EDITORIAL

Antiphospholipid syndrome

Infectious origin of the antiphospholipid syndrome^*

Y Shoenfeld¹, M Blank¹, R Cervera², J Font², E Raschi³, P-L Meroni³

¹ Department of Medicine "B" and Centre for Autoimmune Diseases, Sheba Medical Centre, Tel-Hashomer, and Sackler Faculty of Medicine, Tel-Aviv University, Israel
² Department of Autoimmune Diseases, Institut Clinic de Medicina i Dermatologia, Hospital Clinic, Barcelona, Catalonia, Spain
³ Allergy, Clinical Immunology and Rheumatology Unit, Department of Internal Medicine, University of Milan, IRCCS Istituto Auxologico Italiano, Milan, Italy

Correspondence to:
Correspondence to:
Professor Y Shoenfeld
Head, Department of Medicine "B" and Centre for Autoimmune Diseases, Sheba Medical Centre, Tel-Hashomer 52621, Israel; shoenfel@post.tau.ac.il

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From a systemic disease towards the infectious aetiology

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Keywords: anticardiolipin; antiphospholipid syndrome; autoantibodies; autoimmunity; infection

The first 150 words of the full text of this article appear below.

The general consensus is that autoimmune diseases have a multifactorial aetiology, depending on both genetic and environmental factors. Microbial agents or viruses can induce autoimmune diseases by a variety of mechanisms.¹ For example, proteins of certain infectious agents can act as polyclonal activators on unique lymphocyte subsets. Viruses can preferentially infect/destroy a particular T cell subset, leading to an imbalance in the immune response. Several microbial agents have been found to encode superantigens that can selectively activate subset(s) of T cells. Microbes can also direct the release of cytokines and chemokines, which can act as growth, differentiation, or chemotactic factors for different cell populations and regulate expression of major histocompatibility complex class I and class II as well as costimulatory molecules.²

The healthy immune system is tolerant of the molecules of which the body is composed. However, one can find that among the major antigens recognised during a . . . [Full text of this article]

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