Peripheral T regulatory cells and cytokines in hepatitis E infection

Tripathy, Anuradha S.; Das, Rumki; Rathod, Sanjay; Gurav, Yogesh K.; Arankalle, Vidya A.

doi:10.1007/s10096-011-1291-1

Cited by 41 publications

(35 citation statements)

References 21 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…ALT levels were significantly higher in AVH-E patients compared to the recovered individuals and controls. IgM levels were significantly higher and IgG levels were lower in AVH-E patients compared to the recovered individuals (Table 1) as reported [6–8]. …”

Section: Resultssupporting

confidence: 78%

“…Consumption of IL2 by the Treg cells [23] could be attributed to the absence of IL2 at the protein level of the previous report [8]. Difference in scenario at the gene level for IFN- γ , IL17A, CD95, PD1L, and CD70 for unstimulated and HEV rORF2p stimulated PBMCs suggests that there may be lack of robust HEV rORF2p-specific peripheral response in the HEV-infected patients [7].…”

Section: Discussionmentioning

confidence: 90%

“…Reports from our group and others suggest the involvement of both T cell subsets and antigen nonspecific cells in self-limiting HEV infection [6, 7, 13, 14]. We have recently reported peripheral CD11c, CD80, and CD83 expressions to be high in hepatitis E patients, CD11c expression to be positively associated with HEV replication [14], and association of T regulatory (Treg) cells in acute HEV infection [8]. Higher expressions of CTLA-4, PD1, GITR, CD95, CD103, and CD73 on T regulatory and T effector cells of HEV patients have indicated probable involvement of these molecules in Treg-mediated suppression [9].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Hepatitis E rORF2p Stimulated and Unstimulated Peripheral Expression Profiling in Patients with Self-Limiting Hepatitis E Infection

Rathod

Tripathy

2014

Journal of Immunology Research

View full text Add to dashboard Cite

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.

show abstract

Section: Resultssupporting

confidence: 78%

Section: Discussionmentioning

confidence: 90%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Hepatitis E rORF2p Stimulated and Unstimulated Peripheral Expression Profiling in Patients with Self-Limiting Hepatitis E Infection

Rathod

Tripathy

2014

Journal of Immunology Research

View full text Add to dashboard Cite

show abstract

“…effector T REG cells, suggesting that regulatory T cells are involved in hepatic injury and recovery [47] . The T REG cell pool is depleted during HAV infection due to Fas-mediated cellular apoptosis, resulting in severe liver injury [48] .…”

Section: Insult/injurymentioning

confidence: 99%

Acute-on-chronic liver failure: recent update

Alam

Suen

2016

J Biomed Res

View full text Add to dashboard Cite

Acute on chronic liver failure (ACLF) was first described in 1995 as a clinical syndrome distinct to classic acute decompensation. Characterized by complications of decompensation, ACLF occurs on a background of chronic liver dysfunction and is associated with high rates of organ failure and significant short-term mortality estimated between 45% and 90%. Despite the clinical relevance of the condition, it still remains largely undefined with continued disagreement regarding its precise etiological factors, clinical course, prognostic criteria and management pathways. It is concerning that, despite our relative lack of understanding of the condition, the burden of ACLF among cirrhotic patients remains significant with an estimated prevalence of 30.9%. This paper highlights our current understanding of ACLF, including its etiology, diagnostic and prognostic criteria and pathophysiology. It is evident that further refinement of the ACLF classification system is required in order to detect high-risk patients and improve short-term mortality rates. The field of metabolomics certainly warrants investigation to enhance diagnostic and prognostic parameters, while the use of granulocyte-colony stimulating factor is a promising future therapeutic intervention for patients with ACLF.

show abstract

“…The level of IL-10, a signature cytokine of Tregs, was also elevated in the similar manner. The elevation in frequencies of Treg cells and rise in IL-10 cytokine suggests the role of these cells in infection and recovery of hepatitis E. 107 …”

Section: Pathogenesismentioning

confidence: 99%

Hepatitis E: Molecular Virology and Pathogenesis

Panda

Varma

2013

Journal of Clinical and Experimental Hepatology

View full text Add to dashboard Cite

Hepatitis E virus is a single, positive-sense, capped and poly A tailed RNA virus classified under the family Hepeviridae. Enteric transmission, acute self-limiting hepatitis, frequent epidemic and sporadic occurrence, high mortality in affected pregnants are hallmarks of hepatitis E infection. Lack of an efficient culture system and resulting reductionist approaches for the study of replication and pathogenesis of HEV made it to be a less understood agent. Early studies on animal models, sub-genomic expression of open reading frames (ORF) and infectious cDNA clones have helped in elucidating the genome organization, important stages in HEV replication and pathogenesis. The genome contains three ORF's and three untranslated regions (UTR). The 5 0 distal ORF, ORF1 is translated by host ribosomes in a cap dependent manner to form the non-structural polyprotein including the viral replicase. HEV replicates via a negative-sense RNA intermediate which helps in the formation of the positive-sense genomic RNA and a single bi-cistronic sub-genomic RNA. The 3 0 distal ORF's including the major structural protein pORF2 and the multifunctional host interacting protein pORF3 are translated from the sub-genomic RNA. Pathogenesis in HEV infections is not well articulated, and remains a concern due to the many aspects like host dependent and genotype specific variations. Animal HEV, zoonosis, chronicity in immunosuppressed patients, and rapid decompensation in affected chronic liver diseased patients warrants detailed investigation of the underlying pathogenesis. Recent advances about structure, entry, egress and functional characterization of ORF1 domains has furthered our understanding about HEV. This article is an effort to review our present understanding about molecular biology and pathogenesis of HEV. ( J CLIN EXP HEPATOL 2013;3:114-124) H epatitis E virus was first identified in 1983 as the agent responsible for the large scale waterborne epidemics of acute, self-limiting hepatitis in developing nations.1 It was shown to be a naked 28-34 nm virus-like particle with spikes and inundations. 1,2Successful use of non-human primate models for HEV propagation helped in its isolation, cloning and sequencing and as presumed turned out to be an RNA virus.3,4 It had a $7.2 kb single stranded genome with sequence homology to other positive-sense RNA viruses. 4,5 Computer based genome annotation revealed three overlapping open reading frames ORF1, ORF2 and ORF3.4,5 The longest ORF, ORF1 formed the 5 0 distal end of the genome and coded for the non-structural replication proteins including methyltransferase, protease, helicase, and RNA dependent RNA polymerase (RdRp). The 30 distal ORF, ORF2 coded for an arginine rich protein, together with immunodominant sero-reactivity and agglutination against the expressed epitopes, it was predicted to be the major structural protein. A third ORF, ORF3 coded for a small protein thought to be a minor structural protein. [4][5][6] Molecular characterization and replication model of HEV remained...

show abstract

Peripheral T regulatory cells and cytokines in hepatitis E infection

Cited by 41 publications

References 21 publications

Hepatitis E rORF2p Stimulated and Unstimulated Peripheral Expression Profiling in Patients with Self-Limiting Hepatitis E Infection

Hepatitis E rORF2p Stimulated and Unstimulated Peripheral Expression Profiling in Patients with Self-Limiting Hepatitis E Infection

Acute-on-chronic liver failure: recent update

Hepatitis E: Molecular Virology and Pathogenesis

Contact Info

Product

Resources

About