Autoimmune Disease: Pathogenesis

Matteo Bellone, Istituto Scientifico San Raffaele, Milan, Italy

Published online: September 2010

DOI: 10.1002/9780470015902.a0001276.pub3

Autoimmune diseases are a vast array of organ-specific as well as systemic diseases, whose pathogenesis stems from the activation of B- and T lymphocytes reacting against antigens of the body's own tissues (defined as ‘self’). T- and B lymphocytes are the main components of the adaptive arm of the immune system, and their major task is to rapidly and efficiently remove pathogens (e.g. viruses or bacteria) in the absence of relevant tissue damage and self-recognition. In physiologic conditions, the ability of the immune system to avoid responsiveness to self-antigens is obtained by the cooperative efforts of central and peripheral tolerance mechanisms. Alteration of either one of the two mechanisms favours the induction of autoimmune diseases that may either cause complete and irreversible loss of function of the targeted tissue or its hyperfunction.

Key Concepts:

  • Autoimmune diseases are the result of specific immune responses directed against structures of the self.
  • Autoimmune diseases are the consequence of an altered function of the immune system.
  • Autoimmune disease may involve a single tissue or multiple organs.
  • Consequences of an autoimmune reaction may either be the loss of function or the hyperfunction of the target tissue.
  • An autoimmune response may be primarily T- or B-cell-mediated, or both.

Keywords: autoimmunity; autoimmune disease; pathogenesis; tolerance

Figure 1. All types of immune-mediated tissue damage may cause autoimmune diseases. See text for details. Ig, immunoglobulin; NK, natural killer; CD, cluster of differentiation.
Figure 2. In systemic lupus erythematosus (SLE), immune complexes and complement deposited at the renal glomeruli cause glomerulonephritis. (a) Proliferative SLE nephritis (World Health Organisation class IV) with mesangial expansion in all lobules, segmental double contours and abundant, numerous subendothelial linear deposits (AFOG, acid fuchsin orange G; original magnification ×125). (b) Immunofluorescence microscopy showing C1q capillary linear deposits (original magnification ×40). (c) Diffuse subendothelial linear deposits, counterpart to the wire-loop lesion, in a double-contour pattern. Smaller deposits are present in the mesangium. Bar, 2.5 m (uranyl acetate and lead citrate stain; original magnification ×3000). Courtesy of Dr G Dell'Antonio, H San Raffaele, Milan, Italy.
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Article Title: Autoimmune Disease: Pathogenesis
 
How to Cite close
Bellone, Matteo(Sep 2010) Autoimmune Disease: Pathogenesis. In: eLS. John Wiley & Sons Ltd, Chichester. http://www.els.net [doi: 10.1002/9780470015902.a0001276.pub3]