SMAD4 and TGFβ are architects of inverse genetic programs during fate determination of antiviral CTLs.

Animals Cell Differentiation Mice Receptor, Transforming Growth Factor-beta Type II / metabolism Signal Transduction / genetics Smad4 Protein / genetics T-Lymphocytes, Cytotoxic Transforming Growth Factor beta / metabolism
CD8 T cell differentiation CD8 T cells CD8 memory SMAD4 TGFβ cytotoxic T lymphocyte immunology inflammation influenza a virus listeria monocytogenes mouse respiratory virus

Journal

eLife
ISSN: 2050-084X
Titre abrégé: Elife
Pays: England
ID NLM: 101579614

Informations de publication

Date de publication:
09 08 2022
Historique:
received: 17 12 2021
accepted: 05 08 2022
pubmed: 10 8 2022
medline: 27 8 2022
entrez: 9 8 2022
Statut: epublish

Résumé

Transforming growth factor β (TGFβ) is an important differentiation factor for cytotoxic T lymphocytes (CTLs) and alters the expression levels of several of homing receptors during infection. SMAD4 is part of the canonical signaling network used by members of the transforming growth factor family. For this study, genetically modified mice were used to determine how SMAD4 and TGFβ receptor II (TGFβRII) participate in transcriptional programming of pathogen-specific CTLs. We show that these molecules are essential components of opposing signaling mechanisms, and cooperatively regulate a collection of genes that determine whether specialized populations of pathogen-specific CTLs circulate around the body, or settle in peripheral tissues. TGFβ uses a canonical SMAD-dependent signaling pathway to downregulate Eomesodermin (EOMES), KLRG1, and CD62L, while CD103 is induced. Conversely, in vivo and in vitro data show that EOMES, KLRG1, CX

Identifiants

DOI: 10.7554/eLife.76457 PMID: 35942952 PMC: PMC9402230
pubmed: 35942952
doi: 10.7554/eLife.76457
pii: 76457
pmc: PMC9402230
doi:
pii:

Substances chimiques

Smad4 Protein 0
Smad4 protein, mouse 0
Transforming Growth Factor beta 0
Receptor, Transforming Growth Factor-beta Type II EC 2.7.11.30
Tgfbr2 protein, mouse EC 2.7.11.30

Banques de données

GEO
['GSE151637', 'GSE39152', 'GSE107281', 'GSE70813', 'GSE125471', 'GSE135533']

Types de publication

Journal Article Research Support, Non-U.S. Gov't Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : NCI NIH HHS
ID : P30 CA014195
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI123864
Pays : United States

Informations de copyright

© 2022, Chandiran et al.

Déclaration de conflit d'intérêts

KC, JS, YH, EJ, ZU, JL, BM, SK, LC No competing interests declared

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Auteurs

Karthik Chandiran (K)

Department of Immunology, University of Connecticut Health Center, Farmington, United States.
ORCID: 0000-0003-2118-7946

Jenny E Suarez-Ramirez (JE)

Department of Immunology, University of Connecticut Health Center, Farmington, United States.

Yinghong Hu (Y)

Department of Microbiology and Immunology, Emory Vaccine Center, Emory University, Atlanta, United States.

Evan R Jellison (ER)

Department of Immunology, University of Connecticut Health Center, Farmington, United States.

Zeynep Ugur (Z)

Department of Immunology, University of Connecticut Health Center, Farmington, United States.

Jun Siong Low (JS)

Department of Immunobiology, Yale University School of Medicine, New Haven, United States.

Bryan McDonald (B)

NOMIS Center for Immunobiology and Microbial Pathogenesis, Salk Institute for Biological Studies, La Jolla, United States.

Susan M Kaech (SM)

NOMIS Center for Immunobiology and Microbial Pathogenesis, Salk Institute for Biological Studies, La Jolla, United States.

Linda S Cauley (LS)

Department of Immunology, University of Connecticut Health Center, Farmington, United States.
ORCID: 0000-0001-9488-0341

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Classifications MeSH

Recherchemedicale.com › Eucaryotes › Animaux › SMAD4 and TGFβ are architects of inverse...
Recherchemedicale.com › Phénomènes physiologiques cellulaires › Différenciation cellulaire › SMAD4 and TGFβ are architects of inverse...
Recherchemedicale.com › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Rodentia › Muridae › Murinae › Souris › SMAD4 and TGFβ are architects of inverse...
Recherchemedicale.com › Acides aminés, peptides et protéines › Protéines › Protéines membranaires › Récepteurs de surface cellulaire › Récepteurs peptidiques › Récepteur facteur croissance › Récepteurs TGF-bêta › Récepteur de type II du facteur de croissance transformant bêta › SMAD4 and TGFβ are architects of inverse...
Recherchemedicale.com › Phénomènes physiologiques cellulaires › Transduction du signal › SMAD4 and TGFβ are architects of inverse...
Recherchemedicale.com › Acides aminés, peptides et protéines › Protéines › Facteurs de transcription › Protéines Smad › Protéine Smad-4 › SMAD4 and TGFβ are architects of inverse...
Recherchemedicale.com › Systèmes sanguin et immunitaire › Système immunitaire › Leucocytes › Agranulocytes › Lymphocytes › Lymphocytes T › Sous-populations de lymphocytes T › Lymphocytes T cytotoxiques › SMAD4 and TGFβ are architects of inverse...
Recherchemedicale.com › Facteurs biologiques › Protéines et peptides de signalisation intercellulaire › Protéines de la superfamille du TGF bêta › Facteur de croissance transformant bêta › SMAD4 and TGFβ are architects of inverse...