Cytokine Networks Dysregulation during HTLV-1 Infection and Associated Diseases

Author(s)

Futsch, Nicolas ^[1] ; Prates, Gabriela ^{[2, 3]} ; Mahieux, Renaud ^[1] ; Casseb, Jorge ^{[2, 3]} ; Dutartre, Helene ^[1]

Affiliation

^[1] Univ Claude Bernard Lyon 1, Equipe Oncogenese Retrovirale, CNRS, ENS Lyon, INSERM, U1111, CIRI, UMR5308, Labex Ecofect, Equipe Labellise FRM, F-69007 Lyon - France

^[2] Inst Trop Med Sao Paulo, BR-05403000 Sao Paulo, SP - Brazil

^[3] Univ Sao Paulo, Dept Dermatol, Lab Dermatol & Immunodeficiencies, Med Sch, BR-01246100 Sao Paulo, SP - Brazil

• Document type: Review article
• Source: Viruses-Basel; v. 10, n. 12 DEC 2018.
• Web of Science Citations: 0

Abstract

Human T-cell leukemia virus type 1 (HTLV-1) is the causative agent of a neural chronic inflammation, called HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and of a malignant lymphoproliferation, called the adult T-cell leukemia/lymphoma (ATLL). The mechanisms through which the HTLV-1 induces these diseases are still unclear, but they might rely on immune alterations. HAM/TSP is associated with an impaired production of pro-inflammatory cytokines and chemokines, such as IFN-, TNF-, CXCL9, or CXCL10. ATLL is associated with high levels of IL-10 and TGF-. These immunosuppressive cytokines could promote a protumoral micro-environment. Moreover, HTLV-1 infection impairs the IFN-I production and signaling, and favors the IL-2, IL-4, and IL-6 expression. This contributes both to immune escape and to infected cells proliferation. Here, we review the landscape of cytokine dysregulations induced by HTLV-1 infection and the role of these cytokines in the HTLV-1-associated diseases progression. (AU)

• FAPESP's process: 14/22827-7 - Prevalence and incidence of early central nervous system disturbance in HTLV-1-infected subjects in Brazil
• Grantee: Jorge Simao do Rosario Casseb
• Support Opportunities: Regular Research Grants