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Mimotope‐hormesis and mortalin/grp75/mthsp70: a new hypothesis on how infectious disease‐associated epitope mimicry may explain low cancer burden in developing nations
Author(s) -
Deocaris Custer C.,
Taira Kazunari,
Kaul Sunil C.,
Wadhwa Renu
Publication year - 2005
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2004.11.108
Subject(s) - molecular mimicry , autoimmunity , immunology , biology , mimotope , epitope , cancer , disease , immune system , cancer immunotherapy , carcinogenesis , heat shock protein , immunotherapy , antibody , medicine , genetics , gene
It is generally observed that countries with heavy infectious burden show lower cancer incidence as compared to more affluent nations. With the emerging paradigm on microbial heat shock proteins (hsps) as molecular link between infections and autoimmune diseases, we posit a new hypothesis, the “mimotope‐hormesis”, on the immunologic impact of infections on regional cancer prevention. According to this, assaults of infection during early adulthood could fortify the immune system to evoke more potent defenses against late‐onset diseases, such as cancer, via autoimmunity. Interestingly, both experimental and clinical data support the beneficial role of autoimmunity in long‐term cancer survivors. We illustrate this by a comprehensive in silico mimotope (epitope mimicry) analysis of human infectious pathogens against mortalin (mthsp70/PB74/GRP75), a type of hsp70 protein involved in control of cell proliferation, immortalization and tumorigenesis.