Literature DB >> 20146719

Cross-presentation of peptides from intracellular pathogens by MHC class I molecules.

Nicolas Blanchard1, Nilabh Shastri.   

Abstract

Many prokaryotic and eukaryotic parasites multiply in specialized subcellular niches in the host cell. The invading microbes hijack key cellular functions to establish the intracellular niches but, unlike viruses, do not need the protein synthesis machinery of host cells to replicate. Circulating CD8+ T cells provide protective immunity by recognizing pathogen-derived peptide major histocompatibility complex class I molecules (pMHC I) expressed by infected cells. Here, we review studies on the complex and varied pathways that produce the appropriate pMHC I as ligands for the CD8+ T cells. We also discuss possible explanations for the curious observations that CD8+ T cells are specific for fewer pMHC I ligands in parasite infections compared to the diversity of pMHC I ligands in viral infections.

Entities:  

Mesh:

Substances:

Year:  2010        PMID: 20146719     DOI: 10.1111/j.1749-6632.2009.05135.x

Source DB:  PubMed          Journal:  Ann N Y Acad Sci        ISSN: 0077-8923            Impact factor:   5.691


  10 in total

1.  Both Major Histocompatibility Complex Class I (MHC-I) and MHC-II Molecules Are Required, while MHC-I Appears To Play a Critical Role in Host Defense against Primary Coxiella burnetii Infection.

Authors:  Laura Buttrum; Lindsey Ledbetter; Rama Cherla; Yan Zhang; William J Mitchell; Guoquan Zhang
Journal:  Infect Immun       Date:  2018-03-22       Impact factor: 3.441

Review 2.  Induction and function of virus-specific CD4+ T cell responses.

Authors:  Jason K Whitmire
Journal:  Virology       Date:  2011-01-14       Impact factor: 3.616

3.  Efficacy of intracellular activated promoters for generation of Salmonella-based vaccines.

Authors:  Xin Xu; Mohamed I Husseiny; Andreas Goldwich; Michael Hensel
Journal:  Infect Immun       Date:  2010-08-23       Impact factor: 3.441

4.  Immune regulation and evasion of Mammalian host cell immunity during viral infection.

Authors:  B M Pratheek; Soham Saha; Prasanta K Maiti; Soma Chattopadhyay; Subhasis Chattopadhyay
Journal:  Indian J Virol       Date:  2013-03-15

5.  Limited transplantation of antigen-expressing hematopoietic stem cells induces long-lasting cytotoxic T cell responses.

Authors:  Warren L Denning; Jun Xu; Siqi Guo; Christopher A Klug; Zdenek Hel
Journal:  PLoS One       Date:  2011-02-17       Impact factor: 3.240

6.  Bacteria modulate the CD8+ T cell epitope repertoire of host cytosol-exposed proteins to manipulate the host immune response.

Authors:  Yaakov Maman; Ran Nir-Paz; Yoram Louzoun
Journal:  PLoS Comput Biol       Date:  2011-10-13       Impact factor: 4.475

7.  Bacteria-host transcriptional response during endothelial invasion by Staphylococcus aureus.

Authors:  Rasmus Birkholm Grønnemose; Christian Garde; Claes Søndergaard Wassmann; Janne Kudsk Klitgaard; Ronni Nielsen; Susanne Mandrup; Andreas Holm Mattsson; Thomas Emil Andersen
Journal:  Sci Rep       Date:  2021-03-16       Impact factor: 4.379

8.  Location of the CD8 T cell epitope within the antigenic precursor determines immunogenicity and protection against the Toxoplasma gondii parasite.

Authors:  Virginie Feliu; Virginie Vasseur; Harshita S Grover; H Hamlet Chu; Mark J Brown; Jeremy Wang; Jon P Boyle; Ellen A Robey; Nilabh Shastri; Nicolas Blanchard
Journal:  PLoS Pathog       Date:  2013-06-20       Impact factor: 6.823

Review 9.  Host-Brucella interactions and the Brucella genome as tools for subunit antigen discovery and immunization against brucellosis.

Authors:  Gabriel Gomez; Leslie G Adams; Allison Rice-Ficht; Thomas A Ficht
Journal:  Front Cell Infect Microbiol       Date:  2013-05-16       Impact factor: 5.293

10.  Escape from the Phagosome: The Explanation for MHC-I Processing of Mycobacterial Antigens?

Authors:  Melanie J Harriff; Georgiana E Purdy; David M Lewinsohn
Journal:  Front Immunol       Date:  2012-03-05       Impact factor: 7.561

  10 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.