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Autoimmunity - an Introduction

Autoimmune Diseases II

Hughes-Syndrome or antiphospholipid syndrome (APS) is an autoimmune disease that affects predominantly young women in their reproductive ages. The disease causes thromboses, recurring miscarriage and intrauterine fetal death without any explicable reason. The blood of these patients contains specific autoantibodies against phospholipids like cardiolipin or phospholipid-binding proteins.

Fig.1
Structure of cardiolipin

-O-C(O)R: saturated or unsaturated fatty acids

Fig.2
Barley (Hordeum vulgare)
Foto "Ährengold" © 2010 stormpic / aboutpixel.de

Celiac disease is a chronic autoimmune disease triggered by intolerance to the grain component gluten.

In celiac disease, local autoimmune reactions in the mucosa of the small intestine develop after intake of gliadin, a protein from wheat. Proteins such as gliadin can pass through the layer of epithelial cells of the intestinal lining. The damaged mucosa is not able to absorb essential nutrients, leading to deficiencies and developmental disorders if children are affected.

Fig.3
Wheat (Triticum aestivum L. subsp. aestivum)
Urheber: Franz Eugen Köhler, Köhler's Medizinal-Pflanzen

Recent research has also shown that autoimmune processes are implicated in cases of arteriosclerosis. After all, diseases basing on an autoreactive meachanisms are quite common.

Further readings

  • Antiphospholipid Syndrome - a Challenge for Laboratory Diagnostics (PDF-Download). In: Up-to-Date 2009, Publisher Orgentec Diagnostika, Mainz, Germany.
  • Celiac Disease - From Childhood Disease to Common Ailment (PDF-Download). In: Up-to-Date 2008, Publisher Orgentec Diagnostika, Mainz, Germany.

Literature

Wick, G.; Knoflach, M.; Xu, Q. (2004): Autoimmune and Inflammatory Mechanisms in Atherosclerosis.. In: Annual Review of Immunology. 22 (1) , 361-403
Titel des Artikels
Autoimmune and Inflammatory Mechanisms in Atherosclerosis.
Abstract
The present review focuses on the concept that cellular and humoral immunity to the phylogenetically highly conserved antigen heat shock protein 60 (HSP60) is the initiating mechanism in the earliest stages of atherosclerosis. Subjecting arterial endothelial cells to classical atherosclerosis risk factors leads to the expression of HSP60 that then may serve as a target for pre-existent cross-reactive antimicrobial HSP60 immunity or bona fide autoimmune reactions induced by biochemically altered autologous HSP60. Endothelial cells can also bind microbial or autologous HSP60 via Toll-like receptors, providing another possibility for targetting adaptive or innate immunological effector mechanisms.
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