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Monitoring of peptide-specific and gamma interferon-productive T cells in patients with active and convalescent tuberculosis using an enzyme-linked immunosorbent spot assay.

Clin Vaccine Immunol

March 2012

Department of Microbiology, Ministry of Education Key Laboratory of Tropical Diseases Control, Guangdong Provincial Research Center for Severe Infectious Disease Prevention and Control Technology, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, People's Republic of China.

To establish a high-efficiency gamma interferon-specific enzyme-linked immunosorbent spot assay (IFN-γ ELISPOT assay) for detection of tuberculosis (TB), peptides (E6, E7, and C14) and peptide mixtures (E6 plus E7 and E6 plus E7 plus C14) were used to monitor peripheral blood (PBL) samples from patients with pulmonary TB (PTB), as well as control samples. The positive detection rates of the five IFN-γ ELISPOT assays were 78.38%, 74.

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Siglec-1 on monocytes is a potential risk marker for monitoring disease severity in coronary artery disease.

Clin Biochem

July 2009

Department of Laboratory Medicine, Changzheng Hospital, Second Military Medical University and Clinical Immunology Center of PLA, 415 Feng Yang Road, Huang Pu District, Shanghai 200003, People's Republic of China.

Objectives: Siglec-1 has long been considered as an important biomarker of the activation of monocyte/macrophage and a type I interferon-specific imprint, but its role in atherosclerosis has not been elucidated.

Methods: We examined the expression of Siglec-1 by flow cytometry and RT-PCR in 83 CAD patients and 38 healthy controls. In addition, the levels of serum lipids, Gensini score, hs-CRP and homocysteine were determined.

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Albumin-interferon-alpha (alb-IFN) is a novel recombinant protein derived from IFN-alpha2b genetically fused to human albumin. The resulting single polypeptide combines in one molecule the antiviral properties of IFN-alpha with the long serum half-life of albumin. IFN-mediated biological responses stem from the engagement of IFN-alpha with its target receptor and subsequent modulation of IFN-specific gene (ISG) expression.

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Expression of toll-like receptors and type 1 interferon specific protein MxA in biliary atresia.

Lab Invest

January 2007

Department of Pediatrics, Chang Gung Memorial Hospital-Kaohsiung Medical Center and the Graduate Institute of Clinical Medical Sciences, Chang Gung University College of Medicine, Kaohsiung, Taiwan, ROC.

Viral infection and type I interferon have been implicated in the pathogenesis of biliary atresia (BA), but the expression of toll-like receptors (TLRs) that recognize viruses, as well as of type 1 interferon specific signaling molecules are still unknown in BA. Fresh liver tissues were obtained from patients in early and late stage of BA and from patients with choledochal cyst (CC), as well as from normal controls receiving liver resection for benign lesion other than cholestasis or fibrosis. Archived liver tissues from patients with neonatal hepatitis (NH) were obtained for immunohistochemical studies.

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The pathogenic NY-1 hantavirus G1 cytoplasmic tail inhibits RIG-I- and TBK-1-directed interferon responses.

J Virol

October 2006

Molecular and Cellular Biology Graduate Program, SUNY at Stony Brook, Stony Brook, NY 11794, USA.

Hantaviruses cause two diseases with prominent vascular permeability defects, hemorrhagic fever with renal syndrome and hantavirus pulmonary syndrome. All hantaviruses infect human endothelial cells, although it is unclear what differentiates pathogenic from nonpathogenic hantaviruses. We observed dramatic differences in interferon-specific transcriptional responses between pathogenic and nonpathogenic hantaviruses at 1 day postinfection, suggesting that hantavirus pathogenesis may in part be determined by viral regulation of cellular interferon responses.

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