Impact of Microbes on Autoimmune Diseases
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REVIEW
Impact of Microbes on Autoimmune Diseases Claudia Danzer • Jochen Mattner
Received: 11 July 2012 / Accepted: 1 February 2013 / Published online: 16 February 2013 Ó L. Hirszfeld Institute of Immunology and Experimental Therapy, Wroclaw, Poland 2013
Abstract Autoimmune and autoinflammatory diseases arise as a consequence of complex interactions of environmental factors with genetic traits. Although specific allelic variations cluster in predisposed individuals and promote the generation and/or expansion of autoreactive T and B lymphocytes, autoimmunity appears in various disease phenotypes and localizes to diverging tissues. Furthermore, the discovery that allelic variations within genes encoding components of the innate immune system drive self-reactive immune responses as well, led to the distinction of immune responses against host tissues into autoimmune and autoinflammatory diseases. In both categories of disorders, different pathogenic mechanisms and/or subsequent orders of tissue assaults may underlie the target cell specificity of the respective autoimmune attack. Furthermore, the transition from the initial tissue assault to the development of full-blown disease is likely driven by several factors. Thus, the development of specific forms of autoimmunity and autoinflammation reflects a multi-factorial process. The delineation of the specific factors involved in the pathogenic process is hampered by the fact that certain symptoms are assembled under the umbrella of a specific disease, although they might originate from diverging pathogenic pathways. These multi-factorial triggers and pathogenic pathways may also explain the inter-individual divergent courses and outcomes of diseases among humans. Here, we will discuss the impact of different environmental factors in general
C. Danzer J. Mattner (&) Mikrobiologisches Institut, Klinische Mikrobiologie, Immunologie Und Hygiene, Universita¨tsklinikum Erlangen and Friedrich-Alexander Universita¨t Erlangen-Nu¨rnberg, Wasserturmstr. 3/5, 91054 Erlangen, Germany e-mail: [email protected] J. Mattner Division of Cellular and Molecular Immunology, Cincinnati Children’s Hospital, Cincinnati, OH 45229, USA
and microbial pathogens in particular on the regulation/ expression of genes encoded within susceptibility alleles, and its consequences on subsequent autoimmune and/or autoinflammatory tissue damage utilizing primarily the chronic cholestatic liver disease primary biliary cirrhosis as model. Keywords Autoimmunity Autoinflammation Genetic susceptibility Infection Host–pathogen interactions Abbreviations AMA Antimitochondrial antibodies APC Antigen-presenting cell CTLA-4 Cytotoxic T lymphocyte antigen 4 DC Dendritic cell GSL Glycosphingolipid IgM Immunoglobulin M IL-10 Interleukin 10 MS Multiple sclerosis NKT Natural killer T cell PBC Primary biliary cirrhosis PDC-E2 Pyruvate dehydrogenase complex E2 subunit RA Rheumatoid arthritis SLE Systemic lupus erythematosus SNP Single nucleotide polymorphism TCR T cell receptor Th cells T helper cell
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