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Mediators of Inflammation
Volume 2015, Article ID 351732, 11 pages
http://dx.doi.org/10.1155/2015/351732
Review Article

Selected Aspects in the Pathogenesis of Autoimmune Diseases

1Department of Genetics, Cell and Immunobiology, Semmelweis University, Budapest 1089, Hungary
2Centre for Immune Regulation and Department of Immunology, University of Oslo and Oslo University Hospital, Rikshospitalet, 0372 Oslo, Norway
3K.G. Jebsen Center for Influenza Vaccine Research, Institute of Immunology, University of Oslo and Oslo University Hospital, 0372 Oslo, Norway
4Department of Medicine, Institute of Clinical Medicine, Helsinki University Central Hospital and ORTON Orthopaedic Hospital of the Invalid Foundation, 0280 Helsinki, Finland

Received 23 December 2014; Accepted 24 February 2015

Academic Editor: Anshu Agrawal

Copyright © 2015 György Nagy et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Autoimmune processes can be found in physiological circumstances. However, they are quenched with properly functioning regulatory mechanisms and do not evolve into full-blown autoimmune diseases. Once developed, autoimmune diseases are characterized by signature clinical features, accompanied by sustained cellular and/or humoral immunological abnormalities. Genetic, environmental, and hormonal defects, as well as a quantitative and qualitative impairment of immunoregulatory functions, have been shown in parallel to the relative dominance of proinflammatory Th17 cells in many of these diseases. In this review we focus on the derailed balance between regulatory and Th17 cells in the pathogenesis of autoimmune diseases. Additionally, we depict a cytokine imbalance, which gives rise to a biased T-cell homeostasis. The assessment of Th17/Treg-cell ratio and the simultaneous quantitation of cytokines, may give a useful diagnostic tool in autoimmune diseases. We also depict the multifaceted role of dendritic cells, serving as antigen presenting cells, contributing to the development of the pathognomonic cytokine signature and promote cellular and humoral autoimmune responses. Finally we describe the function and role of extracellular vesicles in particular autoimmune diseases. Targeting these key players of disease progression in patients with autoimmune diseases by immunomodulating therapy may be beneficial in future therapeutic strategies.