ArticleInflammation1988
Stimulation of human neutrophils, monocytes, and platelets by modified C-reactive protein (CRP) expressing a neoantigenic specificity.
Article in Inflammation, 1988. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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.
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
23 citing papers in PubMed, 87 citations in OpenAlex.
- Effect of short-term aspirin use on C-reactive protein.Journal of thrombosis and thrombolysis · 2000Trial
- CRP (C-Reactive Protein) Revisited: An Old Yet New Biomarker of Acute and Chronic Inflammation.Cells · 2026Review
- The Pathogenesis, Potential Biomarkers and Novel Therapeutic Strategies for Tubulointerstitial Nephritis in Systemic Lupus Erythematosus-A Narrative Review.International journal of molecular sciences · 2025Review
- Redefining CRP in tissue injury and repair: more than an acute pro-inflammatory mediator.Frontiers in immunology · 2025Review
- A biofunctional review of C-reactive protein (CRP) as a mediator of inflammatory and immune responses: differentiating pentameric and modified CRP isoform effects.Frontiers in immunology · 2023Review
- Associations of C-reactive protein isoforms with systemic lupus erythematosus phenotypes and disease activity.Arthritis research & therapy · 2022Article
- Anti-Pentraxin Antibodies in Autoimmune Diseases: Bystanders or Pathophysiological Actors?Frontiers in immunology · 2020Review
- Presence of multimeric isoforms of human C-reactive protein in tissues and blood.Molecular medicine reports · 2016Article
- Prognostic value of anti-CRP antibodies in lupus nephritis in long-term follow-up.Arthritis research & therapy · 2015Article
- The role of genetic variants in CRP in radiographic severity in African Americans with early and established rheumatoid arthritis.Genes and immunity · 2015Article
- Targeting C-Reactive Protein in Inflammatory Disease by Preventing Conformational Changes.Mediators of inflammation · 2015Review
- Article
- Does C-reactive protein contribute to atherothrombosis via oxidant-mediated release of pro-thrombotic factors and activation of platelets?Frontiers in physiology · 2012Article
- C-reactive protein (CRP) aptamer binds to monomeric but not pentameric form of CRP.Analytical and bioanalytical chemistry · 2011Article
- C-reactive protein induced rearrangement of phosphatidylcholine on nanoparticle mimics of lipoprotein particles.The journal of physical chemistry. B · 2010Article
- C-reactive protein exists in an NaCl concentration-dependent pentamer-decamer equilibrium in physiological buffer.The Journal of biological chemistry · 2010Article
- Article
- Carbohydrate ligands of human C-reactive protein: binding of neoglycoproteins containing galactose-6-phosphate and galactose-terminated disaccharide.Glycoconjugate journal · 2006Article
- Antibodies to C reactive protein.Annals of the rheumatic diseases · 2006Article
- Autoantibodies to C-reactive protein (CRP) and other acute-phase proteins in systemic autoimmune diseases.Clinical and experimental immunology · 1998Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
C-reactive protein (CRP) can be structurally modified by heat, acid, or urea-chelation to express a neoantigen designated by us as neo-CRP. This antigen is also expressed on the in vitro primary protein translation products of both human and rabbit CRP. Unmodified CRP and CRP complexed with pneumococcal C-polysaccharide (CPS) do not express neo-CRP. Forms of CRP expressing neo-CRP but not native CRP antigenicity (even in the presence of CPS) consistently and in a dose-dependent manner potentiated the respiratory burst response of human polymorphonuclear leukocytes and peripheral blood monocytes to heat-modified IgG. Forms of CRP expressing neo-CRP antigenicity also induced reactions of aggregation and secretion from isolated platelets and potentiated platelet activation stimulated by ADP in platelet-rich-plasma, while native CRP alone or complexed with CPS again did not. Unlike CRP-CPS complexes, forms of CRP expressing neo-CRP were not able to activate the complement system. These data emphasize the biologic potential inherent in this humoral acute-phase reactant, particularly in the activation of the formed elements of the blood important in the inflammatory response. Since these cell-activating properties are preferentially observed when CRP is structurally modified to express the neo-CRP antigen, such a molecular conversion may be central to the structure-function relationships of CRP at local sites of inflammation and tissue injury.
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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.