Autoimmunity and infection: a bidirectional relationship
Abstract number: S68
The hypothesis of an infectious origin for autoimmune diseases has received great attention during the recent years. Microbial agents or viruses can induce autoimmune diseases by a variety of mechanisms. 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. In other instances, infectious agents can up-regulate Th1 cytokines, thereby increasing selected expression of molecules such as major histocompatibility complex (MHC) glycoproteins, as well as activation of costimulatory molecules. Several microbial agents have been found to encode superantigens that can selectively activate subsets of T cells. Microbes can also direct the release of cytokines and chemokines, which can act as growth, differentiation, or chemotactic factors for different Th populations and regulate expression of MHC class I and class II molecules.
On the other hand, the healthy immune system is tolerant to the molecules of which the body is composed of. However, one can find that among the major antigens recognized during a wide variety of bacterial viral and parasitic diseases, many belong to conserved protein families, sharing extensive sequence identity or conformational fits, with host's molecules, namely molecular mimicry. Antigenic similarity of either molecules' linear amino-acid sequences or their conformational structure between antigens of infectious agents and host tissues might trigger an immune response against the shared determinant. As a result, the tolerance to autoantigens breaks down, and the pathogen-specific immune response that is generated cross-react with host structures to cause tissue damage and disease.
In this presentation, the cases of Sjögren's syndrome, systemic lupus erythematosus and the antiphospholipid syndrome, among others, will be reviewed as clear examples of autoimmune diseases where an infectious origin is postulated.
|Session name:||Abstracts 20th European Congress of Clinical Microbiology and Infectious Diseases|
|Location:||Vienna, Austria, 10 - 13 April 2010|
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