CD4 + T Cell Help Confers a Cytotoxic T Cell Effector Program Including Coinhibitory Receptor Downregulation and Increased Tissue Invasiveness

CD4 T cells optimize the cytotoxic T cell (CTL) response in magnitude and quality, by unknown molecular mechanisms. We here present the transcriptomic changes in CTLs resulting from CD4 T cell help after anti-cancer vaccination or virus infection. The gene expression signatures revealed that CD4 T c...

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Vydané v:	Immunity (Cambridge, Mass.) Ročník 47; číslo 5; s. 848
Hlavní autori:	Ahrends, Tomasz, Spanjaard, Aldo, Pilzecker, Bas, Bąbała, Nikolina, Bovens, Astrid, Xiao, Yanling, Jacobs, Heinz, Borst, Jannie
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	United States 21.11.2017
Predmet:	Animals CD27 Ligand - physiology CD4-Positive T-Lymphocytes - physiology Cell Differentiation Cell Movement CX3C Chemokine Receptor 1 - physiology Down-Regulation Mice Mice, Inbred C57BL Receptors, CXCR4 - physiology T-Lymphocytes, Cytotoxic - immunology Tumor Necrosis Factor Receptor Superfamily, Member 7 - physiology CD4 T cell help CD8 T cell costimulation CTL differentiation transcriptome migration coinhibition tumor immunity vaccination virus infection
ISSN:	1097-4180, 1097-4180
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Abstract	CD4 T cells optimize the cytotoxic T cell (CTL) response in magnitude and quality, by unknown molecular mechanisms. We here present the transcriptomic changes in CTLs resulting from CD4 T cell help after anti-cancer vaccination or virus infection. The gene expression signatures revealed that CD4 T cell help during priming optimized CTLs in expression of cytotoxic effector molecules and many other functions that ensured efficacy of CTLs throughout their life cycle. Key features included downregulation of PD-1 and other coinhibitory receptors that impede CTL activity, and increased motility and migration capacities. "Helped" CTLs acquired chemokine receptors that helped them reach their tumor target tissue and metalloprotease activity that enabled them to invade into tumor tissue. A very large part of the "help" program was instilled in CD8 T cells via CD27 costimulation. The help program thus enhances specific CTL effector functions in response to vaccination or a virus infection.
AbstractList	CD4+ T cells optimize the cytotoxic T cell (CTL) response in magnitude and quality, by unknown molecular mechanisms. We here present the transcriptomic changes in CTLs resulting from CD4+ T cell help after anti-cancer vaccination or virus infection. The gene expression signatures revealed that CD4+ T cell help during priming optimized CTLs in expression of cytotoxic effector molecules and many other functions that ensured efficacy of CTLs throughout their life cycle. Key features included downregulation of PD-1 and other coinhibitory receptors that impede CTL activity, and increased motility and migration capacities. "Helped" CTLs acquired chemokine receptors that helped them reach their tumor target tissue and metalloprotease activity that enabled them to invade into tumor tissue. A very large part of the "help" program was instilled in CD8+ T cells via CD27 costimulation. The help program thus enhances specific CTL effector functions in response to vaccination or a virus infection.CD4+ T cells optimize the cytotoxic T cell (CTL) response in magnitude and quality, by unknown molecular mechanisms. We here present the transcriptomic changes in CTLs resulting from CD4+ T cell help after anti-cancer vaccination or virus infection. The gene expression signatures revealed that CD4+ T cell help during priming optimized CTLs in expression of cytotoxic effector molecules and many other functions that ensured efficacy of CTLs throughout their life cycle. Key features included downregulation of PD-1 and other coinhibitory receptors that impede CTL activity, and increased motility and migration capacities. "Helped" CTLs acquired chemokine receptors that helped them reach their tumor target tissue and metalloprotease activity that enabled them to invade into tumor tissue. A very large part of the "help" program was instilled in CD8+ T cells via CD27 costimulation. The help program thus enhances specific CTL effector functions in response to vaccination or a virus infection. CD4 T cells optimize the cytotoxic T cell (CTL) response in magnitude and quality, by unknown molecular mechanisms. We here present the transcriptomic changes in CTLs resulting from CD4 T cell help after anti-cancer vaccination or virus infection. The gene expression signatures revealed that CD4 T cell help during priming optimized CTLs in expression of cytotoxic effector molecules and many other functions that ensured efficacy of CTLs throughout their life cycle. Key features included downregulation of PD-1 and other coinhibitory receptors that impede CTL activity, and increased motility and migration capacities. "Helped" CTLs acquired chemokine receptors that helped them reach their tumor target tissue and metalloprotease activity that enabled them to invade into tumor tissue. A very large part of the "help" program was instilled in CD8 T cells via CD27 costimulation. The help program thus enhances specific CTL effector functions in response to vaccination or a virus infection.
Author	Bąbała, Nikolina Jacobs, Heinz Bovens, Astrid Xiao, Yanling Spanjaard, Aldo Ahrends, Tomasz Pilzecker, Bas Borst, Jannie
Author_xml	– sequence: 1 givenname: Tomasz surname: Ahrends fullname: Ahrends, Tomasz organization: Division of Tumor Biology and Immunology, the Netherlands Cancer Institute-Antoni van Leeuwenhoek, 1066 CX Amsterdam, the Netherlands – sequence: 2 givenname: Aldo surname: Spanjaard fullname: Spanjaard, Aldo organization: Division of Tumor Biology and Immunology, the Netherlands Cancer Institute-Antoni van Leeuwenhoek, 1066 CX Amsterdam, the Netherlands – sequence: 3 givenname: Bas surname: Pilzecker fullname: Pilzecker, Bas organization: Division of Tumor Biology and Immunology, the Netherlands Cancer Institute-Antoni van Leeuwenhoek, 1066 CX Amsterdam, the Netherlands – sequence: 4 givenname: Nikolina surname: Bąbała fullname: Bąbała, Nikolina organization: Division of Tumor Biology and Immunology, the Netherlands Cancer Institute-Antoni van Leeuwenhoek, 1066 CX Amsterdam, the Netherlands – sequence: 5 givenname: Astrid surname: Bovens fullname: Bovens, Astrid organization: Division of Tumor Biology and Immunology, the Netherlands Cancer Institute-Antoni van Leeuwenhoek, 1066 CX Amsterdam, the Netherlands – sequence: 6 givenname: Yanling surname: Xiao fullname: Xiao, Yanling organization: Division of Tumor Biology and Immunology, the Netherlands Cancer Institute-Antoni van Leeuwenhoek, 1066 CX Amsterdam, the Netherlands – sequence: 7 givenname: Heinz surname: Jacobs fullname: Jacobs, Heinz organization: Division of Tumor Biology and Immunology, the Netherlands Cancer Institute-Antoni van Leeuwenhoek, 1066 CX Amsterdam, the Netherlands – sequence: 8 givenname: Jannie surname: Borst fullname: Borst, Jannie email: j.borst@nki.nl organization: Division of Tumor Biology and Immunology, the Netherlands Cancer Institute-Antoni van Leeuwenhoek, 1066 CX Amsterdam, the Netherlands. Electronic address: j.borst@nki.nl
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/29126798$$D View this record in MEDLINE/PubMed
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PublicationTitle	Immunity (Cambridge, Mass.)
PublicationTitleAlternate	Immunity
PublicationYear	2017
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Snippet	CD4 T cells optimize the cytotoxic T cell (CTL) response in magnitude and quality, by unknown molecular mechanisms. We here present the transcriptomic changes... CD4+ T cells optimize the cytotoxic T cell (CTL) response in magnitude and quality, by unknown molecular mechanisms. We here present the transcriptomic changes...
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SubjectTerms	Animals CD27 Ligand - physiology CD4-Positive T-Lymphocytes - physiology Cell Differentiation Cell Movement CX3C Chemokine Receptor 1 - physiology Down-Regulation Mice Mice, Inbred C57BL Receptors, CXCR4 - physiology T-Lymphocytes, Cytotoxic - immunology Tumor Necrosis Factor Receptor Superfamily, Member 7 - physiology
Title	CD4 + T Cell Help Confers a Cytotoxic T Cell Effector Program Including Coinhibitory Receptor Downregulation and Increased Tissue Invasiveness
URI	https://www.ncbi.nlm.nih.gov/pubmed/29126798 https://www.proquest.com/docview/1963271554
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