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Differential Regional Immune Response in Chagas Disease
Following infection, lymphocytes expand exponentially and differentiate into effector cells to control infection and coordinate the multiple effector arms of the immune response. Soon after this expansion, the majority of antigen-specific lymphocytes die, thus keeping homeostasis, and a small pool o...
Autores principales: | , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2009
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2700264/ https://www.ncbi.nlm.nih.gov/pubmed/19582140 http://dx.doi.org/10.1371/journal.pntd.0000417 |
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author | de Meis, Juliana Morrot, Alexandre Farias-de-Oliveira, Désio Aurélio Villa-Verde, Déa Maria Serra Savino, Wilson |
author_facet | de Meis, Juliana Morrot, Alexandre Farias-de-Oliveira, Désio Aurélio Villa-Verde, Déa Maria Serra Savino, Wilson |
author_sort | de Meis, Juliana |
collection | PubMed |
description | Following infection, lymphocytes expand exponentially and differentiate into effector cells to control infection and coordinate the multiple effector arms of the immune response. Soon after this expansion, the majority of antigen-specific lymphocytes die, thus keeping homeostasis, and a small pool of memory cells develops, providing long-term immunity to subsequent reinfection. The extent of infection and rate of pathogen clearance are thought to determine both the magnitude of cell expansion and the homeostatic contraction to a stable number of memory cells. This straight correlation between the kinetics of T cell response and the dynamics of lymphoid tissue cell numbers is a constant feature in acute infections yielded by pathogens that are cleared during the course of response. However, the regional dynamics of the immune response mounted against pathogens that are able to establish a persistent infection remain poorly understood. Herein we discuss the differential lymphocyte dynamics in distinct central and peripheral lymphoid organs following acute infection by Trypanosoma cruzi, the causative agent of Chagas disease. While the thymus and mesenteric lymph nodes undergo a severe atrophy with massive lymphocyte depletion, the spleen and subcutaneous lymph nodes expand due to T and B cell activation/proliferation. These events are regulated by cytokines, as well as parasite-derived moieties. In this regard, identifying the molecular mechanisms underlying regional lymphocyte dynamics secondary to T. cruzi infection may hopefully contribute to the design of novel immune intervention strategies to control pathology in this infection. |
format | Text |
id | pubmed-2700264 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2009 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-27002642009-07-07 Differential Regional Immune Response in Chagas Disease de Meis, Juliana Morrot, Alexandre Farias-de-Oliveira, Désio Aurélio Villa-Verde, Déa Maria Serra Savino, Wilson PLoS Negl Trop Dis Review Following infection, lymphocytes expand exponentially and differentiate into effector cells to control infection and coordinate the multiple effector arms of the immune response. Soon after this expansion, the majority of antigen-specific lymphocytes die, thus keeping homeostasis, and a small pool of memory cells develops, providing long-term immunity to subsequent reinfection. The extent of infection and rate of pathogen clearance are thought to determine both the magnitude of cell expansion and the homeostatic contraction to a stable number of memory cells. This straight correlation between the kinetics of T cell response and the dynamics of lymphoid tissue cell numbers is a constant feature in acute infections yielded by pathogens that are cleared during the course of response. However, the regional dynamics of the immune response mounted against pathogens that are able to establish a persistent infection remain poorly understood. Herein we discuss the differential lymphocyte dynamics in distinct central and peripheral lymphoid organs following acute infection by Trypanosoma cruzi, the causative agent of Chagas disease. While the thymus and mesenteric lymph nodes undergo a severe atrophy with massive lymphocyte depletion, the spleen and subcutaneous lymph nodes expand due to T and B cell activation/proliferation. These events are regulated by cytokines, as well as parasite-derived moieties. In this regard, identifying the molecular mechanisms underlying regional lymphocyte dynamics secondary to T. cruzi infection may hopefully contribute to the design of novel immune intervention strategies to control pathology in this infection. Public Library of Science 2009-07-07 /pmc/articles/PMC2700264/ /pubmed/19582140 http://dx.doi.org/10.1371/journal.pntd.0000417 Text en Meis et al. http://creativecommons.org/licenses/by/4.0/ 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 properly credited. |
spellingShingle | Review de Meis, Juliana Morrot, Alexandre Farias-de-Oliveira, Désio Aurélio Villa-Verde, Déa Maria Serra Savino, Wilson Differential Regional Immune Response in Chagas Disease |
title | Differential Regional Immune Response in Chagas Disease |
title_full | Differential Regional Immune Response in Chagas Disease |
title_fullStr | Differential Regional Immune Response in Chagas Disease |
title_full_unstemmed | Differential Regional Immune Response in Chagas Disease |
title_short | Differential Regional Immune Response in Chagas Disease |
title_sort | differential regional immune response in chagas disease |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2700264/ https://www.ncbi.nlm.nih.gov/pubmed/19582140 http://dx.doi.org/10.1371/journal.pntd.0000417 |
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