Evidence map›Paper›PMID 12519387›Full record

ArticleClinical and experimental immunology2003

T cell activation by soluble C1q-bearing immune complexes: implications for the pathogenesis of rheumatoid arthritis.

K Jiang, Y Chen, C-S Xu, J N Jarvis

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

14 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Hypocomplementemic urticarial vasculitis syndrome.Current rheumatology reports · 2009
    Review
  11. Neutrophils: the forgotten cell in JIA disease pathogenesis.Pediatric rheumatology online journal · 2007
    Article
  12. Article
  13. Review
  14. Article
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 3 institutions in 1 country.

K JiangDepartment of Pediatrics, Oklahoma University Health Sciences Center, Oklahoma City, OK 73104, USA.
Y Chen
C-S Xu
J N Jarvis
OU HealthUniversity of Oklahoma · USUniversity of Oklahoma Health Sciences Center · US

Funding

IMMUNE COMPLEXES IN THE PATHOPHYSIOLOGY OF JRAR01AR043967 · NIAMS · WAYNE STATE UNIVERSITY · PI JARVIS, JAMES N · 1995 to 1997
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NIAMS NIH HHS R01-AR43967
6 · The paper itself

Abstract

Both innate and adaptive immune systems are thought to participate in the pathogenesis of rheumatoid arthritis in adults and children. The experiments reported here were undertaken to examine how immune complexes, potent stimulators of inflammation, may regulate cells of the adaptive immune system. Human T cells were prepared from peripheral blood by negative selection and incubated with bovine serum albumin (BSA)-anti-BSA immune complexes that were formed in the presence or absence of human C1q. C1q-bearing immune complexes, but not unopsonized complexes, elicited both TNF-alpha and IFN-gamma secretion from human T cells. Secretion of both cytokines was time- and dose-dependent. Cross-linking C1q on the cell surface of T cells produced the same results. Cytokine secretion was not inhibited by blocking the C3b receptor (CR1, CD35) on T cells prior to incubation with immune complexes. Reverse transcriptase polymerase chain reaction (RT-PCR) of immune complex-stimulated cells revealed accumulation of both TNF-alpha and IFN-gamma mRNA within 2 h post-stimulation. IL-2 was not detected in cell culture supernatants, but IL-2 receptor alpha chain (CD25) was detected in low density on a small proportion of T cells activated by C1q-bearing immune complexes. Secretion of both cytokines was inhibited partially, but not completely, by IL-10. These experiments show that immune complexes, potent inflammatory mediators, may activate T cells through a novel mechanism. These findings have implications for chronic inflammatory diseases in humans.

Indexed as

Antigen-Antibody ComplexArthritis, RheumatoidCells, CulturedComplement C1qFlow CytometryHumansInterferon-gammaInterleukin-10Lymphocyte ActivationReceptors, Interleukin-2Reverse Transcriptase Polymerase Chain ReactionRNA, MessengerT-LymphocytesTumor Necrosis Factor-alphaAntigen-Antibody ComplexComplement C1qInterferon-gammaInterleukin-10Receptors, Interleukin-2RNA, MessengerTumor Necrosis Factor-alpha

Identifiers

PMID12519387
PMCPMC1808608
OpenAlexW2007732050

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.