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Open research questions in interferon and immune responses

771 gap statements mined from interferon and immune responses papers in our 7.9M-paper local library, which holds 3,146 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.

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What the literature leaves open

  • The need to integrate multiple functional modalities to characterize the impact of viral transcriptional regulators on host gene expression. The challenge of identifying the extensive rewiring of host pathways by viral transcriptional regulators.

    Functional characterization of viral transcriptional regulators reveals extensive rewiring of host pathways · 2026 · DOI

  • The mechanisms of action of viral transcriptional regulators are not well understood. The impact of viral transcriptional regulators on host gene expression is not well characterized. There is a need for a framework to understand how viral transcriptional regulators contribute to viral replication, persistence, and pathogenesis.

    Functional characterization of viral transcriptional regulators reveals extensive rewiring of host pathways · 2026 · DOI

  • The role of TRIM28 in DLBCL progression and glycolytic reprogramming is unclear. The molecular mechanisms underlying TRIM28's effects on DLBCL cell growth, migration, and glycolytic activity are not well understood.

    TRIM28 facilitates diffuse large B-cell lymphoma progression by inducing glycolytic reprogramming through the E2F1/PKM2 axis · 2026 · DOI

  • The need to develop effective methods to study the role of TRIM69 in suppressing viral replication. The difficulty of translating the findings to primary human cells and in vivo models.

    TRIM69 Suppresses the Cellular AMPK Pathway to Inhibit Viral Replication · 2026 · DOI

  • The specific role of ISG20 against PEDV remains poorly understood. The underlying mechanism of ISG20 during PEDV infection is not well characterized.

    Porcine ISG20 Restricts PEDV Replication Independent of Its Exonuclease Activity and Is Associated with Enhanced IRF3 Activation · 2026 · DOI

  • The complex roles of the ETS family in immune cells and immune-related diseases are not fully understood. The correlation between the ETS family and various diseases and disease processes needs to be thoroughly analyzed. The difficulty of research on the ETS family is increased due to their complex roles.

    ETS Transcription Factors in Immune Cells and Immune-Related Diseases · 2024 · DOI

  • The pathogenicity mechanism of AIV is still not clear. The role of TRIM21 in promoting oxidative stress and ferroptosis is not well understood.

    TRIM21 Promotes Oxidative Stress and Ferroptosis through the SQSTM1-NRF2-KEAP1 Axis to Increase the Titers of H5N1 Highly Pathogenic Avian Influenza Virus · 2024 · DOI

  • However, how HHARI drives interferon signalling is not fully understood and the function of the unique, highly conserved acidic N-terminal domain of the protein is unknown.

    The acidic N-terminus of HHARI and neddylation are essential for the activation and maintenance of RIG-I-mediated type I interferon response · 2026 · DOI

  • While the cGAS-STING pathway is well characterized in detecting non-self-DNA, its response to self-DNA originating from the host nucleus remains unclear.

    Uncoupling of STING Accumulation and Activation upon Chromosome-Derived Extrachromosomal Circular DNA Formation · 2026 · DOI

  • How these antibodies emerge, mature, and function at the molecular level remains unclear.

    Developmental and molecular features shaping broad and synergistic actions of human autoantibodies targeting interferon-α · 2026 · DOI

  • Early life is characterized by heightened susceptibility to respiratory pathogens, yet the immune mechanisms that predispose infants to infection remain poorly defined.

    Delayed IL-17RA signaling in early life promotes type I interferon/CXCL10-dependent inhibition of pneumococcal clearance · 2026 · DOI

  • However, the role of kinases in modulating RIG-I in a catalytically-independent manner is not well known.

    DYRK1B: A Novel positive regulator of RIG-I in antiviral innate immunity · 2026 · DOI

  • However, its function in negative-strand RNA virus infection and innate immune responses remains poorly understood.

    ACBD3 promotes the antiviral innate immune response against vesicular stomatitis virus infection by stabilizing MAVS through TRIM21 · 2026 · DOI

  • Although it has been demonstrated that ECs can be infected by respiratory viruses and that hypoxia can affect their function, the impact of hypoxia on the antiviral capabilities of the endothelium remains poorly understood.

    Different Effects of Acute and Chronic Hypoxia on Antiviral Capacity of Pulmonary Vascular Endothelial Cells · 2026 · DOI

  • However, the viral sensing pathways that regulate induction of IFN-λ, as well as the specific activity of IFN-λ in viral control and regulation of cellular tropism, remain to be defined for muAstV.

    MDA5-MAVS and interferon-lambda signaling in the intestinal epithelium limit murine astrovirus infection · 2025 · DOI

  • Although CQ exhibits broad-spectrum antiviral activity, its effect on host innate immune responses remains incompletely understood.

    Chloroquine Enhances Mitochondrial Antiviral Signaling-Mediated Cytokine Induction and Alters Mitochondrial Morphology · 2025 · DOI

  • Intestinal epithelial cell (IEC) responses to interferon (IFN) favor antiviral defense with minimal cytotoxicity, but IEC-specific factors that regulate these responses remain poorly understood.

    Interferon regulatory factor 6 (IRF6) determines intestinal epithelial cell development and immunity · 2024 · DOI

  • Despite this growing interest, the functional role of TRIM21 during viral infection remains incompletely understood, with seemingly conflicting findings describing it as either antiviral or proviral63.

    TRIM21 is a molecular rheostat for influenza A virus replication · 2026 · DOI

  • MSC-exo has emerged as a potent immunomodulatory agent in autoimmune conditions, including SLE; however, the underlying mechanisms remain incompletely elucidated.

    MSC-derived exosomes ameliorate systemic lupus erythematosus by reprogramming macrophage mitochondrial homeostasis via the CMPK2-cGAS-STING axis · 2026 · DOI

  • Moreover, we focused on the downstream consequences of STING activation, while the upstream mechanisms remain unexplored. While the STING/ZBP1 axis remains to be validated in human AKI samples, this study clarifies key pathogenic mechanisms in the tubular epithelium.

    STING-STAT1-ZBP1 axis orchestrates PANoptotic signaling in ischemia-reperfusion induced acute kidney injury · 2026 · DOI

  • Lack of specific clinical manifestations in the early stages of HCC. Need for optimization of early diagnostic systems for HCC and development of individualized treatment strategies.

    ​​Integrating machine learning and spatial transcriptomics uncovers shared immunomodulatory deubiquitinases in MAFLD and HCC · 2026 · DOI

  • Determine the relative contribution of AMPK inhibition to the overall antiviral phenotype - Establish direct causality between reduced AMPK activation and inhibition of viral replication using genetic or pharmacological rescue approaches - Determine whether AMPK suppression represents a general feature of TRIM69 antiviral activity or whether TRIM69 employs distinct mechanisms depending on the viral…

    TRIM69 Suppresses the Cellular AMPK Pathway to Inhibit Viral Replication · 2026 · DOI

  • The study was conducted in mice, - The study focused on a specific model antigen (HOD), - The study used a limited number of recipient mice, - The study did not investigate the mechanisms of TLR9-mediated alloimmunization…

    TLR9 is required in donor blood for inflammation-induced immunization to an alloantigen on transfused RBCs in mice · 2026 · DOI

  • Investigating the mechanisms of TLR9-mediated alloimmunization, - Studying the effects of TLR9 antagonists on RBC alloimmunization, - Examining the role of TLR9 in human RBC alloimmunization, - Investigating the potential of selecting RBC units from donors with known hypomorphic TLR9 gene…

    TLR9 is required in donor blood for inflammation-induced immunization to an alloantigen on transfused RBCs in mice · 2026 · DOI

  • Further study on the molecular mechanism of TRIM21 in regulating ferroptosis, - Investigation on how TRIM21 regulates the SQSTM1-NRF2-KEAP1 axis to regulate oxidative stress homeostasis, - Research on the role of TRIM21 in other virus…

    TRIM21 Promotes Oxidative Stress and Ferroptosis through the SQSTM1-NRF2-KEAP1 Axis to Increase the Titers of H5N1 Highly Pathogenic Avian Influenza Virus · 2024 · DOI

Most-cited papers in interferon and immune responses

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Open questions raised by papers listed on this page include: (1) The mechanisms of action of viral transcriptional regulators are not well understood (“Functional characterization of viral transcriptional regulators reveals…”, 2026); (2) The role of TRIM28 in DLBCL progression and glycolytic reprogramming is unclear (“TRIM28 facilitates diffuse large B-cell lymphoma progression by inducing…”, 2026); (3) The specific role of ISG20 against PEDV remains poorly understood (“Porcine ISG20 Restricts PEDV Replication Independent of Its Exonuclease…”, 2026); (4) How HHARI drives interferon signalling is not fully understood and the function of the unique, highly conserved acidic N-terminal domain of the protein is unknown (“The acidic N-terminus of HHARI and neddylation are essential for the activation…”, 2026); (5) While the cGAS-STING pathway is well characterized in detecting non-self-DNA, its response to self-DNA originating from the host nucleus remains unclear (“Uncoupling of STING Accumulation and Activation upon Chromosome-Derived…”, 2026). 771 gap statements have been mined from interferon and immune responses papers in our 7.9M-paper local library, which holds 3,146 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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