Autoimmune Diseases

The textbook term "autoimmune disease" might be a misnomer - this is not a mischievous challenge, but since our immune system scans our body at each moment, recognising it as self, the disease process stands only for failure of such recognition. Should this occur, then the immune system arrives to the fallacy of self being foreign and agresses it: autoagressive disease is the term. Between may and june 2011, an outbreak of diarrhea and the hemolytic uremic syndrome (HUS)caused by Escherichia coli O104:H4 began in Germany early may 2011 to dwindle 2 months late. The shiga-toxin producing E. coli makes HUS and an autoantibody against complement factor C. HUS was lethal for 34 patients. Infectious agents display molecular mimicry with autoantigens, e.g. viral peptides may be presented by infected antigen presenting cells to myelin basic protein and other viruses and Bacteria (Campylobacter jejuni in Guillain-Barré disease) become associated with postinfectious autoimmune disease, the following events underlying their pathogenicity: infectious agent fixes to the host cell or mimicks autoantigens by expressing partial sequence homology between the microbial antigen and a self-determinant. Tissue injury by the infectious agent might break tolerance to self antigen thus perpetuating injury by an autoagressive process, or the infectious agent might enhance expression of MHC antigens. A complex network of cytokines that includes tumor necrosis factor (TNF), interleukin (IL)-1,-6,-8,-12,-15 and -17 mediates inflammation of autoimmunity involving, as a newcomer in our knowledge, TNF-like ligand 1A (TL1A). The anti-TNF monoclonal antibody adalimumab might well act through suppressing TL1A.

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