In 1974, in Nature, we hypothesized that removal of cytokines can be effective in the treatment of certain inflammatory diseases, e.g., rheumatoid arthritis (RA). We call this approach anticytokino-therapy. Later it was shown that neutralization of pro-inflammatory cytokines, such as tumor necrosis factor alpha (TNF-α), interferon alpha (IFN-α), interferon gamma (IFN-γ), and interleukin 6 (IL-6), leads to a good therapeutic effect. Anticytokinotherapy is currently used around the world for the treatment of rheumatoid arthritis, psoriasis, psoriatic arthritis, and other Th-1-mediated inflammatory diseases. Pro-inflammatory cytokines have also been found in other conditions (myocardial infarctions, strokes, chronic pain syndromes, etc.). This leads us to believe that hyper- production of pro-inflammatory cytokines forms a basis of a variety of pathological conditions and represents a uniform response of the organism to a wide variety of insults in any part of the body. Thus, we propose to add monoclonal antibodies to (or other blockers of) pro-inflammatory cytokines to the treatment regimens for myocardial infarctions, strokes, and possibly other Th-1-mediated diseases.
References
[1]
Skurkovich, S.V., Klinova, E.G., Aleksandrovskaya, I.M., Levina, N.V., Arkhipova, N.A. and Bulicheva, T.I. (1973) Stimulation of Transplantation Immunity and Plasma Cell Reaction by Interferon in Mice. Immunology, 25, 317-322.
[2]
Skurkovich, S.V., Klinova, E.G., Eremkina, E.I. and Levina, N.V. (1974) Immunosuppressive Effect of an Anti-Interferon Serum. Nature, 247, 551-552. http://dx.doi.org/10.1038/247551a0
[3]
Skurkovich, S. and Skurkovich, B. (1989) The Development of Autoimmune Diseases is Connected with the Initial Disturbance of Interferon Synthesis in the Cells. Journal of Interferon Research, 9, S305.
[4]
Skurkovich, S.V., Loukina, G.V., Sigidin, Y.A. and Skurkovich, B. (1998) Successful First-Time Use of Antibodies to Interferon-Gamma Alone and Combined with Antibodies to Tumor Necrosis Factor Alpha to Treat Rheumatic Diseases (Rheumatoid Arthritis, Systemic Lupus Erythemotosus, Psoriatic Arthritis, Behcet’s Syndrome). Intern Journal of Immunotherapy, 14, 23-32.
[5]
Elliott, M.J., Maini, R.N., Feldmann, M., Kalden, J.R., Antoni, C., Smolen, J.S., Leeb, B., Breedveld, F.C., Macfarlane, J.D., Bijl, H. and Woody, J.N. (1994) Randomized Double-Blind Comparison of Chimeric Monoclonal Antibody to Tumor Necrosis Factor Alpha (cA2) versus Placebo in Rheumatoid Arthritis. Lancet, 344, 1105-1110. http://dx.doi.org/10.1016/S0140-6736(94)90628-9
[6]
Skurkovich, B. and Skurkovich, S. (2006) Inhibition of IFN-as a Method of Treatment of Various Autoimmune Diseases, Including Skin Diseases. Ernst Schering Res Found Workshop, 56, 1-27.
http://dx.doi.org/10.1007/3-540-37673-9_1
[7]
Sharma, H.S. and Das, D.K. (1997) Role of Cytokines in Myocardial Ischemia and Reperfusion. Mediators Inflammation, 6, 175-183. http://dx.doi.org/10.1080/09629359791668
[8]
Starke, R.M., Raper, D.M., Ding, D., Chalouhi, N., Owens, G.K., Hasan, D.M., Mendel, R. and Dumont, A.S. (2013) Tumor Necrosis Factor-Modulates Cerebral Aneurism Formation and Rupture. Translational Stroke Research, 5, 269- 277. http://www.ncbi.nlm.nih.gov/pubmed/24323710
[9]
Simms, R.W. and Korn, J.H. (2002) Cytokine Directed Therapy in Scleroderma: Rationale, Current Status, and the Future. Current Opinion in Rheumatology, 14, 717-722. http://dx.doi.org/10.1097/00002281-200211000-00015
[10]
Canady, J., Karrer, S., Fleck, M. and Bosserhoff, A.K. (2013) Fibrosing Connective Tissue Disorders of the Skin: Molecular Similarities and Distinctions. Journal of Dermatological Science, 70, 151-158.
http://dx.doi.org/10.1016/j.jdermsci.2013.03.005