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Memory T Cell Migration.

Zhang Q, Lakkis FG - Front Immunol (2015)

Bottom Line: This review will focus on the mechanisms by which memory T cells migrate to the site where their target antigen is present, with particular emphasis on their migration to transplanted organs.First, we will define the known subsets of memory T cells (central, effector, and tissue resident) and their circulation patterns.Second, we will review the cellular and molecular mechanisms by which memory T cells migrate to inflamed and non-inflamed tissues and highlight the emerging paradigm of antigen-driven, trans-endothelial migration.

View Article: PubMed Central - PubMed

Affiliation: Tsinghua University School of Medicine , Beijing , China ; University of Pittsburgh School of Medicine , Pittsburgh, PA , USA.

ABSTRACT
Immunological memory is a key feature of adaptive immunity. It provides the organism with long-lived and robust protection against infection. In organ transplantation, memory T cells pose a significant threat by causing allograft rejection that is generally resistant to immunosuppressive therapy. Therefore, a more thorough understanding of memory T cell biology is needed to improve the survival of transplanted organs without compromising the host's ability to fight infections. This review will focus on the mechanisms by which memory T cells migrate to the site where their target antigen is present, with particular emphasis on their migration to transplanted organs. First, we will define the known subsets of memory T cells (central, effector, and tissue resident) and their circulation patterns. Second, we will review the cellular and molecular mechanisms by which memory T cells migrate to inflamed and non-inflamed tissues and highlight the emerging paradigm of antigen-driven, trans-endothelial migration. Third, we will discuss the relevance of this knowledge to organ transplantation and the prevention or treatment of allograft rejection.

No MeSH data available.


Related in: MedlinePlus

TCR-mediated integrin activation inside-out signaling. This figure outlines the key mediators in the TCR signaling-mediated integrin (LFA-1) activation pathway. ADAP and SKAP1 are two adaptor proteins involved in this pathway, functioning by synergistically recruiting RapL–Rap1–GTP complex to the integrin cytosolic tail and leading to integrin confirmation changes and membrane clustering [modified from Ref. (34)].
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Figure 1: TCR-mediated integrin activation inside-out signaling. This figure outlines the key mediators in the TCR signaling-mediated integrin (LFA-1) activation pathway. ADAP and SKAP1 are two adaptor proteins involved in this pathway, functioning by synergistically recruiting RapL–Rap1–GTP complex to the integrin cytosolic tail and leading to integrin confirmation changes and membrane clustering [modified from Ref. (34)].

Mentions: As noted previously, integrin activation is essential for T cell arrest and firm adhesion on blood vessel walls, which are critical steps that trigger memory T cell transmigration across the endothelium and into peripheral tissues. There are two well-known modalities of integrin activation: conformational changes leading to increased affinity of individual integrin molecule and lateral mobility (clustering) of the integrin molecules contributing to an overall enhanced cell avidity (Figure 1) (32). Structural studies of LFA-1, a common integrin involved in cell adhesion and migration, indicated that integrins dynamically equilibrate in three distinct conformational states, which are designated as folded, extended-closed, and extended-open conformations. Both folded and extended-closed integrins display relatively low affinity, while extended-open integrin affinity is 103–104-fold higher. These integrin conformational changes are consequences of inside-out signaling: signals that are first triggered by a receptor on the cell surface (outside-in) but then signal from inside the cell (inside-out) to activate integrin molecules (33).


Memory T Cell Migration.

Zhang Q, Lakkis FG - Front Immunol (2015)

TCR-mediated integrin activation inside-out signaling. This figure outlines the key mediators in the TCR signaling-mediated integrin (LFA-1) activation pathway. ADAP and SKAP1 are two adaptor proteins involved in this pathway, functioning by synergistically recruiting RapL–Rap1–GTP complex to the integrin cytosolic tail and leading to integrin confirmation changes and membrane clustering [modified from Ref. (34)].
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4591505&req=5

Figure 1: TCR-mediated integrin activation inside-out signaling. This figure outlines the key mediators in the TCR signaling-mediated integrin (LFA-1) activation pathway. ADAP and SKAP1 are two adaptor proteins involved in this pathway, functioning by synergistically recruiting RapL–Rap1–GTP complex to the integrin cytosolic tail and leading to integrin confirmation changes and membrane clustering [modified from Ref. (34)].
Mentions: As noted previously, integrin activation is essential for T cell arrest and firm adhesion on blood vessel walls, which are critical steps that trigger memory T cell transmigration across the endothelium and into peripheral tissues. There are two well-known modalities of integrin activation: conformational changes leading to increased affinity of individual integrin molecule and lateral mobility (clustering) of the integrin molecules contributing to an overall enhanced cell avidity (Figure 1) (32). Structural studies of LFA-1, a common integrin involved in cell adhesion and migration, indicated that integrins dynamically equilibrate in three distinct conformational states, which are designated as folded, extended-closed, and extended-open conformations. Both folded and extended-closed integrins display relatively low affinity, while extended-open integrin affinity is 103–104-fold higher. These integrin conformational changes are consequences of inside-out signaling: signals that are first triggered by a receptor on the cell surface (outside-in) but then signal from inside the cell (inside-out) to activate integrin molecules (33).

Bottom Line: This review will focus on the mechanisms by which memory T cells migrate to the site where their target antigen is present, with particular emphasis on their migration to transplanted organs.First, we will define the known subsets of memory T cells (central, effector, and tissue resident) and their circulation patterns.Second, we will review the cellular and molecular mechanisms by which memory T cells migrate to inflamed and non-inflamed tissues and highlight the emerging paradigm of antigen-driven, trans-endothelial migration.

View Article: PubMed Central - PubMed

Affiliation: Tsinghua University School of Medicine , Beijing , China ; University of Pittsburgh School of Medicine , Pittsburgh, PA , USA.

ABSTRACT
Immunological memory is a key feature of adaptive immunity. It provides the organism with long-lived and robust protection against infection. In organ transplantation, memory T cells pose a significant threat by causing allograft rejection that is generally resistant to immunosuppressive therapy. Therefore, a more thorough understanding of memory T cell biology is needed to improve the survival of transplanted organs without compromising the host's ability to fight infections. This review will focus on the mechanisms by which memory T cells migrate to the site where their target antigen is present, with particular emphasis on their migration to transplanted organs. First, we will define the known subsets of memory T cells (central, effector, and tissue resident) and their circulation patterns. Second, we will review the cellular and molecular mechanisms by which memory T cells migrate to inflamed and non-inflamed tissues and highlight the emerging paradigm of antigen-driven, trans-endothelial migration. Third, we will discuss the relevance of this knowledge to organ transplantation and the prevention or treatment of allograft rejection.

No MeSH data available.


Related in: MedlinePlus