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Contains fulltext : 299955.pdf (Publisher’s version ) (Closed access), 01 december 2023

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1 juni 2012, Item does not contain fulltext

1 april 2010, Contains fulltext : 88209.pdf (publisher's version ) (Closed access), OBJECTIVE: CD55 (decay-accelerating factor) is best known for its role in the negative regulation of the complement system. Indeed, lack of this molecule leads to disease aggravation in many autoimmune disease models. However, CD55 is abundantly present on fibroblast-like synoviocytes and is also a ligand of the adhesion-class heptahelical receptor CD97, which is expressed by infiltrating macrophages. Treatment with antibodies to CD97 ameliorates the collagen-induced model of rheumatoid arthritis (RA) in DBA/1 mice, but the net contribution of CD55 is unknown. This study was undertaken to investigate the role of CD55 in experimental RA. METHODS: Arthritis was induced in wild-type, CD55(-/-), and CD97(-/-) mice using collagen-induced and K/BxN serum-transfer models. Incidence of arthritis was monitored over time, and disease activity was assessed by clinical and immunohistochemical evaluation. RESULTS: In contrast to observations in many inflammatory disease models, lack of CD55 resulted in decreased arthritis in experimental models of RA. Consistent with the previously reported effects of anti-CD97 antibody treatment, CD97(-/-) mice had reduced arthritis activity compared with wild-type controls. CONCLUSION: Our findings indicate that the lack of CD55 or CD97 in 2 different models of arthritis increases resistance to the disease. These findings provide insight into a role for CD55 interaction with CD97 in the pathogenesis of RA and suggest that therapeutic strategies that disrupt CD55/CD97 may be clinically beneficial.

Item does not contain fulltext, Efalizumab 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.

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.