Rheumatoid Arthritis: Eming R

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A digest of articles written 1999 and later, on the topic "Arthritis, Rheumatoid," originating from Planet Earth —» Eming R.  Display:  All Citations ·  All Abstracts
1 Review B-cell-directed therapy for inflammatory skin diseases. 2009

Nagel A, Hertl M, Eming R. · Department of Dermatology and Allergology, Philipps University, Marburg, Germany. · J Invest Dermatol. · Pubmed #19148218 No free full text.

Abstract: The basic understanding of inflammatory dermatoses and autoimmune-mediated skin disorders has greatly advanced and broadened our understanding of underlying immune mechanisms that shape the complex network of chronic inflammation and autoimmunity. The new treatment options for psoriasis exemplify how new insights into (auto)immune responses, especially the role and function of various immune cells and proinflammatory cytokines, may lead to new therapeutic strategies. The concept of targeting B cells in autoimmune-mediated disorders is closely related to the discovery of autoantibodies and their cellular origin. However, the appreciation of B cells in autoimmunity has significantly changed and is not limited to their role as progenitors of autoantibody secreting plasma cells. Recent investigations of various inflammatory skin diseases, that is, autoimmune blistering disorders, collagen vascular diseases, and atopic dermatitis, actually support the concept that B cells might be as important as T cells in the etiopathogenesis of these disorders. The striking clinical improvement seen in patients with rheumatoid arthritis following B-cell depletion with the anti-CD20 mAb rituximab has tremendously catalyzed the interest in B-cell-targeted therapies in different autoimmune diseases. Future translational and clinical investigations are mandatory to precisely define the role and the contribution of impaired B-cell function in (auto)immune-mediated skin diseases.

2 Review [B-cell-depleting antibodies in skin diseases] 2008

Nagel A, Hertl M, Eming R. · Klinik für Dermatologie and Allergologie, Philipps Universität Marburg, Deutschhausstrasse 9, 35037, Marburg, Deutschland. · Hautarzt. · Pubmed #18779943 No free full text.

Abstract: Basic insight into immune mechanisms, particularly the role and function of various immune cells and proinflammatory cytokines in the etiopathogenesis of inflammatory dermatoses and autoimmune skin disorders, has made possible the development of novel therapeutic strategies. Because of their properties as antigen presenting cells and progenitors of autoantibody-secreting plasma cells, B cells have a major impact in different autoimmune diseases and represent an important therapeutic target. The remarkable clinical improvement seen in patients with rheumatoid arthritis after treatment with the monoclonal anti-CD20 antibody, rituximab, has strongly augmented the interest in B-cell-targeted therapies in different autoimmune diseases. Future clinical and immunological investigations are mandatory to precisely define the contribution of impaired B-cell function in development and progression of autoimmune mediated skin disorders.

3 Review Humanized mice as a model for rheumatoid arthritis. 2002

Eming R, Visconti K, Hall F, Sekine C, Kobayashi K, Chen Q, Cope A, Kanazawa S, Peterlin M, Rijnders A, Boots A, Meijerink J, Sønderstrup G. · Department of Microbiology and Immunology, Stanford University School of Medicine, California 94305, USA. · Arthritis Res. · Pubmed #12110132 No free full text.

Abstract: Genetic susceptibility to rheumatoid arthritis (RA), a common autoimmune disease, is associated with certain HLA-DR4 alleles. Treatments are rarely curative and are often tied to major side effects. We describe the development of a humanized mouse model wherein new, less toxic, vaccine-like treatments for RA might be pretested. This model includes four separate transgenes: HLA-DR*0401 and human CD4 molecules, a RA-related human autoantigenic protein (HCgp-39), and a T-cell receptor (TCRalphabeta) transgene specific for an important HCgp-39 epitope, eliciting strong Th1 responses in the context of HLA-DR*0401.