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Open research questions in Phagocytosis and Immune Regulation

96 gap statements mined from Phagocytosis and Immune Regulation papers in our 4.5M-paper local library, which holds 287 papers on the topic — drawn mostly from each paper's own stated research gap, future-work, challenge and limitation notes, and its abstract. The ones listed below are a selection still marked open; each names the study that raised it, with a DOI link where the paper has one.

What the literature leaves open

  • Abstract Highly accessible genomic super-enhancers often drive tumor-promoting programs, yet the impact of genomic variation within these regulatory elements remains unclear.

    An InDel genomic variant within a bifunctional super-enhancer for LINC00636 and CD47 regulation in breast cancer · 2026 · DOI

  • Liver inflammation and damage are well-known features of COVID-19 pathogenesis; however, little is known about FGL-1 expression patterns in COVID-19 and other infectious diseases.

    FGL-1 plasma levels correlate with markers of inflammation and severe disease during SARS-CoV-2 infection · 2026 · DOI

  • Live T cells, however, have been shown to externalize PS, and the role of cell surface-exposed PS in T-cell function remains unclear.

    Targeting Exposed Phosphatidylserine Boosts Antigen-Specific T-Cell Response · 2026 · DOI

  • However, the precise mechanism through which PAI-1 exacerbates inflammation remains unclear.

    Inflammatory macrophage-derived plasminogen activator inhibitor-1 exacerbates inflammation through efferocytosis inhibition · 2026 · DOI

  • Glioblastomas (GBMs) are uniformly fatal brain tumors resistant to immunotherapy, yet the mechanisms driving immune dysfunction remain poorly understood.

    Radiation therapy synergizes with mRNA vaccination to overcome microglia-mediated suppression of dendritic cell migration and T cell priming in glioblastoma · 2026 · DOI

  • Therefore, future investigations are warranted to elucidate the roles of ACE2-independent mechanisms in immune-mediated pathology and viral evolution, independent of immune pressure targeting ACE2-mediated entry in previously infected or vaccinated individuals.

    ACE2-independent entry factors for SARS-CoV-2 infection and immune activation · 2025 · DOI

  • However, the mechanism by which intracellular lipid accumulation impairs macrophage efferocytosis remains unclear.

    TRIB3 Links Endoplasmic Reticulum Stress to Impaired Efferocytosis in Atherosclerosis · 2025 · DOI

  • However, Kras mutation alone is insufficient to transform precancerous cells into metastatic PDAC.

    Intercellular TIMP-1-CD63 signaling directs the evolution of immune escape and metastasis in KRAS-mutated pancreatic cancer cells · 2025 · DOI

  • BACKGROUND: While immunotherapy-chemotherapy combinations are approved for programmed death-ligand 1 (PD-L1)-positive advanced triple-negative breast cancer (TNBC), the therapeutic potential of sitravatinib-enhanced immunotherapy remains unexplored.

    Sitravatinib plus tislelizumab in locally recurrent or metastatic triple-negative breast cancer: a multi-cohort, single-arm, phase II clinical trial (SPARK Trial) · 2025 · DOI

  • While the mechanisms involved in this heterogeneity in the tumor microenvironment (TME) of early-stage EC remain poorly defined.

    Targeting the CD47-HCK-LGALS9 axis disrupts proliferation-immunosuppression coupling in early-stage endometrial cancer · 2025 · DOI

  • The details of adaptive immune remodeling in liver metastasis, especially the role of neutrophils, remain elusive.

    NFE2-driven neutrophil polarization promotes pancreatic cancer liver metastasis progression · 2025 · DOI

  • However, the precise function and regulatory mechanisms of SIRPα in efferocytosis remain unclear.

    SIRPα modulates microglial efferocytosis and neuroinflammation following experimental subarachnoid hemorrhage via the SHP1/STAT6 axis · 2025 · DOI

  • However, its antibacterial role in vivo and the underlying mechanisms have been insufficiently explored.

    ATP7A Maintains Bactericidal Function of Neutrophils and Macrophages via Regulating the Formation and Activation of Phagolysosomes · 2025 · DOI

  • Successfully inhibiting sepsis-induced acute lung injury (ALI) hinges on clearing apoptotic neutrophils; however, the underlying mechanisms of this process remain elusive.

    Blocking the ADAM9 / ITGAV Pathway Ameliorates Sepsis‐Induced Acute Lung Injury by Promoting Macrophage Efferocytosis · 2025 · DOI

  • However, the specific molecular mechanisms underlying the defective immune functions of BM-MSCs in patients with SLE remain unclear.

    The aryl hydrocarbon receptor affects the inflammatory response of bone marrow mesenchymal stem cell via the hippo– YAP pathway to exacerbate systemic lupus erythematosus · 2025 · DOI

  • However, compared to small extracellular vesicles, the preparation, characterization, and biological properties of ApoBDs remain underexplored.

    Comparison of in-vitro immunomodulatory capacity between large and small apoptotic bodies from human bone marrow mesenchymal stromal cells · 2025 · DOI

  • M2 microglia efferocytosis is essential for resolving neuroinflammation, but its regulatory mechanisms remain unclear.

    GAS6/AXL signaling promotes M2 microglia efferocytosis to alleviate neuroinflammation in sepsis-associated encephalopathy · 2025 · DOI

  • However, the antitumor activity of gilteritinib in solid tumors remains poorly elucidated.

    Antitumor activity of gilteritinib, an inhibitor of AXL, in human solid tumors · 2025 · DOI

  • Despite the significant impact of CAKI on COVID-19-related mortality and its enduring effects in long COVID, the underlying causes and molecular mechanisms of CAKI remain elusive.

    SARS-CoV-2 ORF3a induces COVID-19-associated kidney injury through HMGB1-mediated cytokine production · 2024 · DOI

  • BACKGROUND: The Gas6/TAM (Tyro3, Axl, and Mer) receptor system has been implicated in demyelination and delayed remyelination in experimental animal models, but data in humans are scarce.

    Tyro3 and Gas6 are associated with white matter and myelin integrity in multiple sclerosis · 2024 · DOI

  • However, the best strategies to use these therapies remain unknown, and ongoing studies suggest they may be most effective when used in combination with other anticancer agents.

    Targeted therapies prime oncogene-driven lung cancers for macrophage-mediated destruction · 2024 · DOI

  • Although extracellular vesicles derived from mesenchymal stem cells (MSC-EVs) have shown substantial potentials in cell replacement therapy of various organ ischemia reperfusion injuries (IRIs), the precise mechanisms remain unclear.

    Extracellular vesicles containing GAS6 protect the liver from ischemia-reperfusion injury by enhancing macrophage efferocytosis via MerTK-ERK-COX2 signaling · 2024 · DOI

  • The complex pathogenesis of rheumatoid arthritis, - The limited curative therapies available for RA, - The potential off-target effects of CD47 antibodies

    Commentary: the TSP-1-CD47-integrin α4β1 axis—deciphering pathogenic mechanisms and therapeutic horizons in rheumatoid arthritis · 2026 · DOI

  • The study identifies a gap in the understanding of the molecular mechanisms underlying CD47-mediated T cell infiltration. The role of the TSP-1-CD47-integrin α4β1 axis in rheumatoid arthritis is not fully understood.

    Commentary: the TSP-1-CD47-integrin α4β1 axis—deciphering pathogenic mechanisms and therapeutic horizons in rheumatoid arthritis · 2026 · DOI

  • The geometric origins of the physical limit of frustrated phagocytosis remain poorly defined. There is a need for a quantitative framework to interpret stalled engulfment and nuclear deformation-dependent responses.

    A Geometric Model of Nucleus-Constrained Frustrated Phagocytosis · 2026 · DOI

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96 gap statements have been mined from Phagocytosis and Immune Regulation papers in our 4.5M-paper local library, which holds 287 papers on the topic; the gaps come from whichever of those papers state one. They are mostly the research gaps the authors state and the papers' abstracts, plus future-work, limitations and challenges passages. The ones listed below are a selection still marked open; each names the study that raised it, with a DOI link where the paper has one, so you can read the original claim in context.

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