ArticleAutophagy2015
The human CD5L/AIM-CD36 axis: A novel autophagy inducer in macrophages that modulates inflammatory responses.
Article in Autophagy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 113 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Apoptosis inhibitor of macrophage (AIM/CD5L) as a potential immunomodulator in feline injection-site sarcoma: a hypothesis on tumor-macrophage interactions.The veterinary quarterly · 2026Review
- Editorial: Investigating lung biology, metabolism, and host susceptibility in mycobacterial infections.Frontiers in cellular and infection microbiology · 2026Article
- Border-associated macrophages: an emerging perspective from physiological basis and multi-disease roles to the mechanism of vascular cognitive impairment and dementia.Journal of neuroinflammation · 2025Review
- DENetwork unveils non-differentially expressed genes with functional relevance across conditions through information flow perturbation.Nucleic acids research · 2025Article
- The role of an anti-inflammatory molecule AIM/CD5L in gut ischemia/reperfusion injury of male mice.Molecular medicine (Cambridge, Mass.) · 2025Article
- Senescent-like border-associated macrophages regulate cognitive aging via migrasome-mediated induction of paracrine senescence in microglia.Nature aging · 2025Article
- Inhibiting CD36 palmitoylation improves cardiac function post-infarction by regulating lipid metabolic homeostasis and autophagy.Nature communications · 2025Article
- Transforming heart transplantation care with multi-omics insights.Journal of translational medicine · 2025Review
- Endogenous CD5L controls the metabolic and inflammatory state of human macrophages.Frontiers in immunology · 2025Article
- AIMing for survival: The impact of the free and total AIM concentration in septic patients.Frontiers in immunology · 2025Article
- Gas6 induces AIM to suppress acute lung injury in mice by inhibiting NLRP3 inflammasome activation and inducing autophagy.Frontiers in immunology · 2025Article
- Article
- The effects of apoptosis inhibitor of macrophage in kidney diseases.European journal of medical research · 2024Review
- Macrophage lineage cells-derived migrasomes activate complement-dependent blood-brain barrier damage in cerebral amyloid angiopathy mouse model.Nature communications · 2023Article
- The comprehensive role of apoptosis inhibitor of macrophage (AIM) in pathological conditions.Clinical and experimental immunology · 2023Review
- Contribution of Elevated Glucose and Oxidized LDL to Macrophage Inflammation: A Role for PRAS40/Akt-Dependent Shedding of Soluble CD14.Antioxidants (Basel, Switzerland) · 2023Article
- [CD5L is elevated in the serum of patients with candidemia and promotes disease progression in mouse models].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- The Presence of Psoriasis, Metabolic Syndrome and Their Combination Increases the Serum Levels of CRP and CD5L but Not sCD200R1 and sTLR2 in Participants.Journal of personalized medicine · 2022Article
- TIMELESS is a key gene mediating thrombogenesis in COVID-19 and antiphospholipid syndrome.Scientific reports · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CD5L (CD5 molecule-like) is a secreted glycoprotein that participates in host response to bacterial infection. CD5L influences the monocyte inflammatory response to the bacterial surface molecules lipopolysaccharide (LPS) and lipoteichoic acid (LTA) by inhibiting TNF secretion. Here we studied the intracellular events that lead to macrophage TNF inhibition by human CD5L. To accomplish this goal, we performed functional analyses with human monocytic THP1 macrophages, as well as with peripheral blood monocytes. Inhibition of phosphatidylinositol 3-kinase (PtdIns3K) reversed the inhibitory effect of CD5L on TNF secretion. Among the various PtdIns3K isoforms, our results indicated that CD5L activates PtdIns3K (whose catalytic subunit is termed PIK3C3), a key modulator involved in autophagy. Further analysis revealed a concomitant enhancement of autophagy markers such as cellular LC3-II content, increased LC3 puncta, as well as LC3-LysoTracker Red colocalization. Moreover, electron microscopy showed an increased presence of cytosolic autophagosomes in THP1 macrophages overexpressing CD5L. Besides preventing TNF secretion, CD5L also inhibited IL1B and enhanced IL10 secretion. This macrophage anti-inflammatory pattern of CD5L was reverted upon silencing of autophagy protein ATG7 by siRNA transfection. Additional siRNA experiments in THP1 macrophages indicated that the induction of autophagy mechanisms by CD5L was achieved through cell-surface scavenger receptor CD36, a multiligand receptor expressed in a wide variety of cell types. Our data represent the first evidence that CD36 is involved in autophagy and point to a significant contribution of the CD5L-CD36 axis to the induction of macrophage autophagy.
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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.