Normal Development and Function of T Cells in Proline Rich 7 (Prr7) Deficient Mice
Transmembrane adaptor proteins (TRAPs) are important organisers for the transduction of immunoreceptor-mediated signals. Prr7 is a TRAP that regulates T cell receptor (TCR) signalling and potently induces cell death when overexpressed in human Jurkat T cells. Whether endogenous Prr7 has a similar fu...
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creator | Hrdinka, Matous Sudan, Kritika Just, Sissy Drobek, Ales Stepanek, Ondrej Schlüter, Dirk Reinhold, Dirk Jordan, Bryen A Gintschel, Patricia Schraven, Burkhart Kreutz, Michael R |
description | Transmembrane adaptor proteins (TRAPs) are important organisers for the transduction of immunoreceptor-mediated signals. Prr7 is a TRAP that regulates T cell receptor (TCR) signalling and potently induces cell death when overexpressed in human Jurkat T cells. Whether endogenous Prr7 has a similar functional role is currently unknown. To address this issue, we analysed the development and function of the immune system in Prr7 knockout mice. We found that loss of Prr7 partially impairs development of single positive CD4+ T cells in the thymus but has no effect on the development of other T cell subpopulations, B cells, NK cells, or NKT cells. Moreover, Prr7 does not affect the TCR signalling pathway as T cells derived from Prr7 knockout and wild-type animals and stimulated in vitro express the same levels of the activation marker CD69, and retain their ability to proliferate and activate induced cell death programs. Importantly, Prr7 knockout mice retained the capacity to mount a protective immune response when challenged with Listeria monocytogenes infection in vivo. In addition, T cell effector functions (activation, migration, and reactivation) were normal following induction of experimental autoimmune encephalomyelitis (EAE) in Prr7 knockout mice. Collectively, our work shows that loss of Prr7 does not result in a major immune system phenotype and suggests that Prr7 has a dispensable function for TCR signalling. |
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Prr7 is a TRAP that regulates T cell receptor (TCR) signalling and potently induces cell death when overexpressed in human Jurkat T cells. Whether endogenous Prr7 has a similar functional role is currently unknown. To address this issue, we analysed the development and function of the immune system in Prr7 knockout mice. We found that loss of Prr7 partially impairs development of single positive CD4+ T cells in the thymus but has no effect on the development of other T cell subpopulations, B cells, NK cells, or NKT cells. Moreover, Prr7 does not affect the TCR signalling pathway as T cells derived from Prr7 knockout and wild-type animals and stimulated in vitro express the same levels of the activation marker CD69, and retain their ability to proliferate and activate induced cell death programs. Importantly, Prr7 knockout mice retained the capacity to mount a protective immune response when challenged with Listeria monocytogenes infection in vivo. In addition, T cell effector functions (activation, migration, and reactivation) were normal following induction of experimental autoimmune encephalomyelitis (EAE) in Prr7 knockout mice. Collectively, our work shows that loss of Prr7 does not result in a major immune system phenotype and suggests that Prr7 has a dispensable function for TCR signalling.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0162863</identifier><identifier>PMID: 27657535</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adapter proteins ; Adaptor proteins ; Biology and Life Sciences ; CD4 antigen ; CD69 antigen ; Cell activation ; Cell death ; Cell migration ; Experimental allergic encephalomyelitis ; Immune response ; Immune system ; Immunology ; Listeria ; Listeria monocytogenes ; Lymphatic system ; Lymphocytes ; Lymphocytes B ; Lymphocytes T ; Medical research ; Medicine and Health Sciences ; Mice ; Multiple sclerosis ; Natural killer cells ; Neurobiology ; Neurodegeneration ; Neurosciences ; Phenotypes ; Proline ; Proteins ; Research and Analysis Methods ; Signal transduction ; Signaling ; Subpopulations ; T cell receptors ; T-cell receptor ; Thymus</subject><ispartof>PloS one, 2016-09, Vol.11 (9), p.e0162863-e0162863</ispartof><rights>2016 Hrdinka et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2016 Hrdinka et al 2016 Hrdinka et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c559t-b6bd94f58ca56c8f7f68a8f26d1b2020b49cadec9c79fe33fed8937f044109d13</citedby><cites>FETCH-LOGICAL-c559t-b6bd94f58ca56c8f7f68a8f26d1b2020b49cadec9c79fe33fed8937f044109d13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5033326/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5033326/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27657535$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Labrecque, Nathalie</contributor><creatorcontrib>Hrdinka, Matous</creatorcontrib><creatorcontrib>Sudan, Kritika</creatorcontrib><creatorcontrib>Just, Sissy</creatorcontrib><creatorcontrib>Drobek, Ales</creatorcontrib><creatorcontrib>Stepanek, Ondrej</creatorcontrib><creatorcontrib>Schlüter, Dirk</creatorcontrib><creatorcontrib>Reinhold, Dirk</creatorcontrib><creatorcontrib>Jordan, Bryen A</creatorcontrib><creatorcontrib>Gintschel, Patricia</creatorcontrib><creatorcontrib>Schraven, Burkhart</creatorcontrib><creatorcontrib>Kreutz, Michael R</creatorcontrib><title>Normal Development and Function of T Cells in Proline Rich 7 (Prr7) Deficient Mice</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Transmembrane adaptor proteins (TRAPs) are important organisers for the transduction of immunoreceptor-mediated signals. Prr7 is a TRAP that regulates T cell receptor (TCR) signalling and potently induces cell death when overexpressed in human Jurkat T cells. Whether endogenous Prr7 has a similar functional role is currently unknown. To address this issue, we analysed the development and function of the immune system in Prr7 knockout mice. We found that loss of Prr7 partially impairs development of single positive CD4+ T cells in the thymus but has no effect on the development of other T cell subpopulations, B cells, NK cells, or NKT cells. Moreover, Prr7 does not affect the TCR signalling pathway as T cells derived from Prr7 knockout and wild-type animals and stimulated in vitro express the same levels of the activation marker CD69, and retain their ability to proliferate and activate induced cell death programs. Importantly, Prr7 knockout mice retained the capacity to mount a protective immune response when challenged with Listeria monocytogenes infection in vivo. In addition, T cell effector functions (activation, migration, and reactivation) were normal following induction of experimental autoimmune encephalomyelitis (EAE) in Prr7 knockout mice. Collectively, our work shows that loss of Prr7 does not result in a major immune system phenotype and suggests that Prr7 has a dispensable function for TCR signalling.</description><subject>Adapter proteins</subject><subject>Adaptor proteins</subject><subject>Biology and Life Sciences</subject><subject>CD4 antigen</subject><subject>CD69 antigen</subject><subject>Cell activation</subject><subject>Cell death</subject><subject>Cell migration</subject><subject>Experimental allergic encephalomyelitis</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Immunology</subject><subject>Listeria</subject><subject>Listeria monocytogenes</subject><subject>Lymphatic system</subject><subject>Lymphocytes</subject><subject>Lymphocytes B</subject><subject>Lymphocytes T</subject><subject>Medical research</subject><subject>Medicine and Health Sciences</subject><subject>Mice</subject><subject>Multiple sclerosis</subject><subject>Natural killer 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Development and Function of T Cells in Proline Rich 7 (Prr7) Deficient Mice</title><author>Hrdinka, Matous ; Sudan, Kritika ; Just, Sissy ; Drobek, Ales ; Stepanek, Ondrej ; Schlüter, Dirk ; Reinhold, Dirk ; Jordan, Bryen A ; Gintschel, Patricia ; Schraven, Burkhart ; Kreutz, Michael R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c559t-b6bd94f58ca56c8f7f68a8f26d1b2020b49cadec9c79fe33fed8937f044109d13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adapter proteins</topic><topic>Adaptor proteins</topic><topic>Biology and Life Sciences</topic><topic>CD4 antigen</topic><topic>CD69 antigen</topic><topic>Cell activation</topic><topic>Cell death</topic><topic>Cell migration</topic><topic>Experimental allergic encephalomyelitis</topic><topic>Immune response</topic><topic>Immune system</topic><topic>Immunology</topic><topic>Listeria</topic><topic>Listeria 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Nathalie</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Normal Development and Function of T Cells in Proline Rich 7 (Prr7) Deficient Mice</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2016-09-01</date><risdate>2016</risdate><volume>11</volume><issue>9</issue><spage>e0162863</spage><epage>e0162863</epage><pages>e0162863-e0162863</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Transmembrane adaptor proteins (TRAPs) are important organisers for the transduction of immunoreceptor-mediated signals. Prr7 is a TRAP that regulates T cell receptor (TCR) signalling and potently induces cell death when overexpressed in human Jurkat T cells. Whether endogenous Prr7 has a similar functional role is currently unknown. To address this issue, we analysed the development and function of the immune system in Prr7 knockout mice. We found that loss of Prr7 partially impairs development of single positive CD4+ T cells in the thymus but has no effect on the development of other T cell subpopulations, B cells, NK cells, or NKT cells. Moreover, Prr7 does not affect the TCR signalling pathway as T cells derived from Prr7 knockout and wild-type animals and stimulated in vitro express the same levels of the activation marker CD69, and retain their ability to proliferate and activate induced cell death programs. Importantly, Prr7 knockout mice retained the capacity to mount a protective immune response when challenged with Listeria monocytogenes infection in vivo. In addition, T cell effector functions (activation, migration, and reactivation) were normal following induction of experimental autoimmune encephalomyelitis (EAE) in Prr7 knockout mice. Collectively, our work shows that loss of Prr7 does not result in a major immune system phenotype and suggests that Prr7 has a dispensable function for TCR signalling.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>27657535</pmid><doi>10.1371/journal.pone.0162863</doi><oa>free_for_read</oa></addata></record> |
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subjects | Adapter proteins Adaptor proteins Biology and Life Sciences CD4 antigen CD69 antigen Cell activation Cell death Cell migration Experimental allergic encephalomyelitis Immune response Immune system Immunology Listeria Listeria monocytogenes Lymphatic system Lymphocytes Lymphocytes B Lymphocytes T Medical research Medicine and Health Sciences Mice Multiple sclerosis Natural killer cells Neurobiology Neurodegeneration Neurosciences Phenotypes Proline Proteins Research and Analysis Methods Signal transduction Signaling Subpopulations T cell receptors T-cell receptor Thymus |
title | Normal Development and Function of T Cells in Proline Rich 7 (Prr7) Deficient Mice |
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