Rheumatoid Arthritis: Lünemann JD

Münz C, Lünemann JD, Getts MT, Miller SD. · Viral Immunobiology, Institute of Experimental Immunology, University Hospital Zürich, Winterthurerstrasse 190, CH-8057 Zürich, Switzerland. · Nat Rev Immunol. · Pubmed #19319143 No free full text.

Abstract: The predisposition of individuals to several common autoimmune diseases, such as rheumatoid arthritis, systemic lupus erythematosus and multiple sclerosis, is genetically linked to certain human MHC class II molecules and other immune modulators. However, genetic predisposition is only one risk factor for the development of these diseases, and low concordance rates in monozygotic twins, as well as the geographical distribution of disease risk, suggest the involvement of environmental factors in the development of these diseases. Among these environmental factors, infections have been implicated in the onset and/or promotion of autoimmunity. In this Review, we outline the mechanisms by which viral infection can trigger autoimmune disease and describe the pathways by which infection and immune control of infectious disease might be dysregulated during autoimmunity.

Lünemann JD, Kamradt T, Martin R, Münz C. · Laboratory of Viral Immunobiology, Christopher H. Browne Center for Immunology and Immune Diseases, The Rockefeller University, Box 390, 1230 York Avenue, New York, NY 10021-6399, USA. · J Virol. · Pubmed #17459939 links to  free full text

This publication has no abstract.

Lünemann JD, Frey O, Eidner T, Baier M, Roberts S, Sashihara J, Volkmer R, Cohen JI, Hein G, Kamradt T, Münz C. · Laboratory of Viral Immunobiology, Christopher H. Browne Center for Immunology and Immune Diseases, Rockefeller University, New York, NY 10021, USA. · J Immunol. · Pubmed #18606650 links to  free full text

Abstract: EBV is a candidate trigger of rheumatoid arthritis (RA). We determined both EBV-specific T cell and B cell responses and cell-associated EBV DNA copies in patients with RA and demographically matched healthy virus carriers. Patients with RA showed increased and broadened IgG responses to lytic and latent EBV-encoded Ags and 7-fold higher levels of EBV copy numbers in circulating blood cells. Additionally, patients with RA exhibited substantial expansions of CD8(+) T cells specific for pooled EBV Ags expressed during both B cell transformation and productive viral replication and the frequency of CD8(+) T cells specific for these Ags correlated with cellular EBV copy numbers. In contrast, CD4(+) T cell responses to EBV and T cell responses to human CMV Ags were unchanged, altogether arguing against a defective control of latent EBV infection in RA. Our data show that the regulation of EBV infection is perturbed in RA and suggest that increased EBV-specific effector T cell and Ab responses are driven by an elevated EBV load in RA.