The role of non-cognate T cell stimulation during intracellular bacterial infection

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Intra-macrophage bacterial infections cause significant morbidity and mortality in both the developed and developing world. Protective host immune responses to these infections initially requires the activation and expansion of pathogen-specific CD4 Th1 cells within lymphoid tissues and subsequent relocation of these effector cells to sites of infection. After entering infected tissues, the elicitation of Th1 bactericidal activity can be triggered by cognate or non-cognate signals that are delivered by locally infected antigen-presenting cells and innate cells. However, the contribution of non-cognate stimulation to the resolution of bacterial infection remains poorly understood, especially in the context of a Th1 response. Here, we review the current data on Th1 cell activation and expansion in mouse models of Salmonella and Chlamydia infection and discuss the potential role of non-cognate Th1 cell stimulation in these disease models. Greater understanding of this pathway of T cell activation may lead to the design of therapeutics or vaccines to combat intra-macrophage pathogens.

Original languageEnglish (US)
Article numberArticle 319
JournalFrontiers in Immunology
Volume5
Issue numberJUL
DOIs
StatePublished - 2014

Fingerprint

Th1 Cells
Bacterial Infections
T-Lymphocytes
Macrophages
Chlamydia Infections
Salmonella Infections
Lymphoid Tissue
Antigen-Presenting Cells
Infection
Vaccines
Morbidity
Mortality
Therapeutics

Keywords

  • Bacterial infections
  • IFN-gamma
  • Protective immunity
  • Salmonella
  • T cell

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

Cite this

The role of non-cognate T cell stimulation during intracellular bacterial infection. / Mcsorley, Stephen J.

In: Frontiers in Immunology, Vol. 5, No. JUL, Article 319, 2014.

Research output: Contribution to journalArticle

@article{0893ad9802274057a82a846d89fc6d71,
title = "The role of non-cognate T cell stimulation during intracellular bacterial infection",
abstract = "Intra-macrophage bacterial infections cause significant morbidity and mortality in both the developed and developing world. Protective host immune responses to these infections initially requires the activation and expansion of pathogen-specific CD4 Th1 cells within lymphoid tissues and subsequent relocation of these effector cells to sites of infection. After entering infected tissues, the elicitation of Th1 bactericidal activity can be triggered by cognate or non-cognate signals that are delivered by locally infected antigen-presenting cells and innate cells. However, the contribution of non-cognate stimulation to the resolution of bacterial infection remains poorly understood, especially in the context of a Th1 response. Here, we review the current data on Th1 cell activation and expansion in mouse models of Salmonella and Chlamydia infection and discuss the potential role of non-cognate Th1 cell stimulation in these disease models. Greater understanding of this pathway of T cell activation may lead to the design of therapeutics or vaccines to combat intra-macrophage pathogens.",
keywords = "Bacterial infections, IFN-gamma, Protective immunity, Salmonella, T cell",
author = "Mcsorley, {Stephen J}",
year = "2014",
doi = "10.3389/fimmu.2014.00319",
language = "English (US)",
volume = "5",
journal = "Frontiers in Immunology",
issn = "1664-3224",
publisher = "Frontiers Media S. A.",
number = "JUL",

}

TY - JOUR

T1 - The role of non-cognate T cell stimulation during intracellular bacterial infection

AU - Mcsorley, Stephen J

PY - 2014

Y1 - 2014

N2 - Intra-macrophage bacterial infections cause significant morbidity and mortality in both the developed and developing world. Protective host immune responses to these infections initially requires the activation and expansion of pathogen-specific CD4 Th1 cells within lymphoid tissues and subsequent relocation of these effector cells to sites of infection. After entering infected tissues, the elicitation of Th1 bactericidal activity can be triggered by cognate or non-cognate signals that are delivered by locally infected antigen-presenting cells and innate cells. However, the contribution of non-cognate stimulation to the resolution of bacterial infection remains poorly understood, especially in the context of a Th1 response. Here, we review the current data on Th1 cell activation and expansion in mouse models of Salmonella and Chlamydia infection and discuss the potential role of non-cognate Th1 cell stimulation in these disease models. Greater understanding of this pathway of T cell activation may lead to the design of therapeutics or vaccines to combat intra-macrophage pathogens.

AB - Intra-macrophage bacterial infections cause significant morbidity and mortality in both the developed and developing world. Protective host immune responses to these infections initially requires the activation and expansion of pathogen-specific CD4 Th1 cells within lymphoid tissues and subsequent relocation of these effector cells to sites of infection. After entering infected tissues, the elicitation of Th1 bactericidal activity can be triggered by cognate or non-cognate signals that are delivered by locally infected antigen-presenting cells and innate cells. However, the contribution of non-cognate stimulation to the resolution of bacterial infection remains poorly understood, especially in the context of a Th1 response. Here, we review the current data on Th1 cell activation and expansion in mouse models of Salmonella and Chlamydia infection and discuss the potential role of non-cognate Th1 cell stimulation in these disease models. Greater understanding of this pathway of T cell activation may lead to the design of therapeutics or vaccines to combat intra-macrophage pathogens.

KW - Bacterial infections

KW - IFN-gamma

KW - Protective immunity

KW - Salmonella

KW - T cell

UR - http://www.scopus.com/inward/record.url?scp=84905667465&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84905667465&partnerID=8YFLogxK

U2 - 10.3389/fimmu.2014.00319

DO - 10.3389/fimmu.2014.00319

M3 - Article

AN - SCOPUS:84905667465

VL - 5

JO - Frontiers in Immunology

JF - Frontiers in Immunology

SN - 1664-3224

IS - JUL

M1 - Article 319

ER -