scholarly journals A Mineralocorticoid Receptor Deficiency in Myeloid Cells Reduces Liver Steatosis by Impairing Activation of CD8+ T Cells in a Nonalcoholic Steatohepatitis Mouse Model

2020 ◽  
Vol 11 ◽  
Author(s):  
Natalia Muñoz-Durango ◽  
Marco Arrese ◽  
Alejandra Hernández ◽  
Evelyn Jara ◽  
Alexis M. Kalergis ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Mineralocorticoid Receptor ◽  
Liver Steatosis ◽  
Costimulatory Molecule ◽  
Flow Cytometric Analysis ◽  
Myeloid Cells ◽  
Chow Diet ◽  
Mrna Levels ◽  
Deficient Diet

Background and AimsThe mineralocorticoid receptor (MR) and renin-angiotensin-aldosterone system (RAAS) are implicated in non-alcoholic liver fatty disease (NALFD). However, inflammatory mechanisms linking MR and RAAS with disease pathology remain unclear. Here we aimed to evaluate the contribution of myeloid MR to the inflammatory response in an animal model of non-alcoholic steatohepatitis (NASH), induced with a methionine-choline deficient diet (MCD).MethodsMice with a conditional deficiency of MR in myeloid cells (MyMRKO) and their counterpart floxed control mice (FC) were fed for 18 days with MCD or chow diet, respectively. Serum levels of aminotransferases and aldosterone levels were measured and hepatic steatosis, inflammation and fibrosis scored histologically. Hepatic triglyceride content (HTC) and hepatic mRNA levels of pro-inflammatory pro-fibrotic-associated genes were also assessed. Deep flow cytometric analysis was used to dissect the immune response during NASH development.ResultsMyMRKO mice fed with an MCD diet exhibited reduced hepatic inflammation and lower HTC than controls. Absolute number and percentage of liver inflammatory infiltrate cells (except for CD8+ T lymphocytes) were similar in both MyMRKO and control mice fed with an MCD diet but expression of the costimulatory molecule CD86 by dendritic cells and the CD25 activation marker in CD8+ T cells were significantly reduced in MyMRKO.ConclusionsProinflammatory cells are functionally suppressed in the absence of MR. We hypothesized that loss of MR in myeloid cells reduces lipid accumulation in the liver, in part through modulating the adaptive immune response, which is pivotal for the development of steatosis.

White adipose tissue-infiltrated CD11b+ myeloid cells are a source of S100A4, a new potential marker of hepatic damage

2021 ◽  
Author(s):  
Marjorie Reyes ◽  
Lorena González ◽  
Kevin Ibeas ◽  
Rubén Cereijo ◽  
Siri D. Taxerås ◽  
...  
Keyword(s):  
Gene Expression ◽  
T Cells ◽  
Adipose Tissue ◽  
Potential Role ◽  
Liver Steatosis ◽  
Myeloid Cells ◽  
Hepatic Damage ◽  
Mrna Levels ◽  
Hepatic Inflammation ◽  
Potential Marker

Context The endocrine and immunological properties of subcutaneous vs. visceral adipose tissue (sWAT and vWAT, respectively) have turned a milestone in the study of metabolic diseases. The cytokine S100A4 is increased in obesity and has a role in adipose tissue dysfunction. However, the cellular source and its potential role in hepatic damage in obesity has not been elucidated. Objective We aim to study the regulation of S100A4 in immune cells present in sWAT and vWAT, as well as its potential role as a circulating marker of hepatic inflammation and steatosis. Design A cohort of 60 patients with obesity and distinct metabolic status was analyzed. CD11b+ myeloid cells and T cells were isolated from sWAT and vWAT by magnetic-activating cell sorting, and RNA was obtained. S100A4 gene expression was measured, and correlation analysis with clinical data was performed. Liver biopsies were obtained from 20 patients, and S100A4 circulating levels were measured to check the link with hepatic inflammation and steatosis. Results S100A4 gene expression was strongly upregulated in sWAT- vs. vWAT-infiltrated CD11b+ cells, but this modulation was not observed in T cells. S100A4 mRNA levels from sWAT (and not from vWAT) CD11b+ cells positively correlated with glycemia, triglycerides, TNF-α gene expression and proliferation markers. Finally, circulating S100A4 directly correlated with liver steatosis and hepatic inflammatory markers. Conclusion Our data suggest that sWAT-infiltrated CD11b+ cells could be a major source of S100A4 in obesity. Moreover, our correlations identify circulating S100A4 as a potential novel biomarker of hepatic damage and steatosis.

scholarly journals Impaired Differentiation of Highly Proliferative ICOS+-Tregs Is Involved in the Transition from Low to High Disease Activity in Systemic Lupus Erythematosus (SLE) Patients

2021 ◽  
Vol 22 (17) ◽  
pp. 9501
Author(s):  
Florian Kälble ◽  
Lisa Wu ◽  
Hanns-Martin Lorenz ◽  
Martin Zeier ◽  
Matthias Schaier ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
T Cells ◽  
Lupus Erythematosus ◽  
Costimulatory Molecule ◽  
Flow Cytometric Analysis ◽  
Significant Shift ◽  
Healthy Controls ◽  
Systemic Lupus ◽  
Color Flow ◽  
Active Disease

Dysregulations in the differentiation of CD4+-regulatory-T-cells (Tregs) and CD4+-responder-T-cells (Tresps) are involved in the development of active systemic lupus erythematosus (SLE). Three differentiation pathways of highly proliferative inducible costimulatory molecule (ICOS)+- and less proliferative ICOS−-CD45RA+CD31+-recent-thymic-emigrant (RTE)-Tregs/Tresps via CD45RA−CD31+-memory-Tregs/Tresps (CD31+-memory-Tregs/Tresps), their direct proliferation via CD45RA+CD31−-mature naïve (MN)-Tregs/Tresps, and the production and differentiation of resting MN-Tregs/Tresp into CD45RA−CD31−-memory-Tregs/Tresps (CD31−-memory-Tregs/Tresps) were examined in 115 healthy controls, 96 SLE remission patients, and 20 active disease patients using six color flow cytometric analysis. In healthy controls an appropriate sequence of these pathways ensured regular age-dependent differentiation. In SLE patients, an age-independently exaggerated differentiation was observed for all Treg/Tresp subsets, where the increased conversion of resting MN-Tregs/Tresps particularly guaranteed the significantly increased ratios of ICOS+-Tregs/ICOS+-Tresps and ICOS−-Tregs/ICOS−-Tresps during remission. Changes in the differentiation of resting ICOS+-MN-Tresps and ICOS−-MN-Tregs from conversion to proliferation caused a significant shift in the ratio of ICOS+-Tregs/ICOS+-Tresps in favor of ICOS+-Tresps and a further increase in the ratio of ICOS−-Tregs/ICOS−-Tresps with active disease. The differentiation of ICOS+-RTE-Tregs/Tresps seems to be crucial for keeping patients in remission, where their limited production of proliferating resting MN-Tregs may be responsible for the occurrence of active disease flares.

scholarly journals Street RABV Induces the Cholinergic Anti-inflammatory Pathway in Human Monocyte-Derived Macrophages by Binding to nAChr α7

2021 ◽  
Vol 12 ◽  
Author(s):  
Carmen W. E. Embregts ◽  
Lineke Begeman ◽  
Cees J. Voesenek ◽  
Byron E. E. Martina ◽  
Marion P. G. Koopmans ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
T Cell ◽  
Macrophage Polarization ◽  
Flow Cytometric Analysis ◽  
Human Monocyte ◽  
Host Immune System ◽  
Inflammatory Pathway ◽  
Anti Inflammatory ◽  
Alpha Bungarotoxin

Rabies virus (RABV) is able to reach the central nervous system (CNS) without triggering a strong immune response, using multiple mechanisms to evade and suppress the host immune system. After infection via a bite or scratch from a rabid animal, RABV comes into contact with macrophages, which are the first antigen-presenting cells (APCs) that are recruited to the area and play an essential role in the onset of a specific immune response. It is poorly understood how RABV affects macrophages, and if the interaction contributes to the observed immune suppression. This study was undertaken to characterize the interactions between RABV and human monocyte-derived macrophages (MDMs). We showed that street RABV does not replicate in human MDMs. Using a recombinant trimeric RABV glycoprotein (rRABV-tG) we showed binding to the nicotinic acetylcholine receptor alpha 7 (nAChr α7) on MDMs, and confirmed the specificity using the nAChr α7 antagonist alpha-bungarotoxin (α-BTX). We found that this binding induced the cholinergic anti-inflammatory pathway (CAP), characterized by a significant decrease in tumor necrosis factor α (TNF-α) upon LPS challenge. Using confocal microscopy we found that induction of the CAP is associated with significant cytoplasmic retention of nuclear factor κB (NF-κB). Co-cultures of human MDMs exposed to street RABV and autologous T cells further revealed that the observed suppression of MDMs might affect their function as T cell activators as well, as we found a significant decrease in proliferation of CD8+ T cells and an increased production of the anti-inflammatory cytokine IL-10. Lastly, using flow cytometric analysis we observed a significant increase in expression of the M2-c surface marker CD163, hinting that street RABV might be able to affect macrophage polarization. Taken together, these results show that street RABV is capable of inducing an anti-inflammatory state in human macrophages, possibly affecting T cell functioning.

Immunomodulatory Effects of STI571 in Chronic Myeloid Leukaemia.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 2198-2198
Author(s):  
Dagmar Bund ◽  
Ting Yang ◽  
Raymund Buhmann ◽  
Hans-Jochem Kolb
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Chronic Myeloid Leukaemia ◽  
Myeloid Leukaemia ◽  
Cellular Immune Response ◽  
Myeloid Cells ◽  
Dependent Manner ◽  
Activation Markers ◽  
Cellular Immune ◽  
Antigen Presenting

Abstract Background: The tyrosine kinase inhibitor imatinib (imatinib, STI571, Glivec, and Gleevec) is highly effective in the treatment of chronic myeloid leukaemia (CML) and has already been shown to be effective in the setting of allogeneic stem cell transplantation. But until now, less is known with respect to its immunomodulating effects. Objective: In the present survey we investigated, whether imatinib could modify the antigen-presenting capacity of myeloid cells and in turn affects the cellular immune response. Method: For this purpose, patient derived chronic myeloid cells were incubated with different concentrations of imatinib (0, 1, 2, or 5microM), characterized for their antigen-presenting profile and their stimulatory capacity in the context of HLA-matched and mismatched T-cells. After 5 days, the proliferative immune response was evaluated in presence or absence of different concentrations of imatinib and altered effector-to-target ratios. Thereby, proliferation was detected via a CFDA, SE (5,6-carboxyfluorescein diacetate succinimidyl ester) based assay. Result: The proliferative capacity of the T- cells (allogeneic, HLA-mismatched) was inhibited by imatinib in a dose-dependent manner. Also, the expression of the activation markers was reduced in the presence of the different STI571 concentrations. Moreover, myeloid blasts were sensitized for T cell mediated effector functions by pre-treatment with increasing concentrations of imatinib. Conclusion: Taken together, imatinib can interfere with the T cellular immune response in vitro, and its impact on graft-versus-leukemia (GvL) and graft-versus-host (GvH) reactions will be further investigated.

scholarly journals Protective Killed Leptospira borgpetersenii Vaccine Induces Potent Th1 Immunity Comprising Responses by CD4 and γδ T Lymphocytes

2001 ◽  
Vol 69 (12) ◽  
pp. 7550-7558 ◽  
Author(s):  
Brian M. Naiman ◽  
David Alt ◽  
Carole A. Bolin ◽  
Richard Zuerner ◽  
Cynthia L. Baldwin
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Mononuclear Cells ◽  
Flow Cytometric Analysis ◽  
Γδ T Cells ◽  
Enzyme Linked Immunosorbent Assay ◽  
Specific Response ◽  
Zoonotic Infections ◽  
Leptospira Borgpetersenii ◽  
Ifn Γ

ABSTRACT Leptospira borgpetersenii serovar hardjo is the most common cause of bovine leptospirosis and also causes zoonotic infections of humans. A protective killed vaccine against serovar hardjo was shown to induce strong antigen-specific proliferative responses by peripheral blood mononuclear cells (PBMC) from vaccinated cattle by 2 months after the first dose of vaccine. This response was absent from nonvaccinated control cattle. The mean response peaked by 2 months after completion of the two-dose vaccination regimen, and substantial proliferation was measured in in vitro cultures throughout the 7 months of the study period. Variations in magnitude of the response occurred among the vaccinated animals, but by 7 months postvaccination there was a substantial antigen-specific response with PBMC from all vaccinated animals. Up to one-third of the PBMC from vaccinated animals produced gamma interferon (IFN-γ) after 7 days in culture with antigen, as ascertained by flow cytometric analysis, and significant levels of IFN-γ were measured in culture supernatants by enzyme-linked immunosorbent assay. Two-color immunofluorescence revealed that one-third of the IFN-γ-producing cells were γδ T cells, with the remaining cells being CD4+ T cells. The significance of this study is the very potent Th1-type immune response induced and sustained following vaccination with a killed bacterial vaccine adjuvanted with aluminum hydroxide and the involvement of γδ T cells in the response. Moreover, induction of this Th1-type cellular immune response is associated with the protection afforded by the bovine leptospiral vaccine against L. borgpeterseniiserovar hardjo.

Prognostic impact of PD-1, PD-L1, and CD8 genes expression in peripheral blood in gastric cancer.

2017 ◽  
Vol 35 (15_suppl) ◽  
pp. 11531-11531
Author(s):  
Shuhei Ito ◽  
Takaaki Masuda ◽  
Takeo Fukagawa ◽  
Yuta Kouyama ◽  
Hiroaki Wakiyama ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
T Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Flow Cytometric Analysis ◽  
Predictive Biomarkers ◽  
Prognostic Impact ◽  
Mrna Levels ◽  
Protein Levels ◽  
Flow Cytometric

11531 Background: Programmed death 1 (PD-1)/PD-1 ligand (PD-L1) blocking agents to gastric cancer (GC) in the clinical setting show significant therapeutic promise. However, since these agents are enormously expensive and potentially toxic, it is crucial to identify predictive biomarkers for detecting the best candidate who would benefit from these agents by less invasive and simpler method, such as liquid biopsy. Methods: Expression levels of genes coding for PD-1, PD-L1 and CD8 (CD8+ T cells are closely associated with cellular immune responses to tumors) were assessed in peripheral blood (PB) samples using quantitative RT-PCR. Samples were obtained from 407 GC patients (392 patients with neoadjuvant chemotherapy [NAC] and 15 patients without NAC) before surgery and 23 PB from normal controls (NC). Flow cytometric analysis was performed to identify PD-1-expressed cells in PB mononuclear cells. Results: PD-1, PD-L1 and CD8 mRNA levels of GC patients were significantly higher than those of NC: 4.2-, 3.0- and 6.1-fold increases, respectively (P < 0.0001, P = 0.0001 and P < 0.0001). PD-1 mRNA levels were significantly lower in GC patients with NAC than in GC patients without NAC (P < 0.01). GC patients with low PD-1, high PD-L1 and low CD8 mRNA levels had significantly poorer overall survival (OS) than those with high PD-1, low PD-L1 and high CD8 mRNA levels, respectively (P < 0.05, P < 0.05 and P < 0.05). Multivariate analysis showed that PD-1 low/ PD-L1 high mRNA levels was independent risk factors for OS (OR 2.15, 95%CI 1.29-3.45, P < 0.01). Flow cytometric analysis demonstrated the proportion of CD3 (T cell marker)-positive cells in the PD-1-positive fraction were 95.4 ± 6.9% in GC patients. Thus, most PD-1 protein expression occurred on T cells. Taken together, PD-1, PD-L1 and CD8 mRNAs in PB were overexpressed in GC patients, and PD-1 mRNA levels which was mostly expressed on T cells in protein levels in PB were decreased in GC patients with NAC. Furthermore, relative levels of PD-1, PD-L1 and CD8 were associated with prognosis, respectively. Conclusions: Preoperative PD-1, PD-L1 and CD8 mRNA levels in PB may reflect antitumor immune response, and PD-1 low/ PD-L1 high mRNA levels in PB are markers of poor prognosis in GC patients.

scholarly journals A preliminary Study on the Effect of Head and Neck Chemoradiotherapy on Systematic Immunity

Dose-Response ◽  
2019 ◽  
Vol 17 (4) ◽  
pp. 155932581988418 ◽  
Author(s):  
Weiqiang Huang ◽  
Yao Fan ◽  
Xiaoya Cheng ◽  
Huazhen Liang ◽  
Hua Pan ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Head And Neck ◽  
Concurrent Chemoradiotherapy ◽  
Flow Cytometric Analysis ◽  
Dual Effect ◽  
Blood Tests ◽  
Flow Cytometric ◽  
Before And After ◽  
Preliminary Study

Background: This study was designed initially to explore the effect of chemoradiotherapy on patients diagnosed with head and neck cancer (HNC) with respect to the alteration of systematic immunity. Methods: We did a retrospective study enrolling patients received concurrent chemoradiotherapy (CCRT), with or without induction chemotherapy (IC). Blood tests were performed before IC, before and after CCRT. Flow cytometric analysis and turbidimetric inhibition immunoassay were used for detection. Results: A total number of 58 patients were included from April 1, 2018, to March 31, 2019. Levels of immunoglobulins (Ig), including IgA, IgG, and IgM, declined after 2 to 3 cycles of IC and CCRT, respectively. Serum level of total hemolytic complement (CH50) increased ( P < .001) after IC, but kept stably post-CCRT. Natural killer (NK) cells decreased ( P < .01) after IC and enhanced ( P < .001) post-CCRT. The number of CD3+CD4+ T cells got increased ( P < .01) after IC and decreased ( P < .001) post-CCRT. Consistently, both IC and CCRT induced the increase in CD3+CD8+ T cells significantly ( P < .001 vs P < .01). Conclusion: Both radiotherapy (RT) and chemotherapy (CT) induced dual effect of immune response. Concurrent chemoradiotherapy created an active immune response based on the effect induced by IC, suggesting that RT exerted a potential function on mobilizing immune system.

scholarly journals A Detailed Flow Cytometric Analysis of Immune Activity Profiles in Molecular Subtypes of Colorectal Cancer

Cancers ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3440
Author(s):  
Xingru Li ◽  
Agnes Ling ◽  
Therese G. Kellgren ◽  
Marie Lundholm ◽  
Anna Löfgren-Burström ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Immune Response ◽  
T Cells ◽  
Immune Checkpoint ◽  
Molecular Subtypes ◽  
Personalised Medicine ◽  
Flow Cytometric Analysis ◽  
Molecular Subgroups ◽  
Immune Activity ◽  
Immune Infiltration

The local anti-tumour immune response has important prognostic value in colorectal cancer (CRC). In the era of immunotherapy, a better understanding of the immune response in molecular subgroups of CRC may lead to significant advances in personalised medicine. On this note, microsatellite instable (MSI) tumours have been characterised by increased immune infiltration, suggesting MSI as a marker for immune inhibitor checkpoint therapy. Here, we used flow cytometry to perform a comprehensive analysis of immune activity profiles in tumour tissues, adjacent non-malignant tissues and blood, from a cohort of 69 CRC patients. We found several signs of immune suppression in tumours compared to adjacent non-malignant tissues, including T cells more often expressing the immune checkpoint molecules programmed cell death protein (PD-1) and cytotoxic T lymphocyte-associated protein 4 (CTLA-4). We further analysed immune cell infiltration in molecular subgroups of CRC. MSI tumours were indeed found to be associated with increased immune infiltration, including increased fractions of PD-1+ T cells. No correlation was, however, found between MSI and the fraction of CTLA-4+ T cells. Interestingly, within the group of patients with microsatellite stable (MSS) tumours, some also presented with increased immune infiltration, including comparably high portions of PD-1+ T cells, but also CTLA-4+ T cells. Furthermore, no correlation was found between PD-1+ and CTLA-4+ T cells, suggesting that different tumours may, to some extent, be regulated by different immune checkpoints. We further evaluated the distribution of immune activity profiles in the consensus molecular subtypes of CRC. In conclusion, our findings suggest that different immune checkpoint inhibitors may be beneficial for selected CRC patients irrespective of MSI status. Improved predictive tools are required to identify these patients.

scholarly journals MiR-374b-5p Regulates T Cell Differentiation and Is Associated with rEg.P29 Immunity

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Dongjie Li ◽  
Xiancai Du ◽  
Mingxing Zhu ◽  
Songhao Yang ◽  
Wei Zhao
Keyword(s):  
Flow Cytometry ◽  
Immune Response ◽  
T Cells ◽  
Cell Differentiation ◽  
Echinococcus Granulosus ◽  
Secondary Infection ◽  
T Cell Differentiation ◽  
Mrna Levels ◽  
Th17 Differentiation ◽  
Th1 Immune Response

Cystic echinococcosis (CE) is a zoonotic disease caused by Echinococcus granulosus (Eg) infection. Our previous study confirmed that recombinant Eg.P29 (rEg.P29) could protect against echinococcus granulosus secondary infection in sheep and mice. The aim of the study was to investigate the association between immunoprotection of rEg.P29 vaccine and mmu-miR-374b-5p (miR-374b-5p) and study the immunity influence of miR-374b-5p on CD4+ T cells in mice spleen. MiR-374b-5p level was significantly increased after the second-week and the fourth week of vaccination with rEg.P29. Overexpression of miR-374b-5p increased IFN-γ, IL-2, IL-17A mRNA levels and decreased IL-10 mRNA levels in CD4+ T cells. Moreover, the inhibition of miR-374b-5p decreased IFN-γ and IL-17A and increased IL-10 mRNA levels in CD4+ T cells; this was further confirmed by the flow cytometry. The vaccination of rEg.P29 enhanced miR-374b-5p expression that was associated with a higher Th1 and Th17 immune response, a lower IL-10 mRNA production with miR-374b-5p overexpression, a lower Th1 immune response, and a higher IL-10 mRNA levels with miR-374b-5p inhibitions. To sum up, these data suggest that miR-374b-5p may participate in rEg.P29 immunity by regulating Th1 and Th17 differentiation.

scholarly journals TLR2 Deficiency Exacerbates Imiquimod-Induced Psoriasis-Like Skin Inflammation through Decrease in Regulatory T Cells and Impaired IL-10 Production

2020 ◽  
Vol 21 (22) ◽  
pp. 8560
Author(s):  
Momoko Nakao ◽  
Makoto Sugaya ◽  
Hideki Fujita ◽  
Tomomitsu Miyagaki ◽  
Sohshi Morimura ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Messenger Rna ◽  
Critical Role ◽  
Flow Cytometric Analysis ◽  
Skin Inflammation ◽  
Mrna Levels ◽  
Wild Type ◽  
Flow Cytometric ◽  
Tlr2 Signaling

Emerging evidence has demonstrated that Toll-like receptors (TLRs) are associated with autoimmune diseases. In this study, we investigated the role of TLR2 in psoriasis using imiquimod-induced psoriasis-like dermatitis. Although TLR2 signaling is known to play a critical role in the induction of proinflammatory cytokines by immune cells, such as dendritic cells (DCs), macrophages, and monocytes, TLR2 deficiency unexpectedly exacerbated psoriasiform skin inflammation. Importantly, messenger RNA (mRNA) levels of Foxp-3 and IL-10 in the lesional skin were significantly decreased in TLR2 KO mice compared with wild-type mice. Furthermore, flow cytometric analysis of the lymph nodes revealed that the frequency of regulatory T cells (Tregs) among CD4-positive cells was decreased. Notably, stimulation with Pam3CSK4 (TLR2/1 ligand) or Pam2CSK4 (TLR2/6 ligand) increased IL-10 production from Tregs and DCs and the proliferation of Tregs. Finally, adoptive transfer of Tregs from wild-type mice reduced imiquimod-induced skin inflammation in TLR2 KO mice. Taken together, our results suggest that TLR2 signaling directly enhances Treg proliferation and IL-10 production by Tregs and DCs, suppressing imiquimod-induced psoriasis-like skin inflammation. Enhancement of TLR2 signaling may be a new therapeutic strategy for psoriasis.

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