ReviewJournal of human immunity2026
Apolipoproteins L involvement in immunity.
Review in Journal of human immunity, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
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Corrections and comments
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Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apolipoproteins L (APOLs) are membrane-associated proteins involved in both resistance to pathogens, such as APOL1-mediated killing of African trypanosomes or APOL3-mediated lysis of intracellular bacteria, and induction of diseases, like APOL1-mediated nephropathy or APOL2-mediated liver fibrosis. Accumulating evidence points to APOLs controlling membrane dynamics linked to immunity. APOL1 and APOL3 are induced by inflammatory signalling and play key roles in the initiation and termination of inflammation by promoting the traffic of Golgi-derived membranes involved in STING activation, as well as mitochondrial membrane fission and fusion involved in auto/mitophagy. APOL2, or murine mAPOL8, is required for profibrotic vesicle exocytosis, whereas mAPOL9 triggers bacterial membrane budding linked to gut immunity control. In dendritic cells, APOL3 or the APOL3-like mAPOL7C promote megapore formation in phagosomal membranes, allowing antigen cross-presentation and apoptosis, both probably linked to cardiolipin solubilization. In adipocytes, mAPOL6 controls inflammation-linked lipid droplets dynamics. Through their membrane-remodeling activities, APOLs participate in the control of infection by bacteria, viruses, and parasites. Thus, natural APOLs mutations represent inborn errors of immunity.
Identifiers
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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.