13 research outputs found

    EGF-TM7 receptors in rheumatoid arthritis

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    Else Kop onderzocht de rol van bepaalde receptoren (EGF-TM7) in synoviaal weefsel (de binnenbekleding van de gewrichten) bij patiënten met reumatoïde artritis. Drie van deze receptoren komen in ontstekingscellen veel tot expressie. Bovendien zijn twee bindingspartners van deze receptoren aanwezig op synoviale fibroblasten (bindweefselcellen). Muizen waarin de receptor CD97 was uitgeschakeld, bleken beschermd tegen artritis. EGF-TM7-receptoren dragen wellicht bij aan het vasthouden van ontstekingscellen in het synovium. Onderdrukking van deze receptoren kan een basis zijn voor nieuwe geneesmiddelen

    Differential expression of CD97 on human lymphocyte subsets and limited effect of CD97 antibodies on allogeneic T-cell stimulation.

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    Contains fulltext : 80460.pdf (publisher's version ) (Closed access)CD97 is a large heptahelical EGF-TM7 receptor broadly expressed on hematopoietic cells as three isoforms with respectively three, four, or five epidermal growth factor (EGF)-like domains. We here describe the expression characteristics of CD97 on human lymphocyte subsets. We found CD97 to be present on all lymphocytes in blood and lymphoid tissue. Expression of CD97 on B cells was lower compared to T and NK cells and did not differ between B-cell subsets. In CD4(+) T cells, CD97 expression was higher on memory cells compared to naive cells. In CD8(+) T and NK cells, we found a downregulation of CD97 on cytolytic effector cells. Stimulation through CD3 and CD28 resulted in a rapid upregulation of CD97 in all T-cell subsets within 2-4h. A link between CD97 expression and lymphocyte proliferation was established in NK cells, which markedly upregulated CD97 in response to IL-2 and IL-15. Mixed lymphocyte cultures revealed a limited ability of the stalk region-specific monoclonal antibody CLB-CD97/3 to inhibit CD8(+) and CD4(+) allogeneic T-cell proliferation

    Erythroderma in two patients with psoriasis upon discontinuation of efalizumab treatment.

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    Item does not contain fulltextEfalizumab is therapeutically effective in moderate to severe plaque psoriasis. Rebound after discontinuing therapy affects approximately 14% of patients, while erythroderma occurs in less than 1% of the treated population. In this case report, we describe two non-responding patients with severe plaque psoriasis who developed erythroderma after treatment was ceased. Non-responders are more likely to suffer from rebound. This article emphasizes the importance of close monitoring of non-responders to efalizumab after discontinuance of treatment
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