Data/hora: 04/06/2024 16:25:55

Provedor de dados: | Brazilian Journal of Infectious Diseases
País: | Brazil
Título: | T cell receptor signaling pathway is overexpressed in CD4 + T cells from HAM/TSP individuals
Autores: | Pinto,Mariana Tomazini; Malta,Tathiane Maistro; Rodrigues,Evandra Strazza; Takayanagui,Osvaldo Massaiti; Tanaka,Yuetsu; Covas,Dimas Tadeu; Kashima,Simone.
Data: | 2015-12-01
Ano: | 2015
Palavras-chave: | HTLV-1; HAM/TSP; CD4+ T cell activation; Gene expression.
Resumo: | ABSTRACT Human T-lymphotropic virus type 1 (HTLV-1) is a human retrovirus related to the chronic neuroinflammatory disease HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). CD4+ T cells activation appears to play a key role on HTLV-1 infection. Here we investigated the expression of genes associated to T cell activation CD3e molecule, epsilon (CD3?), lymphocyte-specific protein tyrosine kinase (LCK), vav 1 guanine nucleotide exchange factor (VAV1), and zeta-chain (TCR) associated protein kinase 70 kDa (ZAP70) on T lymphocytes of HTLV-1-infected individuals and compared to healthy uninfected individuals (CT). We observed that CD3?, LCK, ZAP70, and VAV1 gene expression were increased in CD4+ T cells from HAM/TSP group compared to HTLV-1 asymptomatic patients (HAC). Moreover, ZAP70 and VAV1 were also upregulated in HAM/TSP compared to CT group. We detected a positive correlation among all these genes. We also observed that CD3?, LCK, and VAV1 genes had a positive correlation with the proviral load (PVL) and Tax expression. These results suggest that PVL and Tax protein could drive CD3?, LCK, and VAV1 gene expression in CD4+ T cells, and these genes function on a synchronized way on the CD4+ T cell activation. The elucidation of the mechanisms underlying T cell receptor signaling pathway is of considerable interest and might lead to new insights into the mechanism of HAM/TSP.
Tipo: | Info:eu-repo/semantics/article
Idioma: | Inglês
Identificador: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1413-86702015000600578
Editor: | Brazilian Society of Infectious Diseases
Relação: | 10.1016/j.bjid.2015.07.008
Formato: | text/html
Fonte: | Brazilian Journal of Infectious Diseases  v.19 n.6 2015
Fonte: | info:eu-repo/semantics/openAccess