HTLV-1, Immune Response and Autoimmunity |
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Authors: | Juarez A S Quaresma Gilberto T Yoshikawa Roberta V L Koyama George A S Dias Satomi Fujihara Hellen T Fuzii |
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Affiliation: | 1.Science Center of Health and Biology. Pará State University, Rua Perebebuí, 2623, Belém, Pará 66087-670, Brazil; (J.A.S.Q.); (R.V.L.K.); (G.A.S.D.);2.Science Health Institute, Federal University of Pará, Praça Camilo Salgado, 1, Belém, Pará 66055-240, Brazil; ;3.Tropical Medicine Center, Federal University of Pará, Av. Generalíssimo Deodoro, 92, Belém, Pará 66055-240, Brazil; |
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Abstract: | 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. |
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Keywords: | Human T-lymphotropic virus type-1 (HTLV-1) immune response autoimmunity |
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