Evidence map›Paper›PMID 10339588›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America1999

Requirement for membrane lymphotoxin in natural killer cell development.

K Iizuka, D D Chaplin, Y Wang, Q Wu, L E Pegg, W M Yokoyama, Y X Fu

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

40 citing papers in PubMed, 139 citations in OpenAlex.

  1. T-bet Fate Mapping Reveals Gestational Stage-Specific Transcriptional Adaptation of Decidual NK Cells.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026
    Article
  2. Lymphotoxin beta receptorInfection and immunity · 2025
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Molecular Regulation of NK Cell Maturation.Frontiers in immunology · 2020
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. CD69+NK cells contribute to the murine hepatitis virus strain 3-induced murine hepatitis.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2013
    Article
  17. Review
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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

7 authors at 3 institutions in 1 country.

K IizukaDepartments of Internal Medicine and Pathology, Howard Hughes Medical Institute, and Center for Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.
D D Chaplin
Y Wang
Q Wu
L E Pegg
W M Yokoyama
Y X Fu
Howard Hughes Medical Institute · USMonsanto (United States) · USCenter for Rheumatology · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Development of natural killer (NK) cells is thought to depend on interactions between NK progenitors and the bone marrow (BM) microenvironment; however, little is known about the molecular signals involved. Here we show that lymphotoxin (LT) provides an important signal for the development of both NK cells and NK/T cells. LTalpha-/- mice show marked reduction in splenic and BM NK and NK/T cell numbers and dramatically impaired NK and NK/T cell function. Mice deficient in either tumor necrosis factor receptor (TNFR)-I or TNFR-II have normal numbers of NK and NK/T cells, implying that neither of the TNFRs nor soluble LTalpha3 is required for development of these cell types. Reciprocal BM transfers between LTalpha-/- and wild-type mice suggest that close interactions between membrane LT-expressing NK cell precursors and LT-responsive radioresistant stromal cells are necessary for NK cell development. When LT-deficient BM cells are incubated with IL-15, NK cells are formed. In addition, LT-deficient BM cells produce IL-15 after activation. Thus, membrane LT appears to deliver a signal for NK cell development that is either independent of IL-15 or upstream in the IL-15 pathway. These results reveal a novel function for membrane LT in NK and NK/T cell development. They also support a cellular and molecular mechanism by which NK cell precursors themselves deliver essential signals, through the membrane ligand, that induce the microenvironment to promote further NK cell and NK/T cell development.

Indexed as

AnimalsAntigens, CDBone Marrow CellsBone Marrow TransplantationCytotoxicity, ImmunologicGamma RaysGraft RejectionHematopoietic Stem CellsImmunosuppression TherapyInterleukin-15Killer Cells, NaturalLymphocyte TransfusionLymphotoxin-alphaMiceMice, Inbred C57BLMice, Inbred StrainsAntigens, CDInterleukin-15Lymphotoxin-alphaReceptors, Tumor Necrosis FactorReceptors, Tumor Necrosis Factor, Type IReceptors, Tumor Necrosis Factor, Type II

Identifiers

PMID10339588
PMCPMC26882
OpenAlexW1973891072

What OpenQuestion holds

Textmetadata
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.