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-γ, TNF-α, CXCL9, or CXCL10. ATLL is associated with high levels of IL-10 and TGF-β. 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.
Highlights
Human T-cell leukemia virus type 1 (HTLV-1), the first oncogenic retrovirus identified in humans, is the etiological agent of two main diseases—HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and the adult T-cell leukemia/lymphoma (ATLL)
Both diseases generally occur after a long period of latency, with approximatively, 1 to 2% and 2 to 4% of carriers being at risk for HAM/TSP or ATLL development, respectively [1]
IL-4 is undetectable in culture supernatants obtained from ATLL cells or in the supernatant from ATLL cells, before or after stimulation [38,40]. These results suggest that the HTLV-1 infection is not enough to maintain the IL-4 production and IL-4-induced proliferation
Summary
Human T-cell leukemia virus type 1 (HTLV-1), the first oncogenic retrovirus identified in humans, is the etiological agent of two main diseases—HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP) and the adult T-cell leukemia/lymphoma (ATLL). Both diseases generally occur after a long period of latency, with approximatively, 1 to 2% and 2 to 4% of carriers being at risk for HAM/TSP or ATLL development, respectively [1]. ATLL is described as a highly aggressive HTLV-1-infected CD4+ T-cells proliferation and was classified into four clinical subtypes, i.e., smoldering, chronic, acute, and lymphoma subtypes [18] Both diseases are characterized by an alteration in the immune system. We try to explain how the interaction of the HTLV-1 with the immune system leads to a potential dysregulation of cytokines production or signaling, allowing viral persistence and, eventually, pathogenesis
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