypoxia-inducible factor 1a (HIF-1a), c-Kit mutants activate the Ras/Raf/Mek/Erk pathway, stimulate proliferation and transform melanocytes. Proliferation of melanocytes transformed by these mutants was specifically inhibited by imatinib. These results show for the first time that melanocytes require a specific epigenetic environment to be transformed by c-Kit mutants and highlight a distinct molecular mechanism of melanocyte transformation.

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“…MHC Class II products were until recently, considered to be restricted to cells of the immune system, including B lymphocytes, macrophages, vascular endothelial, dendritic and other antigen presenting cells, as well as activated T lymphocytes (Ko et al, 1979). Now in addition, certain epithelia and a significant number of nonlymphoid neoplasms including those of breast, colorectal carcinoma and malignant melanoma are known to display Class II molecules (Natali et al, 1981;Thompson et al, 1982;Whitwell et al, 1984;Daar & Fabre, 1983;Rognum et al, 1983). Currently there is interest in whether this property is a requirement for the induction of autologous lymphoproliferative responses by tumour antigens of the MHC status of tumour cells and the in situ host response in a manner which has hitherto proved impossible using conventional histological techniques.…”

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confidence: 99%