Cited by 463T-cell and B-cell ImmunologyCytokine Signaling Pathways and InteractionsNF-κB Signaling Pathways

The TNF Receptor Superfamily in Co-stimulating and Co-inhibitory Responses

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Ward-Kavanagh, Lindsay K., Lin, Wai Wai, Šedý, John R., Ware, Carl F.·2016·Immunity

Abstract

Cytokines related to tumor necrosis factor (TNF) provide a communication network essential for coordinating multiple cell types into an effective host defense system against pathogens and malignant cells. The pathways controlled by the TNF superfamily differentiate both innate and adaptive immune cells and modulate stromal cells into microenvironments conducive to host defenses. Members of the TNF receptor superfamily activate diverse cellular functions from the production of type 1 interferons to the modulation of survival of antigen-activated T cells. Here, we focus attention on the subset of TNF superfamily receptors encoded in the immune response locus in chromosomal region 1p36. Recent studies have revealed that these receptors use diverse mechanisms to either co-stimulate or restrict immune responses. Translation of the fundamental mechanisms of TNF superfamily is leading to the design of therapeutics that can alter pathogenic processes in several autoimmune diseases or promote immunity to tumors.

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Crossref · 10.1016/j.immuni.2016.04.019

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  • rTregs subset expressed higher levels of quiescence genes Ms4a4b and Sell, whereas aTregs subset expressed higher levels of coinhibitory Pdcd1 and Lag3, costimulatory Tnfrsf9 and Tnfrsf4, activation genes S100a11 and Il1r2, and TF Ikzf2.

    “whereas the rTregs subset expressed higher levels of quiescence genes (e.g., Ms4a4b and Sell), aTregs subset expressed higher levels of coinhibitory (e.g., Pdcd1 and Lag3) and costimulatory genes [e.g., Tnfrsf9 and Tnfrsf4; (38)], activation genes [S100a11 and Il1r2 (IL1 decoy receptor); (39)], and the transcription factor (TF) Ikzf2 (30).”

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Research works printed but not linked: 3

  1. Bekiaris V Sedy JR Macauley MG Rhode-Kurnow A Ware CF The inhibitory receptor BTLA controls gammadelta T cell homeostasis and inflammatory responses Immunity 2013b 39 1082 1094 24315996 PMC3909738
  2. Cai G Anumanthan A Brown JA Greenfield EA Zhu B Freeman GJ CD160 inhibits activation of human CD4+ T cells through interaction with herpesvirus entry mediator Nat Immunol 2008b 9 176 185 18193050
  3. Sedy J Bekiaris V Ware CF Tumor necrosis factor superfamily in innate immunity and inflammation Cold Spring Harb Perspect Biol 2015 7 a016279 25524549 PMC4382740

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Authors
Ward-Kavanagh, L. K., Lin, W. W., Šedý, J. R., & Ware, C. F.
Affiliations
Sanford Burnham Prebys Medical Discovery Institute (US)
Corresponding author
Ware, Carl F.
Venue
Immunity
Publisher
Elsevier BV
Published
2016-05
Volume
44
Issue
5
Pages
1005-1019
ISSN
1074-7613 (ISSN-L)
OpenAlex
W2402789890
Cited by
463
References
225
Citations by year
2026: 25 · 2025: 51 · 2024: 48 · 2023: 51 · 2022: 63 · 2021: 72 · 2020: 60 · 2019: 41 · 2018: 26 · 2017: 18 · 2016: 8
FWCI
2.99
Type
journal article
Language
en
Open access
Locations
  • Immunity (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • American Heart Association
  • Jean Perkins Foundation
  • National Institutes of Health
  • National Cancer Institute (R01CA164679, P01CA177322)
  • National Institute of Allergy and Infectious Diseases (R01AI048073, R01AI067890, R37AI033068)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Keywords
TNF receptor superfamily, costimulation, CO inhibition, 1p36, type I interferon, T cell survival, antitumor immunity, autoimmune disease, cytokine signaling, immune microenvironment
MeSH terms
Animals, Autoimmune Diseases, Chromosome Deletion, Chromosomes, Human, Pair 1, Humans, Immunity, Innate, Immunotherapy, Lymphocyte Activation, Neoplasms, T-Lymphocytes, Signal Transduction, Receptors, Tumor Necrosis Factor, Receptor Cross-Talk, Chromosome Disorders, Neurogenesis, Adaptive Immunity

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