Autonomous TNF is critical for in vivo monocyte survival in steady state and inflammation

Wolf, Yochai; Shemer, Anat; Polonsky, Michal; Gross, Mor; Mildner, Alexander; Yona, Simon; David, Eyal; Kim, Ki Wook; Goldmann, Tobias; Amit, Ido; Heikenwälder, Mathias; Nedospasov, Sergei A.; Prinz, Marco; Friedman, Nir; Jung, Steffen

doi:10.1084/jem.20160499

Cited by 78 publications

(55 citation statements)

References 56 publications

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“…Recent work also revealed that other cytokines were essential for the survival, maintenance and function of the monocytes, like autonomous TNF‐α. The in vivo and in vitro competitive assays showed that TNF‐α or TNF‐α receptor deficiency caused the monocytes out competition by the WT counterparts (Wolf et al, ). The TNF‐α ablation in monocytes and macrophages, not including microglia, delayed the onset of experimental autoimmune encephalomyelitis (EAE), due to the reduced infiltration of Ly6C high monocytes (Wolf et al, ).…”

Section: The Roles Of Local Environment Signals and Transcription Facmentioning

confidence: 99%

“…The in vivo and in vitro competitive assays showed that TNF‐α or TNF‐α receptor deficiency caused the monocytes out competition by the WT counterparts (Wolf et al, ). The TNF‐α ablation in monocytes and macrophages, not including microglia, delayed the onset of experimental autoimmune encephalomyelitis (EAE), due to the reduced infiltration of Ly6C high monocytes (Wolf et al, ). Thus, autonomous TNF‐α plays a crucial role in the maintenance of monocyte homeostasis, recruitment and function in the inflammatory sites.…”

Section: The Roles Of Local Environment Signals and Transcription Facmentioning

confidence: 99%

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The origins and homeostasis of monocytes and tissue‐resident macrophages in physiological situation

Zhao

Zou

Du³

et al. 2018

Journal Cellular Physiology

133

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Monocytes and macrophages are critical effectors and regulators of innate immune response. They not only play crucial and distinctive roles in homeostasis, but also contribute to some pathologic processes. The heterogeneity of the macrophage lineage has been widely recognized and, in part, is a result of the specialization of resident macrophages in particular tissue microenvironments. Monocytes are usually known to originate in the bone marrow from a common myeloid progenitor that is shared with neutrophils, and they are then released into the peripheral blood. However, the origin of tissue-resident macrophages, crucial for homeostasis and immunity, has remained controversial until recently. During embryonic organogenesis, macrophages derived from yolk sac and fetal liver precursors are seeded throughout tissues, persisting in the adulthood as resident, self-maintaining populations. After birth, bone marrow-derived monocytes can replenish tissue resident macrophages following injury, infection and inflammation. In this review, we will mainly summarize our current understanding on the origin, ontogeny and fates of tissue macrophages and will briefly discuss the molecular regulation of resident macrophage homeostasis in physiological situation.

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Section: The Roles Of Local Environment Signals and Transcription Facmentioning

confidence: 99%

Section: The Roles Of Local Environment Signals and Transcription Facmentioning

confidence: 99%

The origins and homeostasis of monocytes and tissue‐resident macrophages in physiological situation

Zhao

Zou

Du³

et al. 2018

Journal Cellular Physiology

133

View full text Add to dashboard Cite

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“…TNF-deficient mice showed reduced EAE during the early stage but exacerbated disease during the chronic stage due to prolonged retention of T cells in the secondary lymphoid organs [51]. TNF-α ablation in monocytes/macrophages delayed the onset of EAE in challenged animals [52]. An interesting evidence by studies with humanized mice indicates that the soluble TNF-α signaling provided a protective effect on EAE induction through TNFR2 on the CD4 + FOXP3 + cells in the spleen, but not T cells in the CNS [53].…”

Section: Discussionmentioning

confidence: 99%

Independent and inter-dependent immunoregulatory effects of NCF1 and NOS2 in experimental autoimmune encephalomyelitis

Zhong

Yau

Holmdahl

2020

J Neuroinflammation

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Background: Increasing evidence has suggested that a single nucleotide polymorphism in the Ncf1 gene is associated with experimental autoimmune encephalomyelitis (EAE). However, the mechanisms of NCF1-induced immunoregulatory effects remain poorly understood. In this study, we focus on NCF1 deficiency-mediated effects on EAE in NOS2 dependent and independent ways. Methods: To determine the effects of NCF1 and NOS2 during EAE development, we have established recombinant mouse strains deficient at NCF1 and/or NOS2 in a crossbreeding system. Different strains allow us to examine the entire course of the disease in the Nos2-null mice bearing a Ncf1 gene that encodes a mutated NCF1, deficient in triggering oxidative burst, after immunization with recombinant myelin oligodendrocyte glycoprotein (MOG) 79-96 peptides. The peptide-induced innate and adaptive immune responses were analyzed by flow cytometry.Results: NCF1-deficient mice developed a reduced susceptibility to EAE, whereas NCF1-NOS2 double-deficient mice developed an enhanced EAE, as compared with NOS2-deficient mice. Flow cytometry analyses show that double deficiencies resulted in an increase of neutrophils in the spleen, accompanied with higher release of interleukin-1β in neutrophils prior to EAE onset. The additional deficiency in NCF1 had no added effect on either interleukin-17 or interferon-γ secretion of T cells during the priming phase.Conclusions: These studies show that NCF1 and NOS2 interact to regulate peptide-induced EAE.

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“…33 In addition, TNF likely also represents a cell-autonomous signal for the survival and maintenance of monocytederived macrophages in the tissue. 35 Cytokine release is a direct response of pattern-recognition receptor (PRR) or cytokine receptor activation and the subsequent c-Jun N-terminal kinase (JNK) and NF-κB dependent upregulation of inflammatory gene expression as well as NOD-, LRR-, and pyrin domain-containing 3 (NLRP3) inflammasome formation. 36 Most macrophages express multiple PRRs, of which TLRs are by far the best characterized.…”

Section: Inflammationmentioning

confidence: 99%

Macrophages in Nonalcoholic Fatty Liver Disease: A Role Model of Pathogenic Immunometabolism

Krenkel

Tacke

2017

Semin Liver Dis

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Nonalcoholic fatty liver disease (NAFLD) and its progressive inflammatory form, nonalcoholic steatohepatitis (NASH), are leading causes of liver cirrhosis and hepatocellular carcinoma. Metabolism and inflammation are intimately interrelated in NAFLD/NASH, as expressed by the term immunometabolism. Hepatic macrophages mediate inflammatory responses during metabolic disorders and can stimulate or dismantle liver fibrosis. Their functional diversity is partly explained by heterogeneous macrophage subsets: tissue-resident Kupffer cells and monocyte-derived macrophages. However, macrophages themselves are altered in their functional polarization by dietary composition and metabolic or inflammatory stimuli in NAFLD. The inflammatory polarization of macrophages correlates with changes in core metabolism pathways like oxidative phosphorylation and glycolysis. The availability of nutrients, such as glucose or fatty acids or oxygen also influences macrophage polarization upon danger signal or cytokine reception. Understanding the interplay of metabolism and macrophage function in NASH may open new approaches to therapeutic targeting of these essential modifiers in metabolic liver diseases.

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Autonomous TNF is critical for in vivo monocyte survival in steady state and inflammation

Cited by 78 publications

References 56 publications

The origins and homeostasis of monocytes and tissue‐resident macrophages in physiological situation

The origins and homeostasis of monocytes and tissue‐resident macrophages in physiological situation

Independent and inter-dependent immunoregulatory effects of NCF1 and NOS2 in experimental autoimmune encephalomyelitis

Macrophages in Nonalcoholic Fatty Liver Disease: A Role Model of Pathogenic Immunometabolism

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