ArticleArthritis & rheumatology (Hoboken, N.J.)2020
Genetic Deficiency of Interferon-γ Reveals Interferon-γ-Independent Manifestations of Murine Hemophagocytic Lymphohistiocytosis.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed.
- Monocyte/macrophages may exert prominent roles in macrophage activation syndrome.Annals of hematology · 2025Article
- The Microbiome Modifies Manifestations of Hemophagocytic Lymphohistiocytosis in Perforin-Deficient Mice.European journal of immunology · 2025Article
- Hemophagocytic lymphohistiocytosis: current treatment advances, emerging targeted therapy and underlying mechanisms.Journal of hematology & oncology · 2024Review
- Early hematopoietic cell transplantation for familial hemophagocytic lymphohistiocytosis in a regional treatment network in Japan.International journal of hematology · 2024Article
- Combined emapalumab and ruxolitinib in patients with haemophagocytic Lymphohistiocytosis.Blood cancer journal · 2024Article
- Hemophagocytic lymphohistiocytosis during treatment of intracranial multifocal germinoma: a case report and literature review.Frontiers in oncology · 2024Article
- Complementary HLH susceptibility factors converge on CD8 T-cell hyperactivation.Blood advances · 2023Article
- CXCL9 inhibition does not ameliorate disease in murine models of both primary and secondary hemophagocytic lymphohistiocytosis.Scientific reports · 2023Article
- Immune Mechanisms in Inflammatory Anemia.Annual review of immunology · 2023Review
- Cellular and transcriptional impacts of Janus kinase and/or IFN-gamma inhibition in a mouse model of primary hemophagocytic lymphohistiocytosis.Frontiers in immunology · 2023Article
- The Role of the IL-33/ST2 Axis in CpG-Induced Macrophage Activation Syndrome.Journal of immunology research · 2023Article
- IL-33 and the Cytokine Storm in COVID-19: From a Potential Immunological Relationship towards Precision Medicine.International journal of molecular sciences · 2022Review
- Excessive IL-10 and IL-18 trigger hemophagocytic lymphohistiocytosis-like hyperinflammation and enhanced myelopoiesis.The Journal of allergy and clinical immunology · 2022Article
- Misdiagnosis of adult primary hemophagocytic lymphohistiocytosis as NK/T-cell lymphoma: A case report.EJHaem · 2022Article
- Familial hemophagocytic lymphohistiocytosis hepatitis is mediated by IFN-γ in a predominantly hepatic-intrinsic manner.PloS one · 2022Article
- Targeting interferon-γ in hyperinflammation: opportunities and challenges.Nature reviews. Rheumatology · 2021Review
- Cleavage of DNA and RNA by PLD3 and PLD4 limits autoinflammatory triggering by multiple sensors.Nature communications · 2021Article
- Immune cartography of macrophage activation syndrome in the COVID-19 era.Nature reviews. Rheumatology · 2021Review
- Neuroinflammation Associated With Inborn Errors of Immunity.Frontiers in immunology · 2021Review
- Analysis of cytokine risk factors in the early death of patients with secondary phagocytic lymphocytic histiocytosis.American journal of translational research · 2021Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
objectiveFamilial hemophagocytic lymphohistiocytosis (FHLH) is a complex cytokine storm syndrome caused by genetic abnormalities rendering CD8+ T cells and natural killer cells incapable of cytolytic killing. In murine models of FHLH, interferon-γ (IFNγ) produced by CD8+ T cells has been identified as a critical mediator of disease, and an IFNγ-blocking antibody (emapalumab) has recently been approved by the Food and Drug Administration. However, development of hemophagocytic lymphohistiocytosis (HLH)/macrophage activation syndrome (MAS) in patients who are genetically unresponsive to IFNγ questions the absolute necessity of IFNγ in driving disease. This study was undertaken to determine the necessity of IFNγ in driving HLH.
methodsIFNγ
resultsLCMV infection of IFNγ
conclusionIFNγ is not necessary for the development of fulminant HLH, requiring physicians to consider case-by-case treatment strategies. Use of therapies that target upstream activators of CD8+ T cells, such as IL-33/ST2 signaling, may be more universally applicable treatment options that ameliorate both IFNγ-dependent and -independent manifestations of HLH/MAS.
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Registered trials
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