ArticleImmunology1994
Effect of C1q on the processing of immune complexes by human neutrophils.
Article in Immunology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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.
Who cites it
1 citing paper in PubMed, 14 citations in OpenAlex.
- Release of calreticulin from neutrophils may alter C1q-mediated immune functions.The Biochemical journal · 1997Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We prepared immune complexes (IC) composed of human anti-tetanus toxoid IgG and tetanus toxoid, and examined the effect of C1q on the processing of IC by human neutrophils. Treating IC with increasing amounts of C1q enhanced the binding and phagocytosis of IC by neutrophils, unless the amounts of C1q added were less than those required to saturate the C1q binding sites of IC. With the increase of unbound excess C1q, the IC processing by neutrophils decreased. Superoxide anions generated during the processing of IC-C1q were entrapped in phagosomes and were not released from neutrophils. The C1q-dependent inhibition of IC processing by neutrophils was not observed when C1q-treated neutrophils were washed and allowed to react with IC, suggesting that the inhibition by excess C1q is due to the hindrance of IC-C1q binding to neutrophils by loosely bound C1q on neutrophils. The C1q-treated, washed neutrophils still showed enhanced responses to IC, suggesting that free C1q as well as the IC-C1q complex can prime neutrophils to enhance Fc receptor (FcR)-mediated cellular responses. Thus, C1q may have two effects on the processing of IC by neutrophils; firstly, it enhances FcR-mediated cellular responses, and secondly, it prevents superoxide anion-induced tissue damage by trapping superoxide anions in phagosomes.
Indexed as
Identifiers
7835978PMC1415047W143758613What OpenQuestion holds
Registered trials
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.