Evidence map›Paper›PMID 15599401›Full record

ArticleThe Journal of clinical investigation2004

EphB6-null mutation results in compromised T cell function.

Hongyu Luo, Guang Yu, Johanne Tremblay, Jiangping Wu

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2004. 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
1.5field-weighted citation impact, top 21% 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, 97 citations in OpenAlex.

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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

4 authors at 2 institutions in 1 country.

Hongyu LuoLaboratory of Immunology, Centre de Recherché, Notre Dame Hospital, Centre Hospitalier de l'Université de Montréal, Pavilion DeSève, 1560 Sherbrooke Street East, Montréal, Quebec H2L 4M1, Canada.
Guang Yu
Johanne Tremblay
Jiangping Wu
Centre Hospitalier de l’Université de Montréal · CAHôpital Notre-Dame · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

So far, there is very limited knowledge about the role of Eph kinases, the largest family of receptor tyrosine kinases, in the immune system. Here, using EphB6(-/-) mice, we demonstrated that in vitro and in vivo T cell responses such as lymphokine secretion, proliferation, and the development of delayed-type skin hypersensitivity and experimental autoimmune encephalitis in EphB6(-/-) mice were compromised. On the other hand, humoral immune responses, such as serum levels of different Ig isotypes and IgG response to tetanus toxoid, were normal in these mice. Mechanistically, we showed that EphB6 migrated to the aggregated TCRs and rafts after TCR activation. Further downstream, in the absence of EphB6, ZAP-70 activation, LAT phosphorylation, the association of PLCgamma1 with SLP-76, and p44/42 MAPK activation were diminished. Thus, we have shown that EphB6 is pivotal in T cell function.

Indexed as

MutationAnimalsAntigensAntigens, CDAntigens, Differentiation, T-LymphocyteBiotinylationCD28 AntigensCD3 ComplexCD69 AntigensCell ProliferationCytokinesDose-Response Relationship, DrugExonsFemaleFlow CytometryGene DeletionAntigensAntigens, CDAntigens, Differentiation, T-LymphocyteCD28 AntigensCD3 ComplexCD69 AntigensCytokinesGreen Fluorescent ProteinsLectins, C-TypeLigandsReceptor, EphB6Receptors, Antigen, T-CellReceptors, Interleukin-2

Identifiers

PMID15599401
PMCPMC535066
OpenAlexW1976819858

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.