Interleukin-19 as an Immunoregulatory Cytokine

2020 ◽  
Vol 14 (2) ◽  
pp. 191-199
Author(s):  
Yasuyuki Fujimoto ◽  
Nobuyuki Kuramoto ◽  
Masanori Yoneyama ◽  
Yasu-Taka Azuma
Keyword(s):  
T Cells ◽  
Inflammatory Cytokine ◽  
The Other ◽  
Acquired Immunity ◽  
Current Role ◽  
Immunoregulatory Cytokine ◽  
Anti Inflammatory ◽  
Anti Inflammatory Cytokine ◽  
Inflammatory Effect

IL-19 is a type of anti-inflammatory cytokine. Since the receptor for IL-19 is common to IL-20 and IL-24, it is important to clarify the role of each of the three cytokines. If three different cytokines bind to the same receptor, these three may have been produced to complement the other two. However, perhaps it is unlikely. Recently, the existence of a novel receptor for IL-19 was suggested. The distinction between the roles of the three cytokines still makes sense. On the other hand, because T cells do not produce IL-19, their role in acquired immunity is limited or indirect. It has been reported that IL-19 causes inflammation in some diseases but does not have an anti-inflammatory effect. In this review, we introduce the current role of IL-19 in each disease. In addition, we will describe the molecular mechanism of IL-19 and its development for the prevention of diseases. IL-19 was previously considered an anti-inflammatory cytokine, but we would like to propose it as an immunoregulatory cytokine.

scholarly journals Elevated vasopressin in pregnant mice induces T-helper subset alterations consistent with human preeclampsia

2018 ◽  
Vol 132 (3) ◽  
pp. 419-436 ◽  
Author(s):  
Sabrina M. Scroggins ◽  
Donna A. Santillan ◽  
Jenna M. Lund ◽  
Jeremy A. Sandgren ◽  
Lindsay K. Krotz ◽  
...  
Keyword(s):  
T Cells ◽  
Cd4 T Cells ◽  
Inflammatory Cytokine ◽  
Maternal Plasma ◽  
Hypertensive Disorder ◽  
Wild Type ◽  
T Helper ◽  
Anti Inflammatory ◽  
Immune Changes ◽  
Anti Inflammatory Cytokine

The pathogenesis of preeclampsia (PreE), a hypertensive disorder of pregnancy, involves imbalanced T helper (TH) cell populations and resultant changes in pro- and anti-inflammatory cytokine release. Elevated copeptin (an inert biomarker of arginine vasopressin (AVP)), secretion precedes the development of symptoms in PreE in humans, and infusion of AVP proximal to and throughout gestation is sufficient to initiate cardiovascular and renal phenotypes of PreE in wild-type C57BL/6J mice. We hypothesize that AVP infusion in wild-type mice is sufficient to induce the immune changes observed in human PreE. AVP infusion throughout gestation in mice resulted in increased pro-inflammatory interferon γ (IFNg) (TH1) in the maternal plasma. The TH17-associated cytokine interleukin (IL)-17 was elevated in the maternal plasma, amniotic fluid, and placenta following AVP infusion. Conversely, the TH2-associated anti-inflammatory cytokine IL-4 was decreased in the maternal and fetal kidneys from AVP-infused dams, while IL-10 was decreased in the maternal kidney and all fetal tissues. Collectively, these results demonstrate the sufficiency of AVP to induce the immune changes typical of PreE. We investigated if T cells can respond directly to AVP by evaluating the expression of AVP receptors (AVPRs) on mouse and human CD4+ T cells. Mouse and human T cells expressed AVPR1a, AVPR1b, and AVPR2. The expression of AVPR1a was decreased in CD4+ T cells obtained from PreE-affected women. In total, our data are consistent with a potential initiating role for AVP in the immune dysfunction typical of PreE and identifies putative signaling mechanism(s) for future investigation.

scholarly journals Role of Interleukin-10 in Malaria: Focusing on Coinfection with Lethal and Nonlethal Murine Malaria Parasites

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Mamoru Niikura ◽  
Shin-Ichi Inoue ◽  
Fumie Kobayashi
Keyword(s):  
Innate Immunity ◽  
T Cells ◽  
Immune Responses ◽  
Malaria Infection ◽  
Inflammatory Cytokine ◽  
Interleukin 10 ◽  
Malaria Parasites ◽  
Severe Pathology ◽  
Anti Inflammatory Cytokine

Interleukin- (IL-) 10, anti-inflammatory cytokine, is known to inhibit the protective immune responses against malaria parasites and to be involved in exacerbating parasitemia duringPlasmodiuminfection. In contrast, IL-10 is regarded as necessary for suppressing severe pathology duringPlasmodiuminfection. Here, we summarize the role of IL-10 during murine malaria infection, focusing especially on coinfection with lethal and nonlethal strains of malaria parasites. Recent studies have demonstrated that the major sources of IL-10 are subpopulations of CD4+T cells in humans and mice infected withPlasmodium. We also discuss the influence of innate immunity on the induction of CD4+T cells during murine malaria coinfection.

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 IFN-τDisplays Anti-Inflammatory Effects onStaphylococcus aureusEndometritis via Inhibiting the Activation of the NF-κB and MAPK Pathways in Mice

2017 ◽  
Vol 2017 ◽  
pp. 1-12
Author(s):  
Zhenbiao Zhang ◽  
Yingfang Guo ◽  
Yuzhu Liu ◽  
Chengye Li ◽  
Mengyao Guo ◽  
...  
Keyword(s):  
Mouse Model ◽  
Protective Effect ◽  
Inflammatory Cytokine ◽  
Inflammatory Diseases ◽  
Potential Drug ◽  
Histopathological Changes ◽  
Uterine Infection ◽  
Anti Inflammatory ◽  
Anti Inflammatory Cytokine ◽  
Inflammatory Effect

The aim of the present study was to determine the anti-inflammatory effect of IFN-τon endometritis using a mouse model ofS. aureus-induced endometritis and to elucidate the mechanism of action underlying these effects. In the present study, the effect of IFN-τonS. aureusgrowth was monitored by turbidimeter at 600 nm. IFN-τdid not affectS. aureusgrowth. The histopathological changes indicated that IFN-τhad a protective effect on uterus tissues withS. aureusinfection. The ELISA and qPCR results showed the production of the proinflammatory cytokines TNF-α, IL-1β, and IL-6 was decreased with IFN-τtreatment. In contrast, the level of the anti-inflammatory cytokine IL-10 was increased. We further studied the signaling pathway associated with these observations, and the qPCR results showed that the expression of TLR2 was repressed by IFN-τ. Furthermore, the western blotting results showed the phosphorylation of IκB, NF-κB p65, and MAPKs (p38, JNK, and ERK) was inhibited by IFN-τtreatment. The results suggested that IFN-τmay be a potential drug for the treatment of uterine infection due toS. aureusor other infectious inflammatory diseases.

T cells producing the anti-inflammatory cytokine IL-10 regulate allergen-specific Th2 responses in human airways

Allergy ◽  
2012 ◽  
Vol 67 (8) ◽  
pp. 1007-1013 ◽  
Author(s):  
A. Faith ◽  
N. Singh ◽  
S. Farooque ◽  
S. Dimeloe ◽  
D. F. Richards ◽  
...  
Keyword(s):  
T Cells ◽  
Inflammatory Cytokine ◽  
Th2 Responses ◽  
Anti Inflammatory ◽  
Human Airways ◽  
Anti Inflammatory Cytokine

Genetic susceptibility to Graves’ ophthalmopathy: The role of polymorphisms in anti-inflammatory cytokine genes

2010 ◽  
Vol 31 (4) ◽  
pp. 215-220 ◽  
Author(s):  
Omid Khalilzadeh ◽  
Mehdi Anvari ◽  
Alireza Esteghamati ◽  
Fatemeh Momen-Heravi ◽  
Armin Rashidi ◽  
...  
Keyword(s):  
Genetic Susceptibility ◽  
Inflammatory Cytokine ◽  
Cytokine Genes ◽  
Graves Ophthalmopathy ◽  
Anti Inflammatory ◽  
Anti Inflammatory Cytokine
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