Evidence map›Paper›PMID 26912039›Full record

ArticleScientific reports2016

Cell intrinsic role of NF-κB-inducing kinase in regulating T cell-mediated immune and autoimmune responses.

Yanchuan Li, Hui Wang, Xiaofei Zhou, Xiaoping Xie, Xiang Chen, Zuliang Jie, Qiang Zou, Hongbo Hu, Lele Zhu, Xuhong Cheng and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
1.7field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

41 citing papers in PubMed, 62 citations in OpenAlex.

  1. NF-κB in inflammation and cancer.Cellular & molecular immunology · 2025
    Review
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Association betweenInternational journal of molecular sciences · 2023
    Article
  9. Article
  10. NFκB signaling in T cell memory.Frontiers in immunology · 2023
    Review
  11. Review
  12. NF-κB in control of regulatory T cell development, identity, and function.Journal of molecular medicine (Berlin, Germany) · 2022
    Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 3 institutions in 2 countries.

Yanchuan LiNational Laboratory of Medical Molecular Biology, Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Tsinghua University, Beijing, China.
Hui WangDepartment of Immunology, The University of Texas MD Anderson Cancer Center, 7455 Fannin Street, Box 902, Houston TX 77030, USA.
Xiaofei ZhouDepartment of Immunology, The University of Texas MD Anderson Cancer Center, 7455 Fannin Street, Box 902, Houston TX 77030, USA.
Xiaoping XieDepartment of Immunology, The University of Texas MD Anderson Cancer Center, 7455 Fannin Street, Box 902, Houston TX 77030, USA.
Xiang ChenDepartment of Immunology, The University of Texas MD Anderson Cancer Center, 7455 Fannin Street, Box 902, Houston TX 77030, USA.
Zuliang JieDepartment of Immunology, The University of Texas MD Anderson Cancer Center, 7455 Fannin Street, Box 902, Houston TX 77030, USA.
Qiang ZouDepartment of Immunology, The University of Texas MD Anderson Cancer Center, 7455 Fannin Street, Box 902, Houston TX 77030, USA.
Hongbo HuState Key Laboratory of Biotherapy, West China Hospital, Si-Chuan University and Collaborative Innovation Center for Biotherapy, Chengdu, 610041, P. R. China.
Lele ZhuDepartment of Immunology, The University of Texas MD Anderson Cancer Center, 7455 Fannin Street, Box 902, Houston TX 77030, USA.
Xuhong ChengDepartment of Immunology, The University of Texas MD Anderson Cancer Center, 7455 Fannin Street, Box 902, Houston TX 77030, USA.
Hans D BrightbillDepartment of Immunology, Genentech Inc., South San Francisco, CA 94080.
Lawren C WuDepartment of Immunology, Genentech Inc., South San Francisco, CA 94080.
Linfang WangNational Laboratory of Medical Molecular Biology, Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, Peking Union Medical College, Tsinghua University, Beijing, China.
Shao-Cong SunDepartment of Immunology, The University of Texas MD Anderson Cancer Center, 7455 Fannin Street, Box 902, Houston TX 77030, USA.
The University of Texas MD Anderson Cancer Center · USTsinghua University · CNState Key Laboratory of Biotherapy

Funding

Tumor Evolution and Metastasis ProgramP30CA016672 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Scott Kopetz · 1985 to 2026
$290.8M
Molecular Studies of Noncanonical NF-kb SignalingR01GM084459 · NIGMS · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SUN, SHAO-CONG · 2008 to 2021
$4.4M
Signaling Functions of the Tumor Suppressor CYLDR01AI064639 · NIAID · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SUN, SHAO-CONG · 2006 to 2014
$3.6M
Regulation of T-cell function and autoimmune inflammation by deubiquitinases.R37AI064639 · NIAID · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI SUN, SHAO-CONG · 2015 to 2021
$2.8M
NCI NIH HHS P30 CA016672NCI NIH HHS P30CA016672NIAID NIH HHS AI064639NIAID NIH HHS R01 AI064639NIAID NIH HHS R37 AI064639NIGMS NIH HHS GM84459NIGMS NIH HHS R01 GM084459
6 · The paper itself

Abstract

NF-κB inducing kinase (NIK) is a central component of the noncanonical NF-κB signaling pathway. Although NIK has been extensively studied for its function in the regulation of lymphoid organ development and B-cell maturation, the role of NIK in regulating T cell functions remains unclear and controversial. Using T cell-conditional NIK knockout mice, we here demonstrate that although NIK is dispensable for thymocyte development, it has a cell-intrinsic role in regulating the homeostasis and function of peripheral T cells. T cell-specific NIK ablation reduced the frequency of effector/memory-like T cells and impaired T cell responses to bacterial infection. The T cell-conditional NIK knockout mice were also defective in generation of inflammatory T cells and refractory to the induction of a T cell-dependent autoimmune disease, experimental autoimmune encephalomyelitis. Our data suggest a crucial role for NIK in mediating the generation of effector T cells and their recall responses to antigens. Together, these findings establish NIK as a cell-intrinsic mediator of T cell functions in both immune and autoimmune responses.

Indexed as

AnimalsAutoimmunityBacterial InfectionsCell DifferentiationCells, CulturedEncephalomyelitis, Autoimmune, ExperimentalHomeostasisImmunity, CellularImmunologic MemoryMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicNF-kappa BNF-kappaB-Inducing KinaseProtein Serine-Threonine KinasesNF-kappa BNF-kappaB-Inducing KinaseProtein Serine-Threonine Kinases

Identifiers

PMID26912039
PMCPMC4766435
OpenAlexW2404315308

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.