title: Hepatitis E rORF2p stimulated and unstimulated peripheral expression profiling in patients with self-limiting hepatitis E infection.
abstract: To improve the current knowledge on the involvement of peripheral lymphocytes in hepatitis E virus (HEV) associated pathogenesis, we analyzed alterations in (1) immunophenotypic expressions (by flow cytometry) and (2) gene expression patterns (by TaqMan Low Density Array) of activatory, inhibitory, integrin, homing, ectonucleotidase machinery, costimulatory, inflammatory markers, and T regulatory cells (Treg) associated cytokines on HEV rORF2p stimulated and unstimulated PBMCs of 43 acute HEV patients, 30 recovered individuals, and 43 controls. The phenotypic expressions of key molecules CTLA-4, GITR, CD103, CD25, CD69, IL10 and TGF- β 1 in the acute patients and TGF- β 1 in the recovered individuals were significantly elevated on both unstimulated and stimulated PBMCs. Gene expression array data revealed upregulations of CD25, PD1, CD103, CCR4, IL10, and TGF- β 1 on both unstimulated and HEV rORF2p stimulated PBMCs of acute patients. The observed upregulations of inhibitory, integrin, activatory, and Treg-associated cytokine genes on the PBMCs of acute HEV patients complemented by their frequency data suggest them as the major players in the fine-tuning of immune response in self-limiting hepatitis E infection.
authors: Hepatitis Group, National Institute of Virology, Pune, 130/1, Sus Road, Pashan, Pune, Maharashtra 411021, India.
authors: Sanjay B
authors: SB
authors: Rathod
authors: Hepatitis Group, National Institute of Virology, Pune, 130/1, Sus Road, Pashan, Pune, Maharashtra 411021, India.
authors: Anuradha S
authors: AS
authors: Tripathy
mesh_terms: D000208:Acute Disease; D000293:Adolescent; D000328:Adult; D015703:Antigens, CD / Q000235:genetics / Q000276:immunology; D060908:CTLA-4 Antigen / Q000235:genetics / Q000276:immunology; D016022:Case-Control Studies; D005260:Female; D020869:Gene Expression Profiling; D005786:Gene Expression Regulation / Q000187:drug effects*; D053450:Glucocorticoid-Induced TNFR-Related Protein / Q000235:genetics / Q000276:immunology; D016751:Hepatitis E / Q000235:genetics* / Q000276:immunology / Q000473:pathology / Q000821:virology; D016752:Hepatitis E virus / Q000276:immunology; D054884:Host-Pathogen Interactions; D006801:Humans; D016753:Interleukin-10 / Q000235:genetics / Q000276:immunology; D008213:Lymphocyte Activation / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D061251:Primary Cell Culture; D011994:Recombinant Proteins / Q000494:pharmacology; D050378:T-Lymphocytes, Regulatory / Q000187:drug effects* / Q000276:immunology / Q000473:pathology / Q000821:virology; D053773:Transforming Growth Factor beta1 / Q000235:genetics / Q000276:immunology; D014764:Viral Proteins / Q000494:pharmacology*
chemical_list: D015703:Antigens, CD; D060908:CTLA-4 Antigen; D053450:Glucocorticoid-Induced TNFR-Related Protein; C508609:IL10 protein, human; C400971:ORF2 protein, Hepatitis E virus; D011994:Recombinant Proteins; C491405:TNFRSF18 protein, human; D053773:Transforming Growth Factor beta1; D014764:Viral Proteins; D016753:Interleukin-10