Increased IL17A, IFNG, and FOXP3 Transcripts in Moderate-Severe Psoriasis: a Major Influence Exerted by IL17A in Disease Severity
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Huil36g 169 Data Sheet
Growth Factor Data Sheet GoldBio growth factors are manufactured for RESEARCH USE ONLY and cannot be sold for human consumption! Interleukin-36G (IL36G) is a pro-inflammatory cytokine that plays an important role in the pathophysiology of several diseases. IL36A, IL36B and IL36G; (formerly IL1F6, IL1F8, and IL1F9) are IL1 family members that signal through the IL1 receptor family members IL1Rrp2 (IL1RL2) and IL1RAcP. IL36B is secreted when transfected into 293-T cells and could constitute part of an independent signaling system analogous to that of IL1A and IL1B receptor agonist and interleukin-1 receptor type I (IL1R1). Furthermore, IL36G also can function as an agonist of NFκB activation through the orphan IL1- receptor-related protein 2. Recombinant human IL36G is synthesized as a protein that contains no signal sequence, no prosegment and no potential N-linked glycosylation site.There is a 53% amino acid homology between human and mouse IL36G. IL36G also has a 25-55% amino acid homology with IL36G and IL1RN, IL1B, IL36RN, IL36A, IL37, IL36B and IL1F10. Catalog Number 1110-36E Product Name IL36G (IL-36 gamma), Human (169 a.a.) Recombinant Human Interleukin-36γ IL36G, IL36γ Interleukin 1 Homolog 1 (IL1H1) Interleukin 1-Related Protein 2 (IL1RP2) Interleukin 1 Family, Member 9 (IL1F9) Source Escherichia coli MW 18.7 kDa (169 amino acids) Sequence MRGTPGDADG GGRAVYQSMC KPITGTINDL NQQVWTLQGQ NLVAVPRSDS VTPVTVAVIT CKYPEALEQG RGDPIYLGIQ NPEMCLYCEK VGEQPTLQLK EQKIMDLYGQ PEPVKPFLFY RAKTGRTSTL ESVAFPDWFI ASSKRDQPII LTSELGKSYN TAFELNIND Accession Number Q9NZH8 Purity >95% by SDS-PAGE and HPLC analyses Biological Activity Fully biologically active when compared to standard. The specific activity is determined by its binding ability in a functional ELISA. -
Genetic Determinants of Circulating Interleukin-1 Receptor Antagonist Levels and Their Association with Glycemic Traits
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Trepo - Institutional Repository of Tampere University GENETIC DETERMINANTS OF CIRCULATING INTERLEUKIN-1 RECEPTOR ANTAGONIST LEVELS AND THEIR ASSOCIATION WITH GLYCEMIC TRAITS Marja-Liisa Nuotio Syventävien opintojen kirjallinen työ Tampereen yliopisto Lääketieteen yksikkö Tammikuu 2015 Tampereen yliopisto Lääketieteen yksikkö NUOTIO MARJA-LIISA: GENETIC DETERMINANTS OF CIRCULATING INTERLEUKIN-1 RECEPTOR ANTAGONIST LEVELS AND THEIR ASSOCIATION WITH GLYCEMIC TRAITS Kirjallinen työ, 57 s. Ohjaaja: professori Mika Kähönen Tammikuu 2015 Avainsanat: sytokiinit, insuliiniresistenssi, tyypin 2 diabetes, tulehdus, glukoosimetabolia, genominlaajuinen assosiaatioanalyysi (GWAS) Tulehdusta välittäviin sytokiineihin kuuluvan interleukiini 1β (IL-1β):n kohonneen systeemisen pitoisuuden on arveltu edesauttavan insuliiniresistenssin kehittymistä ja johtavan haiman β-solujen toimintahäiriöihin. IL-1β:n sisäsyntyisellä vastavaikuttajalla, interleukiini 1 reseptoriantagonistilla (IL-1RA), on puolestaan esitetty olevan suojaava rooli mainittujen fenotyyppien kehittymisessä päinvastaisten vaikutustensa ansiosta. IL-1RA:n suojaavan roolin havainnollistamiseksi työssä Genetic determinants of circulating interleukin-1 receptor antagonist levels and their association with glycemic traits tunnistettiin veren IL-1RA- pitoisuuteen assosioituvia geneettisiä variantteja, minkä jälkeen selvitettiin näiden yhteyttä glukoosi- ja insuliinimetaboliaan liittyvien muuttujien-, sekä -
Interleukin (IL)17A, F and AF in Inflammation: a Study in Collageninduced Arthritis and Rheumatoid Arthritis
bs_bs_banner Clinical and Experimental Immunology ORIGINAL ARTICLE doi:10.1111/cei.12376 Interleukin (IL)-17A, F and AF in inflammation: a study in collagen-induced arthritis and rheumatoid arthritis S. Sarkar,* S. Justa,* M. Brucks,* Summary J. Endres,† D. A. Fox,† X. Zhou,* Interleukin (IL)-17 plays a critical role in inflammation. Most studies to date F. Alnaimat,* B. Whitaker,‡ have elucidated the inflammatory role of IL-17A, often referred to as IL-17. J. C. Wheeler,‡ B. H. Jones§ and IL-17F is a member of the IL-17 family bearing 50% homology to IL-17A S. R. Bommireddy* and can also be present as heterodimer IL-17AF. This study elucidates the *Section of Rheumatology, Department of Medicine, and the Arizona Arthritis Center, distribution and contribution of IL-17A, F and AF in inflammatory arthritis. University of Arizona, Tucson, AZ, †Divison of Neutralizing antibody to IL-17A alone or IL-17F alone or in combination Rheumatology, Department of Internal Medicine, was utilized in the mouse collagen-induced arthritis (CIA) model to eluci- University of Michigan, Ann Arbor, MI, and date the contribution of each subtype in mediating inflammation. IL-17A, F ‡Biologics Research and §Immunology Discovery and AF were all increased during inflammatory arthritis. Neutralization of Research, Janssen Research and Development, IL-17A reduced the severity of arthritis, neutralization of IL-17A+IL-17F had Spring House, PA, USA the same effect as neutralizing IL-17A, while neutralization of IL-17F had no effect. Moreover, significantly higher levels of IL-17A and IL-17F were detected in peripheral blood mononuclear cells (PBMC) from patients with rheumatoid arthritis (RA) in comparison to patients with osteoarthritis (OA). -
Inflammation-Dependent IL18 Signaling Restricts Hepatocellular Carcinoma Growth by Enhancing the Accumulation and Activity of Tumor-Infiltrating Lymphocytes
Published OnlineFirst February 18, 2016; DOI: 10.1158/0008-5472.CAN-15-1548 Cancer Tumor and Stem Cell Biology Research Inflammation-Dependent IL18 Signaling Restricts Hepatocellular Carcinoma Growth by Enhancing the Accumulation and Activity of Tumor- Infiltrating Lymphocytes Geoffrey J. Markowitz1, Pengyuan Yang1,2,3, Jing Fu3, Gregory A. Michelotti4, Rui Chen1, Jianhua Sui5, Bin Yang2, Wen-Hao Qin3, Zheng Zhang6, Fu-Sheng Wang6, Anna Mae Diehl4, Qi-Jing Li7, Hongyang Wang3, and Xiao-Fan Wang1 Abstract Chronic inflammation in liver tissue is an underlying cause of IL18R1 deletion increased tumor burden. Mechanistically, we hepatocellular carcinoma. High levels of inflammatory cytokine foundthatIL18exertedinflammation-dependent tumor-sup- IL18 in the circulation of patients with hepatocellular carcinoma pressive effects largely by promoting the differentiation, activ- correlates with poor prognosis. However, conflicting results have ity, and survival of tumor-infiltrating T cells. Finally, differences been reported for IL18 in hepatocellular carcinoma development in the expression of IL18 in tumor tissue versus nontumor and progression. In this study, we used tissue specimens from tissueweremorepredictiveofpatientoutcomethanoverall hepatocellular carcinoma patients and clinically relevant mouse tissue expression. Taken together, our findings resolve a long- models of hepatocellular carcinoma to evaluate IL18 expression standing contradiction regarding a tumor-suppressive role for and function. In a mouse model of liver fibrosis that recapitulates IL18 in established hepatocellular carcinoma and provide a a tumor-promoting microenvironment, global deletion of the mechanistic explanation for the complex relationship between IL18 receptor IL18R1 enhanced tumor growth and burden. Sim- its expression pattern and hepatocellular carcinoma prognosis. ilarly, in a carcinogen-induced model of liver tumorigenesis, Cancer Res; 76(8); 1–12. -
Interleukin-33 Signaling Exacerbates Experimental Infectious Colitis by Enhancing Gut Permeability and Inhibiting Protective Th17 Immunity
www.nature.com/mi ARTICLE OPEN Interleukin-33 signaling exacerbates experimental infectious colitis by enhancing gut permeability and inhibiting protective Th17 immunity Vittoria Palmieri1, Jana-Fabienne Ebel1, Nhi Ngo Thi Phuong1, Robert Klopfleisch2, Vivian Pham Vu3,4, Alexandra Adamczyk1, Julia Zöller1, Christian Riedel5, Jan Buer1, Philippe Krebs3, Wiebke Hansen1, Eva Pastille1 and Astrid M. Westendorf 1 A wide range of microbial pathogens is capable of entering the gastrointestinal tract, causing infectious diarrhea and colitis. A finely tuned balance between different cytokines is necessary to eradicate the microbial threat and to avoid infection complications. The current study identified IL-33 as a critical regulator of the immune response to the enteric pathogen Citrobacter rodentium.We observed that deficiency of the IL-33 signaling pathway attenuates bacterial-induced colitis. Conversely, boosting this pathway strongly aggravates the inflammatory response and makes the mice prone to systemic infection. Mechanistically, IL-33 mediates its detrimental effect by enhancing gut permeability and by limiting the induction of protective T helper 17 cells at the site of infection, thus impairing host defense mechanisms against the enteric pathogen. Importantly, IL-33-treated infected mice supplemented with IL-17A are able to resist the otherwise strong systemic spreading of the pathogen. These findings reveal a novel IL-33/IL-17A crosstalk that controls the pathogenesis of Citrobacter rodentium-driven infectious colitis. Manipulating the dynamics of cytokines may offer new therapeutic strategies to treat specific intestinal infections. 1234567890();,: Mucosal Immunology (2021) 14:923–936; https://doi.org/10.1038/s41385-021-00386-7 INTRODUCTION epithelial cells, and endothelial cells in response to injury6. -
Cellular and Molecular Signatures in the Disease Tissue of Early
Cellular and Molecular Signatures in the Disease Tissue of Early Rheumatoid Arthritis Stratify Clinical Response to csDMARD-Therapy and Predict Radiographic Progression Frances Humby1,* Myles Lewis1,* Nandhini Ramamoorthi2, Jason Hackney3, Michael Barnes1, Michele Bombardieri1, Francesca Setiadi2, Stephen Kelly1, Fabiola Bene1, Maria di Cicco1, Sudeh Riahi1, Vidalba Rocher-Ros1, Nora Ng1, Ilias Lazorou1, Rebecca E. Hands1, Desiree van der Heijde4, Robert Landewé5, Annette van der Helm-van Mil4, Alberto Cauli6, Iain B. McInnes7, Christopher D. Buckley8, Ernest Choy9, Peter Taylor10, Michael J. Townsend2 & Costantino Pitzalis1 1Centre for Experimental Medicine and Rheumatology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK. Departments of 2Biomarker Discovery OMNI, 3Bioinformatics and Computational Biology, Genentech Research and Early Development, South San Francisco, California 94080 USA 4Department of Rheumatology, Leiden University Medical Center, The Netherlands 5Department of Clinical Immunology & Rheumatology, Amsterdam Rheumatology & Immunology Center, Amsterdam, The Netherlands 6Rheumatology Unit, Department of Medical Sciences, Policlinico of the University of Cagliari, Cagliari, Italy 7Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow G12 8TA, UK 8Rheumatology Research Group, Institute of Inflammation and Ageing (IIA), University of Birmingham, Birmingham B15 2WB, UK 9Institute of -
IL-17-Producing Cells in Tumor Immunity: Friends Or Foes?
Immune Netw. 2020 Feb;20(1):e6 https://doi.org/10.4110/in.2020.20.e6 pISSN 1598-2629·eISSN 2092-6685 Review Article IL-17-Producing Cells in Tumor Immunity: Friends or Foes? Da-Sol Kuen 1,2, Byung-Seok Kim 1, Yeonseok Chung 1,2,* 1Laboratory of Immune Regulation, Institute of Pharmaceutical Sciences, Seoul National University, Seoul 08826, Korea 2BK21 Plus Program, Institute of Pharmaceutical Sciences, Seoul National University, Seoul 08826, Korea Received: Dec 29, 2019 Revised: Jan 25, 2020 ABSTRACT Accepted: Jan 26, 2020 IL-17 is produced by RAR-related orphan receptor gamma t (RORγt)-expressing cells *Correspondence to including Th17 cells, subsets of γδT cells and innate lymphoid cells (ILCs). The biological Yeonseok Chung significance of IL-17-producing cells is well-studied in contexts of inflammation, Laboratory of Immune Regulation and BK21 Plus Program, Institute of Pharmaceutical autoimmunity and host defense against infection. While most of available studies in tumor + Sciences, Seoul National University, 1 Gwanak- immunity mainly focused on the role of T-bet-expressing cells, including cytotoxic CD8 ro, Gwanak-gu, Seoul 08826, Korea. T cells and NK cells, and their exhaustion status, the role of IL-17-producing cells remains E-mail: [email protected] poorly understood. While IL-17-producing T-cells were shown to be anti-tumorigenic in Copyright © 2020. The Korean Association of adoptive T-cell therapy settings, mice deficient in type 17 genes suggest a protumorigenic Immunologists potential of IL-17-producing cells. This review discusses the features of IL-17-producing This is an Open Access article distributed cells, of both lymphocytic and myeloid origins, as well as their suggested pro- and/or anti- under the terms of the Creative Commons tumorigenic functions in an organ-dependent context. -
Evolutionary Divergence and Functions of the Human Interleukin (IL) Gene Family Chad Brocker,1 David Thompson,2 Akiko Matsumoto,1 Daniel W
UPDATE ON GENE COMPLETIONS AND ANNOTATIONS Evolutionary divergence and functions of the human interleukin (IL) gene family Chad Brocker,1 David Thompson,2 Akiko Matsumoto,1 Daniel W. Nebert3* and Vasilis Vasiliou1 1Molecular Toxicology and Environmental Health Sciences Program, Department of Pharmaceutical Sciences, University of Colorado Denver, Aurora, CO 80045, USA 2Department of Clinical Pharmacy, University of Colorado Denver, Aurora, CO 80045, USA 3Department of Environmental Health and Center for Environmental Genetics (CEG), University of Cincinnati Medical Center, Cincinnati, OH 45267–0056, USA *Correspondence to: Tel: þ1 513 821 4664; Fax: þ1 513 558 0925; E-mail: [email protected]; [email protected] Date received (in revised form): 22nd September 2010 Abstract Cytokines play a very important role in nearly all aspects of inflammation and immunity. The term ‘interleukin’ (IL) has been used to describe a group of cytokines with complex immunomodulatory functions — including cell proliferation, maturation, migration and adhesion. These cytokines also play an important role in immune cell differentiation and activation. Determining the exact function of a particular cytokine is complicated by the influence of the producing cell type, the responding cell type and the phase of the immune response. ILs can also have pro- and anti-inflammatory effects, further complicating their characterisation. These molecules are under constant pressure to evolve due to continual competition between the host’s immune system and infecting organisms; as such, ILs have undergone significant evolution. This has resulted in little amino acid conservation between orthologous proteins, which further complicates the gene family organisation. Within the literature there are a number of overlapping nomenclature and classification systems derived from biological function, receptor-binding properties and originating cell type. -
Decrease in Mucosal IL17A, IFN and IL10 Expressions in Active Crohn's
nutrients Article Decrease in Mucosal IL17A, IFNγ and IL10 Expressions in Active Crohn’s Disease Patients Treated with High-Dose Vitamin D Alone or Combined with Infliximab Mia Bendix 1,*, Anders Dige 1, Søren Peter Jørgensen 1, Jens Frederik Dahlerup 1 , Bo Martin Bibby 2, Bent Deleuran 3,4 and Jørgen Agnholt 1 1 Department of Hepatology and Gastroenterology, Aarhus University Hospital, 8200 Aarhus, Denmark; [email protected] (A.D.); [email protected] (S.P.J.); [email protected] (J.F.D.); [email protected] (J.A.) 2 Department of Public Health—Department of Biostatistics, Aarhus University, 8000 Aarhus, Denmark; [email protected] 3 Department of Rheumatology, Aarhus University Hospital, 8200 Aarhus, Denmark; [email protected] 4 Department of Biomedicine, Aarhus University, 8000 Aarhus, Denmark * Correspondence: [email protected] Received: 5 November 2020; Accepted: 26 November 2020; Published: 30 November 2020 Abstract: Background: Vitamin D treatment may reduce Crohn’s disease (CD) activity by modulating the mucosal immune function. We investigated if high-dose vitamin D +/ infliximab modulated − the mucosal cytokine expression in active CD. Methods: Forty CD patients were randomized into: infliximab + vitamin D; infliximab + placebo-vitamin D; placebo-infliximab + vitamin D or placebo-infliximab + placebo-vitamin D. Infliximab (5 mg/kg) and placebo-infliximab were administered at weeks 0, 2 and 6. Oral vitamin D was administered as bolus 200,000 international units (IU) per week 0 followed by 20,000 IU/day for 7 weeks or placebo. Endoscopy with biopsies was performed at weeks 0 and 7 where endoscopic activity was measured and mucosal mRNA cytokine expression was examined. -
Il1f10 (NM 153077) Mouse Tagged ORF Clone – MR223925 | Origene
OriGene Technologies, Inc. 9620 Medical Center Drive, Ste 200 Rockville, MD 20850, US Phone: +1-888-267-4436 [email protected] EU: [email protected] CN: [email protected] Product datasheet for MR223925 Il1f10 (NM_153077) Mouse Tagged ORF Clone Product data: Product Type: Expression Plasmids Product Name: Il1f10 (NM_153077) Mouse Tagged ORF Clone Tag: Myc-DDK Symbol: Il1f10 Synonyms: MGC130267; MGC130268 Vector: pCMV6-Entry (PS100001) E. coli Selection: Kanamycin (25 ug/mL) Cell Selection: Neomycin ORF Nucleotide >MR223925 ORF sequence Sequence: Red=Cloning site Blue=ORF Green=Tags(s) TTTTGTAATACGACTCACTATAGGGCGGCCGGGAATTCGTCGACTGGATCCGGTACCGAGGAGATCTGCC GCCGCGATCGCC ATGTGCTCCCTTCCCATGGCAAGATACTACATAATCAAGGATGCACATCAAAAGGCTTTGTACACACGGA ATGGCCAGCTCCTGCTGGGAGACCCTGATTCAGACAATTATAGTCCAGAGAAGGTCTGTATCCTTCCTAA CCGAGGCCTAGACCGCTCCAAGGTCCCCATCTTCCTGGGGATGCAGGGAGGAAGTTGCTGCCTGGCGTGT GTAAAGACAAGAGAGGGACCTCTCCTGCAGCTGGAGGATGTGAACATCGAGGACCTATACAAGGGAGGTG AACAAACCACCCGTTTCACCTTTTTCCAGAGAAGCTTGGGATCTGCCTTCAGGCTTGAGGCTGCTGCCTG CCCTGGCTGGTTTCTCTGTGGCCCAGCTGAGCCCCAGCAGCCAGTGCAGCTCACCAAAGAGAGTGAACCC TCCACCCATACTGAATTCTACTTTGAGATGAGTCGG ACGCGTACGCGGCCGCTCGAGCAGAAACTCATCTCAGAAGAGGATCTGGCAGCAAATGATATCCTGGATT ACAAGGATGACGACGATAAGGTTTAA Protein Sequence: >MR223925 protein sequence Red=Cloning site Green=Tags(s) MCSLPMARYYIIKDAHQKALYTRNGQLLLGDPDSDNYSPEKVCILPNRGLDRSKVPIFLGMQGGSCCLAC VKTREGPLLQLEDVNIEDLYKGGEQTTRFTFFQRSLGSAFRLEAAACPGWFLCGPAEPQQPVQLTKESEP STHTEFYFEMSR TRTRPLEQKLISEEDLAANDILDYKDDDDKV Restriction Sites: SgfI-MluI This product is to -
Table SII. Significantly Differentially Expressed Mrnas of GSE23558 Data Series with the Criteria of Adjusted P<0.05 And
Table SII. Significantly differentially expressed mRNAs of GSE23558 data series with the criteria of adjusted P<0.05 and logFC>1.5. Probe ID Adjusted P-value logFC Gene symbol Gene title A_23_P157793 1.52x10-5 6.91 CA9 carbonic anhydrase 9 A_23_P161698 1.14x10-4 5.86 MMP3 matrix metallopeptidase 3 A_23_P25150 1.49x10-9 5.67 HOXC9 homeobox C9 A_23_P13094 3.26x10-4 5.56 MMP10 matrix metallopeptidase 10 A_23_P48570 2.36x10-5 5.48 DHRS2 dehydrogenase A_23_P125278 3.03x10-3 5.40 CXCL11 C-X-C motif chemokine ligand 11 A_23_P321501 1.63x10-5 5.38 DHRS2 dehydrogenase A_23_P431388 2.27x10-6 5.33 SPOCD1 SPOC domain containing 1 A_24_P20607 5.13x10-4 5.32 CXCL11 C-X-C motif chemokine ligand 11 A_24_P11061 3.70x10-3 5.30 CSAG1 chondrosarcoma associated gene 1 A_23_P87700 1.03x10-4 5.25 MFAP5 microfibrillar associated protein 5 A_23_P150979 1.81x10-2 5.25 MUCL1 mucin like 1 A_23_P1691 2.71x10-8 5.12 MMP1 matrix metallopeptidase 1 A_23_P350005 2.53x10-4 5.12 TRIML2 tripartite motif family like 2 A_24_P303091 1.23x10-3 4.99 CXCL10 C-X-C motif chemokine ligand 10 A_24_P923612 1.60x10-5 4.95 PTHLH parathyroid hormone like hormone A_23_P7313 6.03x10-5 4.94 SPP1 secreted phosphoprotein 1 A_23_P122924 2.45x10-8 4.93 INHBA inhibin A subunit A_32_P155460 6.56x10-3 4.91 PICSAR P38 inhibited cutaneous squamous cell carcinoma associated lincRNA A_24_P686965 8.75x10-7 4.82 SH2D5 SH2 domain containing 5 A_23_P105475 7.74x10-3 4.70 SLCO1B3 solute carrier organic anion transporter family member 1B3 A_24_P85099 4.82x10-5 4.67 HMGA2 high mobility group AT-hook 2 A_24_P101651 -
IL1F10 Monoclonal Antibody
Product Datasheet IL1F10 Monoclonal Antibody Catalog No: #42049 Orders: [email protected] Description Support: [email protected] Product Name IL1F10 Monoclonal Antibody Host Species Mouse Clonality Monoclonal Purification protein G purifed Applications IHC Species Reactivity Hu Specificity specific for Human IL1F10 denatured and native forms Immunogen Type protein Immunogen Description Recombinant Human IL1F10 protein Target Name IL1F10 Other Names IL-1F10, Family of interleukin 1-theta, FIL1 theta Interleukin-1 HY2, IL-1HY2, Interleukin-1 theta, IL-1 theta Interleukin-38, IL-38 Accession No. Swiss-Prot#: Q8WWZ1 Concentration 1.0mg/mL Formulation Preservative: 0.03% Proclin 300 Constituents: 50% Glycerol, 0.01M PBS, PH 7.4 Storage Store at -20°C Application Details Immunohistochemistry: 1:20 - 1:200 Images Immunohistochemical analysis of paraffin-embedded Human Colon cancer tissue using #42049 at dilution of 1:200. Address: 8400 Baltimore Ave. Suite 302 College Park MD 20740 USA http://www.sabbiotech.com 1 Immunohistochemical analysis of paraffin-embedded Human live cancer tissue using #42049 at dilution of 1:200. Immunohistochemical analysis of paraffin-embedded Human spleen tissue using #42049 at dilution of 1:200. Background Cytokine with immunomodulatory activity. Alone, does not induce cytokine production, but reduces IL22 and IL17A production by T-cells in response to heat-killed Candida albicans. Reduces IL36G-induced production of IL8 by peripheral blood mononuclear cells. Increases IL6 production by dendritic cells stimulated by bacterial lipopolysaccharides (LPS). Ligand for IL-36R/IL1RL2. References "IL-38 binds to the IL-36 receptor and has biological effects on immune cells similar to IL-36 receptor antagonist." van de Veerdonk F.L., Stoeckman A.K., Wu G., Boeckermann A.N., Azam T., Netea M.G., Joosten L.A., van der Meer J.W., Hao R., Kalabokis V., Dinarello C.A.