ReviewClinical and experimental immunology2010
Copy number variation in chemokine superfamily: the complex scene of CCL3L-CCL4L genes in health and disease.
Review in Clinical and experimental immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled 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.
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
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Pooled it
- Unveiling the Role of CCL3: A Driver of CIPN in Colon Cancer Patients?Biomedicines · 2025Review
- Contribution of copy number variations to education, socioeconomic status and cognition from a genome-wide study of 305,401 subjects.Molecular psychiatry · 2025Article
- Blood memory CD8 T cell phenotypes in lung cancer patients predict immune checkpoint treatment responses.Frontiers in oncology · 2025Article
- Transcriptional profiles of peripheral eosinophils in chronic obstructive pulmonary disease and asthma-An exploratory study.Journal of cellular and molecular medicine · 2024Article
- Monocytic myeloid-derived suppressive cells mitigate over-adipogenesis of bone marrow microenvironment in aplastic anemia by inhibiting CD8Cell death & disease · 2022Article
- CCL3L3-null status is associated with susceptibility to systemic lupus erythematosus.Scientific reports · 2021Article
- Accurate diagnosis and heterogeneity analysis of a 17q12 deletion syndrome family with adulthood diabetes onset and complex clinical phenotypes.Endocrine · 2021Article
- CC Chemokines in a Tumor: A Review of Pro-Cancer and Anti-Cancer Properties of Receptors CCR5, CCR6, CCR7, CCR8, CCR9, and CCR10 Ligands.International journal of molecular sciences · 2020Review
- Genetic landscape and autoimmunity of monocytes in developing Vogt-Koyanagi-Harada disease.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Copy number variation of CCL3L1 among three major ethnic groups in Malaysia.BMC genetics · 2020Article
- Syk-dependent tyrosine phosphorylation of 3BP2 is required for optimal FcRγ-mediated phagocytosis and chemokine expression in U937 cells.Scientific reports · 2017Article
- Increased Levels of Macrophage Inflammatory Proteins Result in Resistance to R5-Tropic HIV-1 in a Subset of Elite Controllers.Journal of virology · 2015Article
- Global patterns of apparent copy number variation in birds revealed by cross-species comparative genomic hybridization.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2014Article
- Age-related macular degeneration: insights into inflammatory genes.Journal of ophthalmology · 2014Review
- Genome diversification mechanism of rodent and Lagomorpha chemokine genes.BioMed research international · 2013Article
- Article
- Systematic classification of vertebrate chemokines based on conserved synteny and evolutionary history.Genes to cells : devoted to molecular & cellular mechanisms · 2013Review
- Article
- 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
No grant is acknowledged in the PubMed record.
Abstract
Genome copy number changes (copy number variations: CNVs) include inherited, de novo and somatically acquired deviations from a diploid state within a particular chromosomal segment. CNVs are frequent in higher eukaryotes and associated with a substantial portion of inherited and acquired risk for various human diseases. CNVs are distributed widely in the genomes of apparently healthy individuals and thus constitute significant amounts of population-based genomic variation. Human CNV loci are enriched for immune genes and one of the most striking examples of CNV in humans involves a genomic region containing the chemokine genes CCL3L and CCL4L. The CCL3L-CCL4L copy number variable region (CNVR) shows extensive architectural complexity, with smaller CNVs within the larger ones and with interindividual variation in breakpoints. Furthermore, the individual genes embedded in this CNVR account for an additional level of genetic and mRNA complexity: CCL4L1 and CCL4L2 have identical exonic sequences but produce a different pattern of mRNAs. CCL3L2 was considered previously as a CCL3L1 pseudogene, but is actually transcribed. Since 2005, CCL3L-CCL4L CNV has been associated extensively with various human immunodeficiency virus-related outcomes, but some recent studies called these associations into question. This controversy may be due in part to the differences in alternative methods for quantifying gene copy number and differentiating the individual genes. This review summarizes and discusses the current knowledge about CCL3L-CCL4L CNV and points out that elucidating their complete phenotypic impact requires dissecting the combinatorial genomic complexity posed by various proportions of distinct CCL3L and CCL4L genes among individuals.
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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.