Journal
VIRUSES-BASEL
Volume 10, Issue 12, Pages -Publisher
MDPI
DOI: 10.3390/v10120691
Keywords
HTLV-1; immune system; HAM/TSP; ATLL; cytokines
Categories
Funding
- Ligue Nationale contre le Cancer, equipe labelisee program [EL2013-3Mahieux]
- LabEx Ecofect of the Universite de Lyon [ANR-11-LABX-0048]
- Conselho Nacional de Pesquisa Tecnologico (CNP) [CNPq 301685/2016-9]
- FAPESP (Fundacao de Amparo a Pesquisa do Estado de Sao Paulo) [2014/22827-7]
- Ligue contre le Cancer
- CNPq [133783/2018-9]
- Soroptimist groupe de l'Ariege
- ENS-Lyon
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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.
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