ReviewImmunology2014
Transplantation and inflammation: implications for the modification of chemokine function.
Review in Immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 44 citations in OpenAlex.
- Trial
- Cellular and Molecular Aspects of Chronic Rejection.Results and problems in cell differentiation · 2026Review
- Urinary Chemokines CXCL9 and CXCL10 Are Non-Invasive Biomarkers of Kidney Transplant Rejection.Annals of transplantation · 2024Article
- Mouse Models of Renal Allograft Transplant Rejection: Methods to Investigate Chemokine-GAG Interaction and Therapeutic Blockade.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Cytokines Removal DuringTransplant international : official journal of the European Society for Organ Transplantation · 2023Article
- Virus-Derived Chemokine Modulating Protein Pre-Treatment Blocks Chemokine-Glycosaminoglycan Interactions and Significantly Reduces Transplant Immune Damage.Pathogens (Basel, Switzerland) · 2022Article
- Circulating CXCL10 and IL-6 in solid organ donors after brain death predict graft outcomes.Scientific reports · 2021Article
- A C-terminal CXCL8 peptide based on chemokine-glycosaminoglycan interactions reduces neutrophil adhesion and migration during inflammation.Immunology · 2019Article
- How do chemokines navigate neutrophils to the target site: Dissecting the structural mechanisms and signaling pathways.Cellular signalling · 2019Review
- Cbl-b deficiency provides protection against UVB-induced skin damage by modulating inflammatory gene signature.Cell death & disease · 2018Article
- Novel tumour antigens and the development of optimal vaccine design.Therapeutic advances in vaccines and immunotherapy · 2018Review
- Neutrophils: Beneficial and Harmful Cells in Septic Arthritis.International journal of molecular sciences · 2018Review
- Integrated Proteome and Cytokine Profiles Reveal Ceruloplasmin Eliciting Liver Allograft Tolerance via Antioxidant Cascades.Frontiers in immunology · 2018Article
- Peroxynitrite Exposure of CXCL12 Impairs Monocyte, Lymphocyte and Endothelial Cell Chemotaxis, Lymphocyte ExtravasationFrontiers in immunology · 2018Article
- Pathophysiologic Implications of Cytokines Secretion during Liver Transplantation Surgery.International journal of medical sciences · 2018Review
- Urinary miR-155-5p and CXCL10 as prognostic and predictive biomarkers of rejection, graft outcome and treatment response in kidney transplantation.British journal of clinical pharmacology · 2017Observational
- Regulation of Chemokine Function: The Roles of GAG-Binding and Post-Translational Nitration.International journal of molecular sciences · 2017Review
- CCL2 nitration is a negative regulator of chemokine-mediated inflammation.Scientific reports · 2017Article
- Mechanisms of Regulation of the Chemokine-Receptor Network.International journal of molecular sciences · 2017Review
- Article
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 2 institutions in 1 country.
Funding
Abstract
Oxidative stress is a major and recurring cause of damage during inflammation, especially following organ transplantation. Initial ischaemia-reperfusion injury causes the production of many reactive oxygen and nitrogen species, and subsequent recruitment and activation of inflammatory cells can lead to further oxidative stress. This stress is well known to cause damage at the cellular level, for example by induction of senescence leading to the production of a characteristic senescence-associated secretory phenotype. Chemokines are an important component of the senescence-associated secretory phenotype, recruiting further leucocytes and reinforcing the stress and senescence responses. As well as inducing the production of proteins, including chemokines, oxidative stress can alter proteins themselves, both directly and by induction of enzymes capable of modification. These alterations can lead to important modifications to their biological activity and also alter detection by some antibodies, potentially limiting the biological relevance of some immunochemical and proteomic biomarkers. Peroxynitrite, a reactive nitrogen species generated during inflammation and ischaemia, can cause such modifications by nitrating chemokines. Matrix metalloproteinases, released by many stressed cells, can cleave chemokines, altering function, while peptidylarginine deiminases can inactivate certain chemokines by citrullination. This review discusses the relationship between inflammation and post-translational modification, focusing on the functional modulation of transplant-relevant pro-inflammatory chemokines.
Indexed as
Identifiers
What 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.