Molecular mimicry is the theoretical possibility that sequence similarities between foreign and self-peptides are enough to result in the cross-activation of autoreactive T or B cells by pathogen-derived peptides. Despite the prevalence of several peptide sequences which can be both foreign and self in nature, just a few crucial residues can activate a single antibody or TCR (T cell receptor). This highlights the importance of structural homology in the theory of molecular mimicry. Upon activation, these "peptide mimic" specific T or B cells can cross-react with self-epitopes, thus leading to tissue pathology (autoimmunity).[1] Molecular mimicry is one of several ways in which autoimmunity can be evoked. A molecular mimicking event is more than an epiphenomenon despite its low probability, and these events have serious implications in the onset of many human autoimmune disorders.
One possible cause of autoimmunity, the failure to recognize self antigens as "self", is a loss of immunological tolerance, the ability for the immune system to discriminate between self and non-self. Other possible causes include mutations governing programmed cell death or environmental products that injure target tissues, thus causing a release of immunostimulatory alarm signals.[2][3] Growth in the field of autoimmunity has resulted in more frequent diagnosis of autoimmune diseases. The resulting data show that autoimmune diseases affect approximately 1 in 31 people within the general population.[4] Growth has also led to a greater characterization of what autoimmunity is and how it can be studied and treated. With more research comes growth in the study of the several different ways in which autoimmunity can occur, one of which is molecular mimicry. The mechanism by which pathogens have similar amino acid sequences or the homologous three-dimensional crystal structure of immunodominant epitopes remains a mystery.
^Kohm, A.P., Fuller, K.G. and Miller, S.D. (2003). "Mimicking the way to autoimmunity: an evolving theory of sequence and structural homology". Trends in Microbiology. 11 (3): 101–105. doi:10.1016/S0966-842X(03)00006-4. PMID 12648936.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^Matzinger, P (1998). "An innate sense of Danger". Seminars in Immunology. 10 (5): 399–415. doi:10.1006/smim.1998.0143. PMID 9840976.
^Matzinger, P (2002). "The Danger Model: A Renewed Sense of Self". Science. 296 (5566): 301–5. Bibcode:2002Sci...296..301M. CiteSeerX 10.1.1.127.558. doi:10.1126/science.1071059. PMID 11951032. S2CID 13615808.
^Shoenfeld, Y.; Gershwin, M.E. (2002). "Autoimmunity at a glance". Autoimmunity Reviews. 1 (1–2): 1. doi:10.1016/S1568-9972(01)00011-8.
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