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The effects of TLR activation on T-cell development and differentiation.

Jin B, Sun T, Yu XH, Yang YX, Yeo AE - Clin. Dev. Immunol. (2012)

Bottom Line: Invading pathogens have unique molecular signatures that are recognized by Toll-like receptors (TLRs) resulting in either activation of antigen-presenting cells (APCs) and/or costimulation of T cells inducing both innate and adaptive immunity.T-cell receptor (TCR) activation in distinct T-cell subsets with different TLRs results in differing outcomes, for example, activation of TLR4 expressed in T cells promotes suppressive function of regulatory T cells (Treg), while activation of TLR6 expressed in T cells abrogates Treg function.The current state of knowledge of regarding TLR-mediated T-cell development and differentiation is reviewed.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, The 309th Hospital of The People's Liberation Army, Beijing, China. bjbo.jin@gmail.com

ABSTRACT
Invading pathogens have unique molecular signatures that are recognized by Toll-like receptors (TLRs) resulting in either activation of antigen-presenting cells (APCs) and/or costimulation of T cells inducing both innate and adaptive immunity. TLRs are also involved in T-cell development and can reprogram Treg cells to become helper cells. T cells consist of various subsets, that is, Th1, Th2, Th17, T follicular helper (Tfh), cytotoxic T lymphocytes (CTLs), regulatory T cells (Treg) and these originate from thymic progenitor thymocytes. T-cell receptor (TCR) activation in distinct T-cell subsets with different TLRs results in differing outcomes, for example, activation of TLR4 expressed in T cells promotes suppressive function of regulatory T cells (Treg), while activation of TLR6 expressed in T cells abrogates Treg function. The current state of knowledge of regarding TLR-mediated T-cell development and differentiation is reviewed.

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Related in: MedlinePlus

The effects of TLR on T-cell activation. PAMPs from invading pathogens bind with TLRs expressed in DCs, which causes DC activation. Activated DCs migrate to the draining lymph nodes where, in the presence of co-stimulatory signals and instructing cytokines, they present the antigen epitope with MHC molecules to activate naive T cells. DCs also induce iTreg in the presence of TGF-β and IL-2. These activated T cells move to the site of infection to fight against the invading pathogen. Activation of TLRs in activated T cells induces their survival and clonal expansion. Direct engagement of TLR in iTreg cells promotes their expansion with reduced suppressive function and reprograms them to differentiate into T helper cells, which in turn provide help to effector cells. When the infected pathogen is eliminated, the clearance of TLR ligands results in the suppressive function of the expanded iTreg cells being restored. This serves to regulate the expanded effector T-cell population.
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fig1: The effects of TLR on T-cell activation. PAMPs from invading pathogens bind with TLRs expressed in DCs, which causes DC activation. Activated DCs migrate to the draining lymph nodes where, in the presence of co-stimulatory signals and instructing cytokines, they present the antigen epitope with MHC molecules to activate naive T cells. DCs also induce iTreg in the presence of TGF-β and IL-2. These activated T cells move to the site of infection to fight against the invading pathogen. Activation of TLRs in activated T cells induces their survival and clonal expansion. Direct engagement of TLR in iTreg cells promotes their expansion with reduced suppressive function and reprograms them to differentiate into T helper cells, which in turn provide help to effector cells. When the infected pathogen is eliminated, the clearance of TLR ligands results in the suppressive function of the expanded iTreg cells being restored. This serves to regulate the expanded effector T-cell population.

Mentions: Upon recognition of foreign antigen for DCs via the TLR-PAMP interaction [4, 16], immature DCs resident in tissues mature into professional antigen-presenting cells (APCs) to induce effector and memory T-cell responses in lymphoid organs. Additionally, DCs are capable of inducing antigen-specific T-cell tolerance immunosuppression (Figure 1) [16]. T cells are divided into different subsets based on their phenotypes, intracellular molecules expression, cytokine production, the lengths of telomeres and state of immunity [17]. The current knowledge of TLRs activation in relation to T-cell activation and differentiation is presented here.


The effects of TLR activation on T-cell development and differentiation.

Jin B, Sun T, Yu XH, Yang YX, Yeo AE - Clin. Dev. Immunol. (2012)

The effects of TLR on T-cell activation. PAMPs from invading pathogens bind with TLRs expressed in DCs, which causes DC activation. Activated DCs migrate to the draining lymph nodes where, in the presence of co-stimulatory signals and instructing cytokines, they present the antigen epitope with MHC molecules to activate naive T cells. DCs also induce iTreg in the presence of TGF-β and IL-2. These activated T cells move to the site of infection to fight against the invading pathogen. Activation of TLRs in activated T cells induces their survival and clonal expansion. Direct engagement of TLR in iTreg cells promotes their expansion with reduced suppressive function and reprograms them to differentiate into T helper cells, which in turn provide help to effector cells. When the infected pathogen is eliminated, the clearance of TLR ligands results in the suppressive function of the expanded iTreg cells being restored. This serves to regulate the expanded effector T-cell population.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3376488&req=5

fig1: The effects of TLR on T-cell activation. PAMPs from invading pathogens bind with TLRs expressed in DCs, which causes DC activation. Activated DCs migrate to the draining lymph nodes where, in the presence of co-stimulatory signals and instructing cytokines, they present the antigen epitope with MHC molecules to activate naive T cells. DCs also induce iTreg in the presence of TGF-β and IL-2. These activated T cells move to the site of infection to fight against the invading pathogen. Activation of TLRs in activated T cells induces their survival and clonal expansion. Direct engagement of TLR in iTreg cells promotes their expansion with reduced suppressive function and reprograms them to differentiate into T helper cells, which in turn provide help to effector cells. When the infected pathogen is eliminated, the clearance of TLR ligands results in the suppressive function of the expanded iTreg cells being restored. This serves to regulate the expanded effector T-cell population.
Mentions: Upon recognition of foreign antigen for DCs via the TLR-PAMP interaction [4, 16], immature DCs resident in tissues mature into professional antigen-presenting cells (APCs) to induce effector and memory T-cell responses in lymphoid organs. Additionally, DCs are capable of inducing antigen-specific T-cell tolerance immunosuppression (Figure 1) [16]. T cells are divided into different subsets based on their phenotypes, intracellular molecules expression, cytokine production, the lengths of telomeres and state of immunity [17]. The current knowledge of TLRs activation in relation to T-cell activation and differentiation is presented here.

Bottom Line: Invading pathogens have unique molecular signatures that are recognized by Toll-like receptors (TLRs) resulting in either activation of antigen-presenting cells (APCs) and/or costimulation of T cells inducing both innate and adaptive immunity.T-cell receptor (TCR) activation in distinct T-cell subsets with different TLRs results in differing outcomes, for example, activation of TLR4 expressed in T cells promotes suppressive function of regulatory T cells (Treg), while activation of TLR6 expressed in T cells abrogates Treg function.The current state of knowledge of regarding TLR-mediated T-cell development and differentiation is reviewed.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, The 309th Hospital of The People's Liberation Army, Beijing, China. bjbo.jin@gmail.com

ABSTRACT
Invading pathogens have unique molecular signatures that are recognized by Toll-like receptors (TLRs) resulting in either activation of antigen-presenting cells (APCs) and/or costimulation of T cells inducing both innate and adaptive immunity. TLRs are also involved in T-cell development and can reprogram Treg cells to become helper cells. T cells consist of various subsets, that is, Th1, Th2, Th17, T follicular helper (Tfh), cytotoxic T lymphocytes (CTLs), regulatory T cells (Treg) and these originate from thymic progenitor thymocytes. T-cell receptor (TCR) activation in distinct T-cell subsets with different TLRs results in differing outcomes, for example, activation of TLR4 expressed in T cells promotes suppressive function of regulatory T cells (Treg), while activation of TLR6 expressed in T cells abrogates Treg function. The current state of knowledge of regarding TLR-mediated T-cell development and differentiation is reviewed.

Show MeSH
Related in: MedlinePlus