ReviewJournal of leukocyte biology2016
CD26/dipeptidylpeptidase IV-chemokine interactions: double-edged regulation of inflammation and tumor biology.
Review in Journal of leukocyte biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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
58 citing papers in PubMed, 102 citations in OpenAlex.
- Trial
- LPCAT3 is essential for leukemia progression and represents a therapeutic vulnerability in AML.Blood science (Baltimore, Md.) · 2026Article
- Chemokine-Armed Oncolytic Viruses: Engineering Immune Cell Trafficking to Transform the Tumor Microenvironment.Pharmaceutics · 2026Review
- Refined single-cell profiling captures a CCR5EBioMedicine · 2026Article
- Chemokine receptor expression defines a trajectory from monocytes to mature macrophages in the lung.Journal of leukocyte biology · 2026Article
- Techniques for the determination of dipeptidyl peptidase IV and screening of its inhibitors.Journal of pharmaceutical analysis · 2026Review
- Transcriptome analysis of hepatopancreas of Litopenaeus vannamei after acute exposure to Alexandrium pacificum.PloS one · 2026Article
- Synthesis and preclinical evaluation of FAP-targeting radiotracers for PET and optical imaging.EJNMMI radiopharmacy and chemistry · 2025Article
- Spatial multi-omics identifies aggressive prostate cancer signatures highlighting pro-inflammatory chemokine activity in the tumor microenvironment.Nature communications · 2025Article
- PARP inhibitor-induced anti-tumour chemokine response is suppressed by dipeptidyl peptidase 4 (DPP4) in ovarian cancer.British journal of cancer · 2025Article
- The Role of Fibroblasts in Dystrophic Epidermolysis Bullosa Pathogenesis and Current Treatment Approaches.JID innovations : skin science from molecules to population health · 2025Review
- Incretin-Based Therapies and Cancer: What's New?Medicina (Kaunas, Lithuania) · 2025Review
- Microbial dipeptidyl peptidases of the S9B family as host-microbe isozymes.Science advances · 2025Review
- MAIT cell homing in intestinal homeostasis and inflammation.Science advances · 2025Review
- Chemokines in the resolution of inflammation: key players and targets for therapeutic modulation.Frontiers in immunology · 2025Review
- Single-cell transcriptome analysis of the mouse lungs during the injury and recovery periods after lipopolysaccharide administration.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Comprehensive single-cell profiling of monocytes in HLA-B27-positive ankylosing spondylitis with acute anterior uveitis.MedComm · 2024Article
- The Functions of SARS-CoV-2 Receptors in Diabetes-Related Severe COVID-19.International journal of molecular sciences · 2024Review
- B-1 derived anti-Thy-1 B cells in old aged mice develop lymphoma/leukemia with high expression of CD11b and Hamp2 that different from TCL1 transgenic mice.Immunity & ageing : I & A · 2024Article
- Natural carboxyterminal truncation of human CXCL10 attenuates glycosaminoglycan binding, CXCR3A signaling and lymphocyte chemotaxis, while retaining angiostatic activity.Cell communication and signaling : CCS · 2024Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Post-translational modification of chemokines is an essential regulatory mechanism to enhance or dampen the inflammatory response. CD26/dipeptidylpeptidase IV, ubiquitously expressed in tissues and blood, removes NH2-terminal dipeptides from proteins with a penultimate Pro or Ala. A large number of human chemokines, including CXCL2, CXCL6, CXCL9, CXCL10, CXCL11, CXCL12, CCL3L1, CCL4, CCL5, CCL11, CCL14, and CCL22, are cleaved by CD26; however, the efficiency is clearly influenced by the amino acids surrounding the cleavage site and although not yet proven, potentially affected by the chemokine concentration and interactions with third molecules. NH2-terminal cleavage of chemokines by CD26 has prominent effects on their receptor binding, signaling, and hence, in vitro and in vivo biologic activities. However, rather than having a similar result, the outcome of NH2-terminal truncation is highly diverse. Either no difference in activity or drastic alterations in receptor recognition/specificity and hence, chemotactic activity are observed. Analogously, chemokine-dependent inhibition of HIV infection is enhanced (for CCL3L1 and CCL5) or decreased (for CXCL12) by CD26 cleavage. The occurrence of CD26-processed chemokine isoforms in plasma underscores the importance of the in vitro-observed CD26 cleavages. Through modulation of chemokine activity, CD26 regulates leukocyte/tumor cell migration and progenitor cell release from the bone marrow, as shown by use of mice treated with CD26 inhibitors or CD26 knockout mice. As chemokine processing by CD26 has a significant impact on physiologic and pathologic processes, application of CD26 inhibitors to affect chemokine function is currently explored, e.g., as add-on therapy in viral infection and cancer.
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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.