Evidence map›Paper›PMID 9314551›Full record

ArticleThe Journal of experimental medicine1997

Required early complement activation in contact sensitivity with generation of local C5-dependent chemotactic activity, and late T cell interferon gamma: a possible initiating role of B cells.

R F Tsuji, G P Geba, Y Wang, K Kawamoto, L A Matis, P W Askenase

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

19 citing papers in PubMed, 84 citations in OpenAlex.

  1. Review
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  8. Th-17, monokines, collagen type V, and primary graft dysfunction in lung transplantation.American journal of respiratory and critical care medicine · 2008
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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

6 authors at 3 institutions in 2 countries.

R F TsujiNoda Institute for Scientific Research, Noda-shi, Chiba-ken 278, Japan.
G P Geba
Y Wang
K Kawamoto
L A Matis
P W Askenase
Yale University · USOsaka Prefecture University · JPAlexion Pharmaceuticals (United States) · US

Funding

ALLERGY AND IMMUNOLOGY TRAINING GRANTT32AI007174 · NIAID · YALE UNIVERSITY · PI ASKENASE, PHILIP WILLIAM · 1985 to 2015
$2.6M
IMMUNOLOGY OF CUTANEOUS BASOPHIL HYPERSENSITIVITYR01AI012211 · NIAID · YALE UNIVERSITY · PI ASKENASE, PHILIP W · 1985 to 1986
–
INITIATOR T CELLS IN DELAYED-TYPE HYPERSENSITIVITYR01AI026689 · NIAID · YALE UNIVERSITY · PI ASKENASE, PHILIP W · 1989 to 1996
–
THE IMMUNOBIOLOGY OF CUTANEOUS HYPERSENSITIVITYR37AI012211 · NIAID · YALE UNIVERSITY · PI ASKENASE, PHILIP W · 1987 to 1996
–
NIAID NIH HHS AI-07174NIAID NIH HHS AI-12211NIAID NIH HHS AI-26689NIAID NIH HHS T32 AI007174
6 · The paper itself

Abstract

Complement (C) is an important component of innate immunity, and was also shown recently to participate in induction of acquired B cell humoral immunity. In this study, we present evidence that C also participates in acquired T cell immunity. We found that C was involved in early events of the efferent elicitation phase of contact sensitivity (CS), and delayed-type hypersensitivity (DTH). Thus, CS and DTH were inhibited by administration of a C-blocker, soluble recombinant C receptor-1 (sCR1), when given 30 min before, but not 3 h after local antigen challenge. Among C components, local C5 were thought crucial to elicitation of CS, since local administration of anti-C5 monoclonal antibodies or locally injected C-depleting cobra venom factor also inhibited CS and DTH. These findings were consistent with our previous finding of the importance of C5 for CS elicitation, using congenitally C5-deficient mice. To dissect the mechanism of C dependence in CS, we demonstrated that locally increased early macrophage chemotactic activity (probably C5a) in evolving CS skin extracts, as well as late elaboration of IFN-gamma, were both inhibited by anti-C treatment. In addition, histological analysis showed that leukocyte recruitment into CS ear sites was similarly C-dependent. Furthermore, an initiating role of B cell-derived C-fixing immunoglobulin was suggested by demonstration of impaired CS responses in B cell-deficient mice. In summary, these results suggest that C was activated locally, perhaps via a B cell product, in an important early component of the stepwise events necessary to elicit CS, leading to local production of C5-dependent macrophage chemotactic activity and later IFN-gamma, and subsequently leading to cell infiltration, for development of T cell-dependent CS.

Indexed as

AnimalsAntibodies, MonoclonalB-LymphocytesChemotactic FactorsChemotaxisComplement ActivationComplement C5Complement Inactivator ProteinsDermatitis, ContactElapid VenomsFemaleHypersensitivity, DelayedInterferon-gammaMacrophagesMiceMice, Inbred StrainsAntibodies, MonoclonalChemotactic Factorscobra venom factorComplement C5Complement Inactivator ProteinsElapid VenomsInterferon-gammaReceptors, ComplementRecombinant Proteinssoluble complement inhibitor 1

Identifiers

PMID9314551
PMCPMC2199060
OpenAlexW2034269975

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.