Toxoplasma gondii: bystander or cofactor in rheumatoid arthritis
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ETIO PATHOGENESIS OF AUTOIMMUNITY
Toxoplasma gondii: bystander or cofactor in rheumatoid arthritis Svetlana Fischer • Nancy Agmon-Levin • Yinon Shapira • Bat-Sheva Porat Katz • Eduard Graell • Ricard Cervera • Ljudmila Stojanovich • Jose A. Go´mez Puerta • Raimon Sanmartı´ • Yehuda Shoenfeld
Ó Springer Science+Business Media New York 2013 Yehuda Shoenfeld
Abstract Parasitic infections may induce variable immunomodulatory effects and control of autoimmune disease. Toxoplasma gondii (T. gondii) is a ubiquitous intracellular protozoan that was recently associated with autoimmunity. This study was undertaken to investigate the seroprevalence and clinical correlation of anti-T. gondii antibodies in patients with rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). We evaluated sera from European patients with RA (n = 125) and SLE (n = 164) for the prevalence of anti-T. gondii IgG antibodies (ATXAb), as well as other common infections such as Cytomegalovirus, Epstein-Barr, and Rubella virus. The rates of seropositivity were determined utilizing the LIAISON chemiluminescent immunoassays (DiaSorin, Italy). Our results showed a higher seroprevalence of ATXAb in RA patients, as compared with SLE patients [63 vs. 36 %, respectively (p = 0.01)]. The rates of seropositivity of IgG against other infectious agents were comparable between RA and SLE patients. ATXAb-seropositivity was associated with older age of RA patients, although it did not correlate with RA disease activity and other manifestations of the disease. In conclusion, our data suggest a possible link between exposure to T. gondii infection and RA.
Svetlana Fischer and Nancy Agmon-Levin have contributed equally to this paper. S. Fischer N. Agmon-Levin Y. Shapira Y. Shoenfeld (&) The Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, 52621 Tel HaShomer, Israel e-mail: [email protected] B.-S. Porat Katz Y. Shoenfeld The Hebrew University, Jerusalem, Israel E. Graell J. A. Go´mez Puerta R. Sanmartı´ Arthritis Unit, Rheumatology Department, Hospital Clı´nic, Barcelona, Catalonia, Spain R. Cervera Department of Autoimmune Diseases, Barcelona, Catalonia, Spain L. Stojanovich Bezhanijska Kosa University Medical Center, Belgrade, Serbia Y. Shoenfeld Incumbent of the Laura Schwarz-Kip Chair for Research of Autoimmune Diseases, Tel Aviv University, Tel Aviv, Israel
Keywords Rheumatoid arthritis Systemic lupus erythematosus Toxoplasma gondii Autoimmunity Autoantibodies Parasites
Introduction The development of autoimmunity is believed to involve interaction between genes and the environment [1–9]. Infections may promote the development of autoimmunity by molecular mimicry, epitope spreading, or bystander activation [8, 10]. The relationship between parasitic infections and autoimmunity remains to be elucidated [8, 11]. Recent research on the immunomodulatory effects of parasitic infections highlighted the role of Toll-like receptor (TLR) ligands in development of autoimmunity [12, 13]. Nevertheless, the complex inte
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