Changing the paradigm of IFN-γ at the interface between innate and adaptive immunity: Macrophage-derived IFN-γ

Mezouar, Soraya; Mège, Jean‐Louis

doi:10.1002/jlb.4mir0420-619rr

Cited by 37 publications

(25 citation statements)

References 59 publications

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“…PRR-sensing leads to signaling cascades that induce transcription factors that upregulate antiviral and pro-inflammatory cytokines [90,91]. The antiviral cytokines include type I (IFNα, IFNβ) and type III (IFNλ) interferons (IFNs), whereas type II (IFNγ) IFN promotes immune cell activation [92,93]. Early IFN expression induces IFN-stimulated genes (ISGs) which modify the immune response [94].…”

Section: Innate Responsesmentioning

confidence: 99%

Immunopathology of RSV: An Updated Review

Bergeron

Tripp

2021

Viruses

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RSV is a leading cause of respiratory tract disease in infants and the elderly. RSV has limited therapeutic interventions and no FDA-approved vaccine. Gaps in our understanding of virus–host interactions and immunity contribute to the lack of biological countermeasures. This review updates the current understanding of RSV immunity and immunopathology with a focus on interferon responses, animal modeling, and correlates of protection.

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Section: Innate Responsesmentioning

confidence: 99%

Immunopathology of RSV: An Updated Review

Bergeron

Tripp

2021

Viruses

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“…Isolated placental macrophages from healthy at-term placentas spontaneously produce low levels [61] and secrete high amounts of interferon (IFN)-γ during C. burnetii Nine Mile 1 infection, although the secretion of IFN-γ by macrophage populations is the subject of significant debate [70]. This inflammatory cytokine is involved in the clearance of intracellular pathogens and is implemented as treatment in response to infection by intracellular pathogens.…”

Section: Macrophagesmentioning

confidence: 99%

From Coxiella burnetii Infection to Pregnancy Complications: Key Role of the Immune Response of Placental Cells

2021

Self Cite

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The infection of pregnant animals and women by Coxiella burnetii, an intracellular bacterium, compromises both maternal health and foetal development. The placenta is targeted by C. burnetii, as demonstrated by bacteriological and histological evidence. It now appears that placental strains of C. burnetii are highly virulent compared to reference strains and that placental injury involves different types of placental cells. Trophoblasts, the major placental cells, are largely infected by C. burnetii and may represent a replicating niche for the bacteria. The placenta also contains numerous immune cells, including macrophages, dendritic cells, and mast cells. Placental macrophages are infected and activated by C. burnetii in an unusual way of M1 polarisation associated with bacterial elimination. Placental mast cells eliminate bacteria through a mechanism including the release of extracellular actin filaments and antimicrobial peptides. In contrast, C. burnetii impairs the maturation of decidual dendritic cells, favouring bacterial pathogenicity. Our aim is to review C. burnetii infections of human placentas, paying special attention to both the action and function of the different cell types, immune cells, and trophoblasts targeted by C. burnetii in relation to foetal injury.

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“…IFN-γ, as a main effector factor of group 1 innate lymphocytes, is proved to have the ability to inhibit the proliferation and angiogenesis of tumor cells, and that can also enhance the cytotoxic activity of CTL to promote the anti-tumor effect 11,12 . It is worth noting that IFN-γ can promote the induction of classically activated M1 phenotype macrophage, which can further promote the tumor-inhibiting effect 13,14 . But it remains unclear if group 1 innate lymphocytes could promote the M1 phenotype macrophage polarization in colon cancer.…”

Section: Introductionmentioning

confidence: 99%

Group 1 Innate Lymphocyte-Derived IFN-γ Regulates Macrophage Alternative Activation In Colon Cancer

Zhang

et al. 2021

Preprint

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Background: Tumor-associated macrophage (TAM) is an important innate immune cell-subset in tumor microenvironment, and that is also a pivotal orchestrator of tumor-promoting inflammation and tumor progression. Evidence proved that TAMs are up-regulated in a great number of cancers, and most of them are alternative activated M2 phenotype, which greatly promote the progress of cancer diseases. Group 1 innate lymphocytes including conventional NK cells and type 1 innate lymphocytes (ILC1s), are abundant in intestinal tissue, and characterized by expressing transcription factor T-bet and secreting interferon (IFN)-γ, which can promote the macrophage to classically activated anti-tumor M1 phenotype. However, the relationship between these two cell subsets remains unclear in colon cancer. Methods: Flow cytometry was used to detect the percentage of M1 phenotype macrophage, M2 phenotype macrophage and group 1 innate lymphocytes in colon cancer tissue and paracancer healthy colon tissue of AOM/DSS-induced colon cancer mice model. In vitro isolating group 1 innate lymphocytes and inducing bone marrow-derived macrophage to detect the cross-talk when co-cultured. Adoptively transfer or blocking group 1 innate lymphocytes in vivo to investigate the role of group 1 innate lymphocytes on tumor-infiltrating macrophage and the tumor growth. Results: We found that M1 phenotype macrophage and group 1 innate lymphocytes were down-regulated in colon cancer tissue, and they were positively correlated. Group 1 innate lymphocytes promoted macrophage to classically activated M1 phenotype in vitro, and that could be blocked by anti-IFN-γ. In vivo results showed that the administration of group 1 innate lymphocytes-blocking antibody anti-NK1.1 could decrease the number of M1 phenotype macrophage in tumor tissue of MC38 tumor-bearing mice and promote the tumor growth, while adoptively transferring group 1 innate lymphocytes led to tumor-inhibiting and level of M1 phenotype macrophage up-regulating in MC38 tumor-bearing mice. Conclusions: Our studies preliminarily prove that group 1 innate lymphocytes promote the alternative activation of M1 macrophage by secreting IFN-γ to inhibit the progress of colon cancer for the first time, which may provide an insight in the immunotherapy of colon cancer.

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Changing the paradigm of IFN-γ at the interface between innate and adaptive immunity: Macrophage-derived IFN-γ

Cited by 37 publications

References 59 publications

Immunopathology of RSV: An Updated Review

Immunopathology of RSV: An Updated Review

From Coxiella burnetii Infection to Pregnancy Complications: Key Role of the Immune Response of Placental Cells

Group 1 Innate Lymphocyte-Derived IFN-γ Regulates Macrophage Alternative Activation In Colon Cancer

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