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Lymphocyte Egress Signal Sphingosine...

Robertson, Tanner Ford.

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Lymphocyte Egress Signal Sphingosine-1-Phosphate Promotes ERM-Guided, Bleb-Based Migration.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Lymphocyte Egress Signal Sphingosine-1-Phosphate Promotes ERM-Guided, Bleb-Based Migration./
Author:	Robertson, Tanner Ford.
Published:	Ann Arbor : ProQuest Dissertations & Theses, : 2021,
Description:	116 p.
Notes:	Source: Dissertations Abstracts International, Volume: 83-02, Section: B.
Contained By:	Dissertations Abstracts International83-02B.
Subject:	Immunology. -
Online resource:	https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=28322092
ISBN:	9798516948190

Lymphocyte Egress Signal Sphingosine-1-Phosphate Promotes ERM-Guided, Bleb-Based Migration.
Robertson, Tanner Ford.

Lymphocyte Egress Signal Sphingosine-1-Phosphate Promotes ERM-Guided, Bleb-Based Migration. - Ann Arbor : ProQuest Dissertations & Theses, 2021 - 116 p.

Source: Dissertations Abstracts International, Volume: 83-02, Section: B.

Thesis (Ph.D.)--University of Pennsylvania, 2021.

This item must not be sold to any third party vendors.

Ezrin, radixin, and moesin (ERM) family proteins regulate cytoskeletal responses by tethering the plasma membrane to the underlying actin cortex. Mutations in ERM proteins lead to severe combined immunodeficiency, but the function of these proteins in T cells remains poorly defined. Using mice in which T cells lack all ERM proteins, we demonstrate a selective role for these proteins in facilitating egress from lymphoid organs in response to sphingosine-1-phosphate (S1P), a pleiotropic signaling lipid abundant in the blood and lymph. ERM-deficient T cells display defective S1P-inducedmigration in vitro, despite normal responses to standard protein chemokines that control entry into and migration within lymphoid organs. Analysis of these defects revealed thatS1P promotes a fundamentally different mode of migration than chemokines, characterized by intracellular pressurization and bleb-based motility. ERM proteins facilitate this process, controlling directional migration by limiting blebbing to the leading edge. We propose that the distinct modes of motility induced by S1P and chemokines are specialized to allow T cell migration across lymphatic barriers and through tissue stroma, respectively.

ISBN: 9798516948190Subjects--Topical Terms:

611031
Immunology.
Subjects--Index Terms:

Blebs

Lymphocyte Egress Signal Sphingosine-1-Phosphate Promotes ERM-Guided, Bleb-Based Migration.
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506 $a This item must not be sold to any third party vendors.
520 $a Ezrin, radixin, and moesin (ERM) family proteins regulate cytoskeletal responses by tethering the plasma membrane to the underlying actin cortex. Mutations in ERM proteins lead to severe combined immunodeficiency, but the function of these proteins in T cells remains poorly defined. Using mice in which T cells lack all ERM proteins, we demonstrate a selective role for these proteins in facilitating egress from lymphoid organs in response to sphingosine-1-phosphate (S1P), a pleiotropic signaling lipid abundant in the blood and lymph. ERM-deficient T cells display defective S1P-inducedmigration in vitro, despite normal responses to standard protein chemokines that control entry into and migration within lymphoid organs. Analysis of these defects revealed thatS1P promotes a fundamentally different mode of migration than chemokines, characterized by intracellular pressurization and bleb-based motility. ERM proteins facilitate this process, controlling directional migration by limiting blebbing to the leading edge. We propose that the distinct modes of motility induced by S1P and chemokines are specialized to allow T cell migration across lymphatic barriers and through tissue stroma, respectively.
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