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Review
. 2012 Jan 1;4(5):1864-70.
doi: 10.2741/e508.

Molecular recognition theory and sense-antisense interaction: therapeutic applications in autoimmunity

Affiliations
Review

Molecular recognition theory and sense-antisense interaction: therapeutic applications in autoimmunity

Matthew Thomas Hardison et al. Front Biosci (Elite Ed). .

Abstract

Perhaps behind only the understanding of the genetic code in importance is the comprehension of protein sequence and structure in its effect on modern scientific investigation. How proteins are structured and interact dictates a considerable amount of the body's processes in maintaining homeostasis. Unfortunately, in diseases of autoimmunity, these processes are directed against the body itself and most of the current clinical responses are severely lacking. This review addresses current therapeutics involved in the treatment of various autoimmune diseases and details potential future therapeutics designed with a more targeted approach. Detailed in this manuscript is the concept of utilizing peptides possessing an inverse hydropathy to the immunogenic region of proteins to generate anti-idiotypic (anti-Id) and anti-clonotypic T cell receptor (TCR) antibodies (Abs). Theoretically, the anti-Id Abs cross react with Id Abs and negate the powerful machinery of the adaptive immune response with little to no side effects. A series of studies by a number of groups have shown this to be an exciting and intriguing concept that will likely play a role in the future treatment of autoimmune diseases.

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References

    1. Jacobson DL, Gange SJ, Rose NR, Graham NM. Epidemiology and estimated population burden of selected autoimmune diseases in the United States. Clin Immunol Immunopathol. 1997;84:223–243. - PubMed
    1. Costantino CM, Baecher-Allan CM, Hafler DA. Human regulatory T cells and autoimmunity. Eur J Immunol. 2008;38:921–924. - PMC - PubMed
    1. Sherer Y, Shoenfeld Y. The idiotypic network in antinuclear-antibody-associated diseases. Int Arch Allergy Immunol. 2000;123:10–15. - PubMed
    1. Sakarellos-Daitsiotis M, Cung MT, Sakarellos C, Hilali ZE, Kosmopoulou A, Voitharou C. Complementary peptide epitopes and anti-idiotypic antibodies in autoimmunity. Protein Pept Lett. 2004;11:367–375. - PubMed
    1. Kawahito Y, Cannon GW, Gulko PS, Remmers EF, Longman RE, Reese VR, Wang J, Griffiths MM, Wilder RL. Localization of quantitative trait loci regulating adjuvant-induced arthritis in rats: evidence for genetic factors common to multiple autoimmune diseases. J Immunol. 1998;161:4411–4419. - PubMed

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