Evidence map›Paper›PMID 11285307›Full record

ArticleThe Journal of clinical investigation2001

B7-dependent T-cell costimulation in mice lacking CD28 and CTLA4.

D A Mandelbrot, M A Oosterwegel, K Shimizu, A Yamada, G J Freeman, R N Mitchell, M H Sayegh, A H Sharpe

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

24 citing papers in PubMed, 84 citations in OpenAlex.

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  14. Induction of autoimmune disease in CTLA-4-/- mice depends on a specific CD28 motif that is required for in vivo costimulation.Proceedings of the National Academy of Sciences of the United States of America · 2007
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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

8 authors at 5 institutions in 2 countries.

D A MandelbrotDepartment of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA.
M A Oosterwegel
K Shimizu
A Yamada
G J Freeman
R N Mitchell
M H Sayegh
A H Sharpe
Brigham and Women's Hospital · USHarvard University · USDana-Farber Cancer Institute · USMassachusetts General Hospital · USUniversity Medical Center Utrecht · NL

Funding

Role of Negative Costimulation in Regulation of AutoimmunityP01AI039671 · NIAID · YALE UNIVERSITY · PI David A. Hafler · 1996 to 2026
$51.7M
T Cell Fate as a Determinant of Alloimmune ResponsesP01AI041521 · NIAID · UNIVERSITY OF PENNSYLVANIA · PI STROM, TERRY B. · 1997 to 2011
$15.9M
In Vivo Function of the B7 Family of CostimulatorsR37AI038310 · NIAID · HARVARD MEDICAL SCHOOL · PI SHARPE, ARLENE H. · 2006 to 2015
$4.1M
MOLECULAR PATHWAYS REGULATING T CELL ANERGY TO ALLOANTIGENP01AI041584 · NIAID · DANA-FARBER CANCER INSTITUTE · PI SHARPE, ARLENE H · 1997 to 2001
$1.8M
IN VIVO FUNCTION OF THE B7 FAMILY OF COSTIMULATORSR01AI038310 · NIAID · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI SHARPE, ARLENE H · 1995 to 2004
$1.8M
INTRATHYMIC TRANSPLANTATION TOLERANCE BY MHC PEPTIDESR01AI034965 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI SAYEGH, MOHAMED H · 1999 to 2003
$1.3M
PATHOGENESIS OF TRANSPLANT-ASSOCIATED ARTERIOSCLEROSISR01HL043364 · NHLBI · TUFTS MEDICAL CENTER · PI MITCHELL, RICHARD N · 1990 to 2003
$1.2M
ANTITUMOR AND COSTIMULATORY ACTIVITY OF B7 ON T CELLSR01CA075174 · NCI · BRIGHAM AND WOMEN'S HOSPITAL · PI KUCHROO, VIJAY K · 1999 to 2002
$586k
INTRATHYMIC TRANSPLANTATION TOLERANCE BY MHC PEPTIDESR29AI034965 · NIAID · BRIGHAM AND WOMEN'S HOSPITAL · PI SAYEGH, MOHAMED H · 1994 to 1998
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NCI NIH HHS CA-75174NHLBI NIH HHS HL 43364NIAID NIH HHS AI-34965NIAID NIH HHS AI-38310NIAID NIH HHS AI-39671NIAID NIH HHS AI-41521NIAID NIH HHS AI-41584NIAID NIH HHS P01 AI039671NIAID NIH HHS P01 AI041521NIAID NIH HHS R01 AI034965NIAID NIH HHS R01 AI038310NIAID NIH HHS R37 AI038310
6 · The paper itself

Abstract

To examine whether B7 costimulation can be mediated by a molecule on T cells that is neither CD28 nor CTLA4, we generated mice lacking both of these receptors. CD28/CTLA4(-/-) mice resemble CD28(-/-) mice in having decreased expression of T-cell activation markers in vivo and decreased T-cell proliferation in vitro, as compared with wild-type mice. Using multiple approaches, we find B7-dependent costimulation in CD28/CTLA4(-/-) mice. The proliferation of CD28/CTLA4(-/-) T cells is inhibited by CTLA4-Ig and by the use of antigen-presenting cells lacking both B7-1 and B7-2. CD28/CTLA4(-/-) T-cell proliferation is increased by exposure to Chinese hamster ovary cells transfected with B7-1 or B7-2. Finally, administration of CTLA4-Ig to CD28/CTLA4(-/-) cardiac allograft recipients significantly prolongs graft survival. These data support the existence of an additional receptor for B7 molecules that is neither CD28 nor CTLA4.

Indexed as

ImmunoconjugatesAbataceptAnimalsAntigens, CDAntigens, DifferentiationB7-1 AntigenB7-2 AntigenCD28 AntigensCell DivisionCHO CellsCricetinaeCTLA-4 AntigenGraft RejectionGraft SurvivalHeart TransplantationImmunophenotypingAbataceptAntigens, CDAntigens, DifferentiationB7-1 AntigenB7-2 AntigenCD28 AntigensCd86 protein, mouseCTLA-4 AntigenCtla4 protein, mouseImmunoconjugatesInterferon-gammaMembrane Glycoproteins

Identifiers

PMID11285307
PMCPMC199576
OpenAlexW2041980736

What OpenQuestion holds

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Read underepoch 390

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.