Thromboembolism is being detected at increasing rates in pediatric tertiary care hospitals. The incidence of pediatric thrombophilia differs across countries, and is unknown in Japan. We sent a survey to 520 pediatric department heads and 629 specialists, requesting details on patients who developed symptomatic thromboembolism between 2006 and 2010.
View Article and Find Full Text PDFHuman T-lymphotropic virus type 1 (HTLV-1) is the causative agent of adult T-cell leukemia/lymphoma (ATL). Miscellaneous host immune surveillance systems control T-cell growth/leukemogenesis during HTLV-1 infection. We characterized CD70 and CD27 expression on lymphocytes of HTLV-1 carriers and patients with ATL (study approved by the local Medical Ethical Committee).
View Article and Find Full Text PDFBiochem Biophys Res Commun
October 2014
HTLV-1 infection is a life-long retroviral infection. Chronic viral antigenic stimulation induces persistent infection which results in a clinically asymptomatic carrier state. Only a minor proportion of infected individuals develop adult T cell leukemia/lymphoma (ATLL) or HTLV-1-associated myelopathy/tropical spastic myelopathy (HAM/TSP).
View Article and Find Full Text PDFCD8+ T cell response is important in the response to viral infections; this response though is regulated by inhibitory receptors. Expression of inhibitory receptors has been positively correlated with CD8+ T cell exhaustion; the consequent effect of simultaneous blockade of these inhibitory receptors on CD8+ T cell response in viral infections have been studied, however, the role of individual blockade of receptor-ligand pair is unclear. 2B4/CD48 interaction is involved in CD8+T cell regulation, its signal transducer SAP (signaling lymphocyte activation molecule (SLAM)-associated protein) is required for stimulatory function of 2B4/CD244 on lymphocytes hence, we analyzed 2B4/CD244 (natural killer cell receptor) and SAP (signaling lymphocyte activation molecule(SLAM)-associated protein) on total CD8+ and HTLV-1 specific CD8+T cells in HTLV-1 infection and the effect of blockade of interaction with ligand CD48 on HTLV-1 specific CD8+ T cell function.
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