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Multiple effects of CD40–CD40L axis in immunity against infection and cancer

CD8(+) cytotoxic T lymphocyte (CTL) protects against infection and cancer cells. Understanding the mechanisms involved in generation and maintenance of effective CTL responses is essential for improving disease therapy and vaccine protocols. During CTL responses, immune cells encounter several tight...

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Detalles Bibliográficos
Autores principales: Ara, Anjuman, Ahmed, Khawaja Ashfaque, Xiang, Jim
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6029590/
https://www.ncbi.nlm.nih.gov/pubmed/29988701
http://dx.doi.org/10.2147/ITT.S163614
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author Ara, Anjuman
Ahmed, Khawaja Ashfaque
Xiang, Jim
author_facet Ara, Anjuman
Ahmed, Khawaja Ashfaque
Xiang, Jim
author_sort Ara, Anjuman
collection PubMed
description CD8(+) cytotoxic T lymphocyte (CTL) protects against infection and cancer cells. Understanding the mechanisms involved in generation and maintenance of effective CTL responses is essential for improving disease therapy and vaccine protocols. During CTL responses, immune cells encounter several tightly regulated signaling pathways; therefore, in such a dynamic process, proper integration of critical signals is necessary to orchestrate an effective immune response. In this review, we have focused on CD40–CD40L interactions (a key signal) in the regulation of dendritic cell (DC)–T cell (CD4(+) T and CD8(+) T) cross-talk, rescuing CTL exhaustion, and converting DC tolerization. We have also highlighted the knowledge gap and future directions to design immunotherapies.
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spelling pubmed-60295902018-07-09 Multiple effects of CD40–CD40L axis in immunity against infection and cancer Ara, Anjuman Ahmed, Khawaja Ashfaque Xiang, Jim Immunotargets Ther Review CD8(+) cytotoxic T lymphocyte (CTL) protects against infection and cancer cells. Understanding the mechanisms involved in generation and maintenance of effective CTL responses is essential for improving disease therapy and vaccine protocols. During CTL responses, immune cells encounter several tightly regulated signaling pathways; therefore, in such a dynamic process, proper integration of critical signals is necessary to orchestrate an effective immune response. In this review, we have focused on CD40–CD40L interactions (a key signal) in the regulation of dendritic cell (DC)–T cell (CD4(+) T and CD8(+) T) cross-talk, rescuing CTL exhaustion, and converting DC tolerization. We have also highlighted the knowledge gap and future directions to design immunotherapies. Dove Medical Press 2018-06-28 /pmc/articles/PMC6029590/ /pubmed/29988701 http://dx.doi.org/10.2147/ITT.S163614 Text en © 2018 Ara et al. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.
spellingShingle Review
Ara, Anjuman
Ahmed, Khawaja Ashfaque
Xiang, Jim
Multiple effects of CD40–CD40L axis in immunity against infection and cancer
title Multiple effects of CD40–CD40L axis in immunity against infection and cancer
title_full Multiple effects of CD40–CD40L axis in immunity against infection and cancer
title_fullStr Multiple effects of CD40–CD40L axis in immunity against infection and cancer
title_full_unstemmed Multiple effects of CD40–CD40L axis in immunity against infection and cancer
title_short Multiple effects of CD40–CD40L axis in immunity against infection and cancer
title_sort multiple effects of cd40–cd40l axis in immunity against infection and cancer
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6029590/
https://www.ncbi.nlm.nih.gov/pubmed/29988701
http://dx.doi.org/10.2147/ITT.S163614
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