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Viruses 2016, 8(1), 5;

HTLV-1, Immune Response and Autoimmunity

Science Center of Health and Biology. Pará State University, Rua Perebebuí, 2623, Belém, Pará 66087-670, Brazil
Science Health Institute, Federal University of Pará, Praça Camilo Salgado, 1, Belém, Pará 66055-240, Brazil
Tropical Medicine Center, Federal University of Pará, Av. Generalíssimo Deodoro, 92, Belém, Pará 66055-240, Brazil
These authors contributed equally to this work.
Author to whom correspondence should be addressed.
Academic Editor: Louis M. Mansky
Received: 18 October 2015 / Revised: 27 November 2015 / Accepted: 14 December 2015 / Published: 24 December 2015
(This article belongs to the Special Issue Recent Advances in HTLV Research 2015)
Full-Text   |   PDF [357 KB, uploaded 24 December 2015]   |  


Human T-lymphotropic virus type-1 (HTLV-1) infection is associated with adult T-cell leukemia/lymphoma (ATL). Tropical spastic paraparesis/HTLV-1-associated myelopathy (PET/HAM) is involved in the development of autoimmune diseases including Rheumatoid Arthritis (RA), Systemic Lupus Erythematosus (SLE), and Sjögren’s Syndrome (SS). The development of HTLV-1-driven autoimmunity is hypothesized to rely on molecular mimicry, because virus-like particles can trigger an inflammatory response. However, HTLV-1 modifies the behavior of CD4+ T cells on infection and alters their cytokine production. A previous study showed that in patients infected with HTLV-1, the activity of regulatory CD4+ T cells and their consequent expression of inflammatory and anti-inflammatory cytokines are altered. In this review, we discuss the mechanisms underlying changes in cytokine release leading to the loss of tolerance and development of autoimmunity. View Full-Text
Keywords: Human T-lymphotropic virus type-1 (HTLV-1); immune response; autoimmunity Human T-lymphotropic virus type-1 (HTLV-1); immune response; autoimmunity

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Quaresma, J.A.S.; Yoshikawa, G.T.; Koyama, R.V.L.; Dias, G.A.S.; Fujihara, S.; Fuzii, H.T. HTLV-1, Immune Response and Autoimmunity. Viruses 2016, 8, 5.

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