IL-37 (IL-1F7) the Newest Anti-Inflammatory Cytokine Which Suppresses Immune Responses and Inflammation

2012 ◽  
Vol 25 (1) ◽  
pp. 31-38 ◽  
Author(s):  
S. Tetè ◽  
D. Tripodi ◽  
M. Rosati ◽  
F. Conti ◽  
G. Maccauro ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Immune Responses ◽  
Proinflammatory Cytokines ◽  
Mechanism Of Action ◽  
Inflammatory Cytokine ◽  
Inflammatory Responses ◽  
Detailed Mechanism ◽  
Anti Inflammatory ◽  
And Function ◽  
Anti Inflammatory Cytokine

Cytokines such as interleukins, chemokines and interferons are immunomodulating and inflammatory agents, characterized by considerable redundancy, in that many cytokines appear to share similar functions. Virtually all nucleated cells, but especially epithelial cells and macrophages, are potent producers of cytokines. The objective of this study is to review the detailed mechanism of action and the biological profiles of IL-37, the newest anti-inflammatory cytokine. This review focuses on IL-37, a key cytokine in regulating inflammatory responses, mainly by inhibiting the expression, production and function of proinflammatory cytokines: IL-1 family pro-inflammatory effects are markedly suppressed by IL-37.

scholarly journals Type I and III IFNs produced by the nasal epithelia and dimmed inflammation are key features of alpacas resolving MERS-CoV infection

2020 ◽  
Author(s):  
Nigeer Te ◽  
Jordi Rodon ◽  
Maria Ballester ◽  
Mónica Pérez ◽  
Lola Pailler-García ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Nasal Mucosa ◽  
Inflammatory Cytokine ◽  
Innate Immune ◽  
Type I ◽  
Innate Immune Responses ◽  
Interferon Stimulated Genes ◽  
Anti Inflammatory ◽  
Anti Inflammatory Cytokine

ABSTRACTWhile MERS-CoV (Middle East respiratory syndrome Coronavirus) provokes a lethal disease in humans, camelids, the main virus reservoir, are asymptomatic carriers, suggesting a crucial role for innate immune responses in controlling the infection. Experimentally infected camelids clear infectious virus within one week and mount an effective adaptive immune response. Here, transcription of immune response genes was monitored in the respiratory tract of MERS-CoV infected alpacas. Concomitant to the peak of infection, occurring at 2 days post inoculation (dpi), type I and III interferons (IFNs) were maximally transcribed only in the nasal mucosa of alpacas, provoking the induction of interferon stimulated genes (ISGs) along the whole respiratory tract. Simultaneous to mild focal infiltration of leukocytes in nasal mucosa and submucosa, upregulation of the anti-inflammatory cytokine IL10 and dampened transcription of pro-inflammatory genes under NF-κB control were observed. In the lung, early (1 dpi) transcription of chemokines (CCL2 and CCL3) correlated with a transient accumulation of mainly mononuclear leukocytes. A tight regulation of IFNs in lungs with expression of ISGs and controlled inflammatory responses, might contribute to virus clearance without causing tissue damage. Thus, the nasal mucosa, the main target of MERS-CoV in camelids, is central in driving an efficient innate immune response based on triggering ISGs as well as the dual anti-inflammatory effects of type III IFNs and IL10.IMPORTANCEMiddle East respiratory syndrome coronavirus (MERS-CoV) is the etiological agent of a respiratory disease causing high mortality in humans. In camelids, the main MERS-CoV reservoir host, viral infection leads to subclinical disease. Our study describes transcriptional regulations of innate immunological pathways underlying asymptomatic clinical manifestations of alpacas in response to MERS-CoV. Concomitant to the peak of infection, these animals elicited a strong transient interferon response and induction of the anti-inflammatory cytokine IL10 in the nasal mucosa. This was associated to a dimmed regulation of pro-inflammatory cytokines and induction of interferon stimulated genes along the whole respiratory mucosa, leading to the rapid clearance of the virus. Thus, innate immune responses occurring in the nasal mucosa appear to be the key in controlling MERS-CoV disease by avoiding a cytokine storm. Understanding on how asymptomatic host reservoirs counteract MERS-CoV infection will aid in the development of antiviral drugs and vaccines.

scholarly journals Type I and III IFNs produced by the nasal epithelia and dimmed inflammation are key features of alpacas resolving MERS-CoV infection

2020 ◽  
Author(s):  
Nigeer Te ◽  
Jordi Rodon ◽  
Maria Ballester ◽  
Mónica Pérez ◽  
Lola Pailler-García ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Responses ◽  
Nasal Mucosa ◽  
Inflammatory Cytokine ◽  
Innate Immune ◽  
Type I ◽  
Innate Immune Responses ◽  
Interferon Stimulated Genes ◽  
Anti Inflammatory ◽  
Anti Inflammatory Cytokine

AbstractWhile MERS-CoV (Middle East respiratory syndrome Coronavirus) provokes a lethal disease in humans, camelids, the main virus reservoir, are asymptomatic carriers, suggesting a crucial role for innate immune responses in controlling the infection. Experimentally infected camelids clear infectious virus within one week and mount an effective adaptive immune response. Here, transcription of immune response genes was monitored in the respiratory tract of MERS-CoV infected alpacas. Concomitant to the peak of infection, occurring at 2 days post inoculation (dpi), type I and III interferons (IFNs) were maximally transcribed only in the nasal mucosa of alpacas, provoking the induction of interferon stimulated genes (ISGs) along the whole respiratory tract. Simultaneous to mild focal infiltration of leukocytes in nasal mucosa and submucosa, upregulation of the anti-inflammatory cytokine IL10 and dampened transcription of pro-inflammatory genes under NF-κB control were observed. In the lung, early (1 dpi) transcription of chemokines (CCL2 and CCL3) correlated with a transient accumulation of mainly mononuclear leukocytes. A tight regulation of IFNs in lungs with expression of ISGs and controlled inflammatory responses, might contribute to virus clearance without causing tissue damage. Thus, the nasal mucosa, the main target of MERS-CoV in camelids, is central in driving an efficient innate immune response based on triggering ISGs as well as the dual anti-inflammatory effects of type III IFNs and IL10.Author summaryMiddle East respiratory syndrome coronavirus (MERS-CoV) is the etiological agent of a respiratory disease causing high mortality in humans. In camelids, the main MERS-CoV reservoir host, viral infection leads to subclinical disease. Our study describes transcriptional regulations of innate immunological pathways underlying asymptomatic clinical manifestations of alpacas in response to MERS-CoV. Concomitant to the peak of infection, these animals elicited a strong transient interferon response and induction of the anti-inflammatory cytokine IL10 in the nasal mucosa. This was associated to a dimmed regulation of pro-inflammatory cytokines and induction of interferon stimulated genes along the whole respiratory mucosa, leading to the rapid clearance of the virus. Thus, innate immune responses occurring in the nasal mucosa appear to be the key in controlling MERS-CoV disease by avoiding a cytokine storm. Understanding on how asymptomatic host reservoirs counteract MERS-CoV infection will aid in the development of antiviral drugs and vaccines.

scholarly journals Prototypical anti-inflammatory cytokine IL-10 prevents loss of IGF-I-induced myogenin protein expression caused by IL-1β

2008 ◽  
Vol 294 (4) ◽  
pp. E709-E718 ◽  
Author(s):  
Klemen Strle ◽  
Robert H. McCusker ◽  
Rodney W. Johnson ◽  
Samantha M. Zunich ◽  
Robert Dantzer ◽  
...  
Keyword(s):  
Inflammatory Cytokine ◽  
Muscle Wasting ◽  
Inflammatory Responses ◽  
Mapk Signaling ◽  
Protective Role ◽  
Igf I ◽  
Anti Inflammatory ◽  
Kinase Pathway ◽  
Anti Inflammatory Cytokine

Prolonged and excessive inflammation is implicated in resistance to the biological actions of IGF-I and contributes to the pathophysiology of neurodegenerative, metabolic, and muscle-wasting disorders. IL-10 is a critical anti-inflammatory cytokine that restrains inflammatory responses in macrophages and T cells by inhibiting cytokine and chemokine synthesis and reducing expression of their receptors. Here we demonstrate that IL-10 plays a protective role in nonhematopoietic cells by suppressing the ability of exogenous IL-1β to inhibit IGF-I-induced myogenin and myosin heavy chain expression in myoblasts. This action of IL-10 is not caused by impairment of IL-1β-induced synthesis of IL-6 or the ability of IL-1β to activate two members of the MAPK family, ERK1/2 and p38. Instead, this newly defined protective role of IL-10 occurs by specific reversal of IL-1β activation of the JNK kinase pathway. IL-10 blocks IL-1β-induced phosphorylation of JNK, but not ERK1/2 or p38, indicating that only the JNK component of the IL-1β-induced MAPK signaling pathway is targeted by IL-10. This conclusion is supported by the finding that a specific JNK inhibitor acts similarly to IL-10 to restore IGF-I-induced myogenin expression, which is suppressed by IL-1β. Collectively, these data demonstrate that IL-10 acts in a novel, nonclassical, protective manner in nonhematopoietic cells to inhibit the IL-1β receptor-induced JNK kinase pathway, resulting in prevention of IGF-I resistance.

scholarly journals Functionally distinct subsets of human FOXP3+ Treg cells that phenotypically mirror effector Th cells

Blood ◽  
2012 ◽  
Vol 119 (19) ◽  
pp. 4430-4440 ◽  
Author(s):  
Thomas Duhen ◽  
Rebekka Duhen ◽  
Antonio Lanzavecchia ◽  
Federica Sallusto ◽  
Daniel J. Campbell
Keyword(s):  
Inflammatory Cytokine ◽  
Cytokine Production ◽  
Inflammatory Responses ◽  
Treg Cells ◽  
Receptor Expression ◽  
Inflammatory Cytokine Production ◽  
Th Cell ◽  
Different Types ◽  
Anti Inflammatory ◽  
Anti Inflammatory Cytokine

Abstract FOXP3+ regulatory T (Treg) cells are a broadly acting and potent anti-inflammatory population of CD4+ T cells essential for maintaining immune homeostasis and preventing debilitating autoimmunity. Based on chemokine receptor expression, we identified distinct populations of Treg cells in human blood expected to colocalize with different Th cell subsets. Although each population was functionally suppressive, they displayed unique patterns of pro- and anti-inflammatory cytokine production, differentially expressed lineage-specifying transcription factors, and responded differently to antigens associated with Th1 and Th17 responses. These results highlight a previously unappreciated degree of phenotypic and functional diversity in human Treg cells that allows subsets with unique specificities and immunomodulatory functions to be targeted to defined immune environments during different types of inflammatory responses.

scholarly journals The Strand Specific Regulation of miR-155-3p in Response to Lipopolysaccharide and Interleukin-10 Stimulation Requires FUBP1 Protein

2021 ◽  
Author(s):  
Jeff S. J. Yoon ◽  
Abdulwadood Baksh ◽  
Thomas C. Chamberlain ◽  
Alice L-F. Mui
Keyword(s):  
Inflammatory Cytokine ◽  
Inflammatory Responses ◽  
Interleukin 10 ◽  
Activated Macrophages ◽  
Anti Inflammatory ◽  
Specific Regulation ◽  
Anti Inflammatory Cytokine

MicroRNA-155 (miR-155) expression promotes inflammatory responses in macrophages. Activation of macrophages with lipopolysaccharide (LPS) elevates miR-155, while the anti-inflammatory cytokine interleukin-10 (IL10) reduces miR-155 levels. MiR-155 exists in two forms, miR-155-5p and miR-155-3p, produced from the precursor of miR-155 (pre-miR-155). MiR-155-5p is the most abundant strand in activated macrophages, but in response to LPS, the miR-155-3p level is upregulated first, followed by miR-155-5p later. We have previously identified CELF2 protein which interacts with pre-miR-155 and impairs miR-155-5p expression. We now show that CELF2 only regulates the miR-155-5p expression and that another protein FUBP1 controls miR-155-3p levels in response to LPS and IL10.

scholarly journals Immunoregulatory effects of Imuno TF® (transfer factors) on Th1/Th2/Th17/Treg cytokines

2020 ◽  
Author(s):  
Carlos Rocha Oliveira ◽  
Rodolfo Paula Vieira ◽  
Anderson de Oliveira Ferreira ◽  
Any Elisa de Souza Schmidt Gonçalves ◽  
Hudson Polonini
Keyword(s):  
Immune Responses ◽  
Inflammatory Cytokines ◽  
Inflammatory Cytokine ◽  
Mrna Levels ◽  
Th2 Cytokines ◽  
Transfer Factors ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Th1 Cytokines ◽  
Anti Inflammatory Cytokine

AbstractTransfer factors are known since 1955 due to their activities on the immune system. Although the reports on the effects on diverse immune mechanisms, their role on Th1, Th2, Th17 and Treg responses was still not described. In this sense, the present work focused on the evaluation of such immune responses. For that, human lymphocytes, and mice thymic, splenic and Peyer’s cells were stimulated with Lipopolysaccharides and Concanavalin A, and then treated with isolated transfer factors (Imuno TF®). The culture medium was harvested and the quantification of Th1 cytokines (IL-2 and IFN-γ), Th2 cytokines (IL-4, IL-5, and IL-13), Th17 cytokine (IL- 17), Treg cytokine (IL-35), inflammatory cytokines (IL-6 and TNF-α), and anti-inflammatory cytokine (IL-10) was performed, as well as the quantification of mRNA levels. Imuno TF® positively regulated Th1 cytokines, while decreased Th2 cytokines. It also increased levels of mRNA and secretion of the anti-inflammatory cytokine IL-10, whereas it reduced levels of mRNA and the secretion of pro-inflammatory cytokines IL-6 and TNF-α. Finally, it reversed the hypersecretion of IL-17 and did not promote significant changes in IL-35 secretion. This highlights the role of Imuno TF® in the regulation of the immune responses.

scholarly journals Cytokines Genotype-Phenotype Correlation in Nonalcoholic Steatohepatitis

2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Ioana Corina Bocsan ◽  
Mircea Vasile Milaciu ◽  
Raluca Maria Pop ◽  
Stefan Cristian Vesa ◽  
Lorena Ciumarnean ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Proinflammatory Cytokines ◽  
Negative Correlation ◽  
Inflammatory Cytokine ◽  
Phenotype Correlation ◽  
Pcr Rflp ◽  
Plasmatic Level ◽  
Anti Inflammatory ◽  
High Level ◽  
Anti Inflammatory Cytokine

NASH consists in lipid accumulation in hepatocytes that trigger oxidative stress, secretion of proinflammatory cytokines leading to steatohepatitis (NASH). The study aimed to investigate the levels of proinflammatory (TNF-αand IL-6) along with anti-inflammatory cytokine IL-10 in patients with NASH and to correlate the cytokines’ level with their polymorphism. Sixty-six patients with NASH and 30 healthy volunteers were included in the study. The plasmatic level of IL-6, IL-10, and TNF-αwere determined by ELISA. IL-10 -1082 G/A, IL-6 -174 G/C, and TNF-α-308 G/A polymorphisms were determined using the PCR-RFLP technique. IL-6, TNF-α, and CRP levels were significantly higher in patients with NASH. There was a positive correlation between proinflammatory cytokines and a negative correlation between IL-10 and proinflammatory markers. The G allele and GG genotype of IL-6 -174 G/C polymorphism were more frequently noticed in NASH patients. Regarding IL-10 -1082 G/A polymorphism, the AA genotype was correlated with NASH and with a low plasmatic level of IL-10. The A allele in position 308 of the TNF-αgene was associated with high level of cytokine. In conclusion, there was an imbalance between pro- and anti-inflammatory cytokines in NASH patients. IL-10 -1082 G/A and TNF-α-308 G/A genotypes were correlated with the plasmatic levels of cytokines.

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