alexa
Reach Us +44-1647-403003
Role of USP 18 in Immune Response to Chronic Viral Infection | OMICS International
ISSN: 2161-0703
Journal of Medical Microbiology & Diagnosis

Like us on:

Make the best use of Scientific Research and information from our 700+ peer reviewed, Open Access Journals that operates with the help of 50,000+ Editorial Board Members and esteemed reviewers and 1000+ Scientific associations in Medical, Clinical, Pharmaceutical, Engineering, Technology and Management Fields.
Meet Inspiring Speakers and Experts at our 3000+ Global Conferenceseries Events with over 600+ Conferences, 1200+ Symposiums and 1200+ Workshops on Medical, Pharma, Engineering, Science, Technology and Business

Role of USP 18 in Immune Response to Chronic Viral Infection

Moyen Uddin PKM*

Department of Biochemistry, Primeasia University, Bangladesh

*Corresponding Author:
Moyen Uddin PKM
Department of Biochemistry
Primeasia University
Bangladesh
Tel: 88-01816487617
E-mail: moyen. [email protected]

Received date: April 13, 2015; Accepted date: May 26, 2015; Published date: May 28, 2015

Citation: Uddin PKMM (2015) Role of USP 18 in Immune Response to Chronic Viral Infection. J Med Microb Diagn 4: 189. doi: 10.4172/2161-0703.1000189

Copyright: © 2015 Uddin PKMM. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Visit for more related articles at Journal of Medical Microbiology & Diagnosis

Abstract

Type I IFNs is vital for host defense against viral and bacterial infections. In addition, type I IFNs are also acknowledged to be involved in many immunoregulatory processes, such as NK cell activation and proliferation/survival of CD8+ T cells.

Type I IFNs is vital for host defense against viral and bacterial infections. In addition, type I IFNs are also acknowledged to be involved in many immunoregulatory processes, such as NK cell activation [1] and proliferation/survival of CD8+ T cells [2,3]. Beside their well-known role in innate immunity, type I IFNs are constitutively expressed at a low level to ensure the maintenance of cellular homeostasis and may also play a role in shaping the adaptive immunity [4-6]. This constitutive IFN expression may, however, have detrimental effects if not tightly controlled. Usp18 is an IFN-inducible cysteine protease of the ubiquitin-specific protease family [7] and acts as an ISG15 deconjugating protease in the ISGylation system [8]. Furthermore, Usp18 functions in the type I IFN pathway by down regulating the JAK/STAT pathway independently of its isopeptidase activity through an interaction between Usp18 and the IFNAR2 subunit of the type I IFN receptor complex, whereas neither IFNAR1 nor IFNGR1 (type II IFN) receptor subunits were able to interact with Usp18 [9]. Usp18-deficient cells have enhanced IFN-a/b signaling and more ISG15 modified proteins [10]. As confirmed by gene expression microarray, the expression of IFN-inducible genes is increased and prolonged in the absence of Usp18 [8]. Accordingly, a deficiency in Usp18 increases the sensitivity of cells to IFN-I [9]. Consistently, Usp18-deficient mice exhibit limited viral replication after infection. How Usp18 expression influences the immune response, however, is still not completely understood. The amount of https://www.omicsonline.org/could-human-leukocyte-antigens-(hla)-be-predictive-factors-to-interferon-response-among-chronic-hepatitis-c-virus-hepatitis-2161-0703.S1-003.php?aid=15380 presented is a crucial determinant of the adaptive immune response. In vitro studies found that only 10 peptide–MHC (pMHC) complexes can form an immunological synapse between DCs and T cells [10]. However, lowaffinity T-cell receptors (TCRs) require a larger dose of antigen than high-affinity TCRs [11]. Henrickson et al. found that DCs require at least 2×104pMHC complexes to induce T-cell proliferation in lymph nodes in vivo. Additionally, the duration of the initial priming phase is inversely correlated with the amount of antigen presented [12].These findings suggest that a larger dose of antigen improves T-cell immunity. Consistently, low-dose application of inactivated virus results in limited induction of neutralizing antibodies, whereas replicating virus leads to a strong antibody response [13,14]. Accordingly, a specific compartment that promotes viral replication and increases the presented dose of antigen might improve the adaptive immune response.

References

Select your language of interest to view the total content in your interested language
Post your comment

Share This Article

Article Usage

  • Total views: 14330
  • [From(publication date):
    June-2015 - Apr 03, 2020]
  • Breakdown by view type
  • HTML page views : 10492
  • PDF downloads : 3838
Top