Evidence map›Paper›PMID 10359807›Full record

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

Broad tumor-associated expression and recognition by tumor-derived gamma delta T cells of MICA and MICB.

V Groh, R Rhinehart, H Secrist, S Bauer, K H Grabstein, T Spies

Abstract 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 388 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
388citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

388 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Innate immune cells in chimeric antigen receptor therapy.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Review
  11. Review
  12. Harnessing Vδ1Frontiers in immunology · 2026
    Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review

328 more citing papers are in PubMed but not listed here.

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

6 authors.

V GrohFred Hutchinson Cancer Research Center, Clinical Research Division, 1100 Fairview Avenue North, Seattle, WA 98109, USA.
R Rhinehart
H Secrist
S Bauer
K H Grabstein
T Spies

Funding

Cell-Stress Induced Immune ResponsesR37AI030581 · NIAID · FRED HUTCHINSON CANCER RESEARCH CENTER · PI SPIES, THOMAS · 2001 to 2010
$5.7M
STUDIES ON MARROW GRAFT RESISTANCEP01CA018221 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI STORB, RAINER F. · 1985 to 2001
$2.7M
NOVEL IMMUNE RESPONSE GENES WITHIN THE HUMAN MHCR01AI030581 · NIAID · FRED HUTCHINSON CANCER RESEARCH CENTER · PI SPIES, THOMAS · 1991 to 2000
$366k
NCI NIH HHS CA18221NIAID NIH HHS AI30581NIAID NIH HHS R01 AI030581NIAID NIH HHS R37 AI030581
6 · The paper itself

Abstract

Human MHC class I-related molecules, MICA and MICB, are stress-induced antigens that are recognized by a subset of gamma delta T cells expressing the variable region Vdelta1. This functional association has been found to be limited to intestinal epithelium, where these T cells are prevalent and where MICA and, presumably, MICB are mainly expressed. However, increased frequencies of Vdelta1 gamma delta T cells have been observed in various epithelial tumors; moreover, MICA/B are expressed on diverse cultured epithelial tumor cells. With freshly isolated tumor specimens, expression of MICA/B was documented in many, but not all, carcinomas of the lung, breast, kidney, ovary, prostate, and colon. In tumors that were positive for MICA/B, the frequencies of Vdelta1 gamma delta T cells were significantly higher than in those that were negative. Vdelta1 gamma delta T cell lines and clones derived from different tumors recognized MICA/B on autologous and heterologous tumor cells. In accord with previous evidence, no constraints were observed in these interactions, such as those imposed by specific peptide ligands. Thus, MICA/B are tumor-associated antigens that can be recognized, in an apparently unconditional manner, by a subset of tumor-infiltrating gamma delta T cells. These results raise the possibility that an induced expression of MICA/B, by conditions that may be related to tumor homeostasis and growth, could play a role in immune responses against tumors.

Indexed as

Cytotoxicity, ImmunologicFlow CytometryHistocompatibility Antigens Class IHumansNeoplasmsReceptors, Antigen, T-Cell, gamma-deltaT-LymphocytesHistocompatibility Antigens Class IMHC class I-related chain AMICB antigenReceptors, Antigen, T-Cell, gamma-delta

Identifiers

PMID10359807
PMCPMC22010

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Registered trials

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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.