HTLV-1 bZIP factor induces systemic inflammations in vivo

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HTLV-1 bZIP Factor Induces T-Cell Lymphoma and Systemic Inflammation In Vivo

Human T-cell leukemia virus type 1 (HTLV-1) is the causal agent of a neoplastic disease of CD4+ T cells, adult T-cell leukemia (ATL), and inflammatory diseases including HTLV-1 associated myelopathy/tropical spastic paraparesis, dermatitis, and inflammatory lung diseases. ATL cells, which constitutively express CD25, resemble CD25+CD4+ regulatory T cells (T(reg)). Approximately 60% of ATL cases...

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HTLV-1 bZIP Factor Induces Inflammation through Labile Foxp3 Expression

Human T-cell leukemia virus type 1 (HTLV-1) causes both a neoplastic disease and inflammatory diseases, including HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). The HTLV-1 basic leucine zipper factor (HBZ) gene is encoded in the minus strand of the proviral DNA and is constitutively expressed in infected cells and ATL cells. HBZ increases the number of regulatory T (Treg) ...

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HTLV-1 bZIP factor gene: Its roles in HTLV-1 pathogenesis.

The HTLV-1 bZIP factor (HBZ) gene is transcribed as an anti-sense transcript of HTLV-1 from the 3' long terminal repeat (LTR). Recent studies showed that the HBZ gene was expressed in all ATL cases, suggesting its critical role in leukemogenesis. In addition, only the HBZ gene sequence remains intact, unaffected by nonsense mutations and deletion. HBZ mRNA promotes proliferation of adult T-cell...

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HTLV-1 bZIP Factor RNA and Protein Impart Distinct Functions on T-cell Proliferation and Survival.

Infection of T cells with human T-cell leukemia virus type-1 (HTLV-1) induces clonal proliferation and is closely associated with the onset of adult T-cell leukemia-lymphoma (ATL) and inflammatory diseases. Although Tax expression is frequently suppressed in HTLV-1-infected cells, the accessory gene, HTLV-1 bZIP factor (HBZ), is continuously expressed and has been implicated in HTLV-1 pathogene...

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HTLV-1 bZIP factor HBZ promotes cell proliferation and genetic instability by activating OncomiRs.

Viruses disrupt the host cell microRNA (miRNA) network to facilitate their replication. Human T-cell leukemia virus type I (HTLV-1) replication relies on the clonal expansion of its host CD4(+) and CD8(+) T cells, yet this virus causes adult T-cell leukemia/lymphoma (ATLL) that typically has a CD4(+) phenotype. The viral oncoprotein Tax, which is rarely expressed in ATLL cells, has long been re...

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ژورنال

عنوان ژورنال: Retrovirology

سال: 2011

ISSN: 1742-4690

DOI: 10.1186/1742-4690-8-s1-a8