Relevant bibliographies by topics / IL32

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Academic literature on the topic 'IL32'

Author: Grafiati
Published: 14 March 2023

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Journal articles on the topic "IL32"

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Decombis, Salome, Antonin Papin, Celine Bellanger, Clara Sortais, Christelle Dousset, Yannick Le Bris, Stephanie Blandin, et al. "The IL32/BAFF Axis Supports Prosurvival Dialog in the Lymphoma Ecosystem and Is Disrupted By NIK Inhibition." Blood 138, Supplement 1 (November 5, 2021): 781. http://dx.doi.org/10.1182/blood-2021-144839.

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Abstract Background Aggressive B-cell lymphomas, such as Mantle cell lymphoma (MCL), are microenvironment-dependent tumors but, in contrast to tumoral intrinsic anomalies, complex interplays within their ecosystems are largely ignored. A better understanding of these dialogs could provide new perspectives integrating the key role of the microenvironment to increase treatment efficiency of this hard to cure B-cell malignancy. Methods To identify novel molecular regulations occurring in lymphoma protective ecosystems, we performed a transcriptomic analysis based on the comparison of publicly available datasets from circulating (PB, n=77) versus MCL lymph nodes (LN, n=107) together with deep RNA sequencing of purified CD19+CD5+ MCL (n=8) versus normal B-cells (n=6). This integrated analysis led to the discovery of microenvironment-dependent and tumor-specific secretion of the cytokine IL32β by lymphoma cells. Using in situ multiplex immunohistochemistry , ex vivo models of primary MCL cells (n=23) and IL32 KO MCL cell lines (Crispr/Cas9), we studied the regulation and the functional impact of IL32β in the MCL context, especially in the dialog with tumor-associated macrophages. Results Among the 6887 genes differentially expressed in MCL LN compared to PB in vivo, 70% were confirmed in CD19+ MCL cells cocultured ex vivo and 39% were tumor-specific, that is to say not upregulated in cocultured normal B cells (NBC). Top-genes scoring revealed that IL32 was the most upregulated genes within the "Tumor-specific" transcriptional program. Using ex vivo models of primary MCL cells, we demonstrated that the microenvironment-dependent secretion of IL32β was controlled by the CD40/NFKB2 axis whereas its tumor specificity was the consequence of IL32 promoter hypomethylation in MCL compared to NBC. IL32 protein expression was confirmed in MCL LN in situ by multiplex IHC. The latter allowed the concurrent detection of MCL cells, T cells, macrophages and IL32. Consistently with the microenvironment-dependent induction of IL32 in MCL, we observed that IL32 expression was enriched in situ in tumor zones infiltrated with T cells, compared to tumor-exclusive zones. Based on in vitro experiments using IL32 KO MINO cells (Crispr/Cas9), we demonstrated that, through the secretion of IL32β, the tumor was able to corrupt its microenvironment by polarizing monocytes into specific protumoral CD163 mid MCL-associated macrophages, which secrete both pro- (e.g. IL6, OSM, IL1a/b) and anti- inflammatory (e.g. IL10, IDO, IL18, IL4L1) soluble factors. We next highlighted that IL32β-stimulated macrophages supported tumor survival mostly through a soluble dialog, which is driven by BAFF. Finally, we demonstrated the efficacy of selective NIK/alternative-NFkB inhibition to counteract both microenvironment-dependent induction of IL32β (RNA expression inhibition: 62 % ; n= 3) and BAFF-dependent survival of MCL cells (survival support inhibition : 47 % ; n=6). Conclusions In summary, our data uncovered the IL32β/BAFF axis as a previously undescribed pathway involved in MCL-associated macrophage polarization and tumor survival. Dependent on alternative-NFkB signaling, tumor-specific secretion of IL32β led to the corruption of the microenvironment through the polarization of monocytes into specific MCL-associated macrophages, which in turn favor tumor survival. While IL32β-stimulated macrophages secreted several protumoral factors, they supported MCL survival through BAFF and consequent alternative-NFkB activation in tumor cells. Our data shows that targeting IL32b, BAFF or the alternative NFkB pathway through NIK inhibition could also be of major interest for counteracting the multiple cross-talks that occur in the MCL microenvironment and, especially, the CD40L + T-cell / MCL / CD163 + MCL-associated macrophage triad. Figure 1 Figure 1. Disclosures No relevant conflicts of interest to declare.
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Lu, Huili, Wei Han, Abdulgabar Salama, and Anja Moldenhauer. "CXCL9 and IL32 Regulate Progenitor Expansion and Protect Hematopoietic Progenitor Cells From Chemotherapy." Blood 118, no. 21 (November 18, 2011): 1316. http://dx.doi.org/10.1182/blood.v118.21.1316.1316.

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Abstract Abstract 1316 Background: We have reported that the cytokines CXCL9 and IL32 regulate murine bone marrow regeneration post chemotherapy, but the reasons for this effect and whether they work directly on progenitor cells remain unclear. Methods: Human CD34+ cells from cord blood were incubated with CXCL9 or IL32. Cell numbers were determined on a weekly basis, and one-week expanded cells were seeded on top of a confluent MS-5 stroma cell layer to determine the number of cobblestone-area forming and long-term culture initiating cells (LTC-IC). Apoptosis rates after incubation with CXCL9/IL32 and SCF/G-CSF/IL3 prior to Ara-C treatment (300mM, 1 h) were assessed by Annexin V detection. Subsequently, signaling pathways after stimulation with IL32 or CXCL9 were examined using the luminex map technology. Results: CXCL9 did not influence CD34+ cell expansion, while IL32 enhanced the expansion rates significantly [6.69±1.38 versus to 3.57±0.70 fold in the control group, p<0.05]. However, more LTC-ICs after CXCL9 treatment (1357±123 of CXCL9 group versus 1081±119 of control group, p<0.05) were found, while IL32 reduced the number of LTC-ICs (78±8 of IL32 group, p<0.005). That suggests that CXCL9 kept more primitive LTC-ICs quiescent instead of entering expansion during the one-week incubation, while IL32 rather stimulated the differentiation of LTC-ICs. Since SCF, G-CSF and IL-3 are the most widely used hematopoietic growing factors (HGF) in stem cell expansion, we detected their roles during chemotherapeutical treatment in vitro. We observed enhanced apoptosis during Ara-C treatment when the cells were incubated with SCF or IL3. But when CXCL9 or IL32 were added, results were different. Both CXCL9 and IL-32 reduced the apoptosis rate resulting from Ara-C treatment, when SCF is present (26.37±1.12% of CXCL9+SCF group, 29.97±0.72% of IL32+SCF group, versus 35.52±1.21% of SCF alone, p <0.005 and p<0.05), but none of them affected IL-3 related apoptosis. Especially the effect of CXCL9 was inhibited using antibodies to its receptor CXCR3 (37.97±1.50% with anti-CXCR3 versus 35.52±1.21% of SCF alone, p= 0.09, versus 26.37±1.12% of CXCL9+SCF group p<0.05). G-CSF alone did not influence Ara-C induced apoptosis, but in combination with IL32 the apoptosis rate increased (23.37±0.09% of IL32+G-CSF versus 19.59±0.79% of G-CSF alone, p<0.005). That suggests that IL32 could regulate stem cell expansion differently through various pathways in collaboration with SCF and G-CSF. In fact, IL32 reduced STAT5 and p38 activity, while CXCL9 activated p38 and JNK pathways of CD34+ cells in combination with SCF. Conclusions: Our results demonstrate that both CXCL9 and IL32 can regulate stem cell expansion in vitro; CXCL9 could protect HPCs from chemotherapy and therefore support the following recovery, IL32 could help progenitor cells to expand, differentiate rapidly and thereby enhance the regeneration of the hematologic system. Disclosures: No relevant conflicts of interest to declare.
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Kang, Ji Young, and Kyung Eun Kim. "Prognostic Value of Interleukin-32 Expression and Its Correlation with the Infiltration of Natural Killer Cells in Cutaneous Melanoma." Journal of Clinical Medicine 10, no. 20 (October 13, 2021): 4691. http://dx.doi.org/10.3390/jcm10204691.

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Interleukin-32 (IL-32) is well known as a proinflammatory cytokine that is expressed in various immune cells and cancers. However, the clinical relevance of IL-32 expression in cutaneous melanoma has not been comprehensively studied. Here, we identified the prognostic value of IL32 expression using various systematic multiomic analyses. The IL32 expressions were significantly higher in cutaneous melanoma than in normal tissue, and Kaplan–Meier survival analysis showed a correlation between IL32 expression and good prognosis in cutaneous melanoma patients. In addition, we analyzed the correlation between IL32 expression and the infiltration of natural killer (NK) cells to identify a relevant mechanism between IL32 expression and prognosis in cutaneous melanoma (p = 0.00031). In the relationship between IL32 expression and the infiltration of NK cells, a negative correlation was found in resting NK cells (rho = −0.38, p = 3.95 × 10−17) whereas a strong positive correlation was observed only in active NK cells (rho = 0.374, p = 1.23 × 10−16). Moreover, IL32 expression was markedly positively correlated with the cytolytic molecules, such as granzyme and perforin. These data suggest that IL32 expression may increase patient survival through the infiltration and activation of NK cells, representative anticancer effector cells, in cutaneous melanoma. Collectively, this study provides the prognostic value of IL32 expression and its potential role as an effective predictive biomarker for NK cell infiltration in cutaneous melanoma.
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Baselli, Guido Alessandro, Paola Dongiovanni, Raffaela Rametta, Marica Meroni, Serena Pelusi, Marco Maggioni, Sara Badiali, et al. "Liver transcriptomics highlights interleukin-32 as novel NAFLD-related cytokine and candidate biomarker." Gut 69, no. 10 (January 30, 2020): 1855–66. http://dx.doi.org/10.1136/gutjnl-2019-319226.

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ObjectiveEfforts to manage non-alcoholic fatty liver disease (NAFLD) are limited by the incomplete understanding of the pathogenic mechanisms and the absence of accurate non-invasive biomarkers. The aim of this study was to identify novel NAFLD therapeutic targets andbiomarkers by conducting liver transcriptomic analysis in patients stratified by the presence of the PNPLA3 I148M genetic risk variant.DesignWe sequenced the hepatic transcriptome of 125 obese individuals. ‘Severe NAFLD’ was defined as the presence of steatohepatitis, NAFLD activity score ≥4 or fibrosis stage ≥2. The circulating levels of the most upregulated transcript, interleukin-32 (IL32), were measured by ELISA.ResultsCarriage of the PNPLA3 I148M variant correlated with the two major components of hepatic transcriptome variability and broadly influenced gene expression. In patients with severe NAFLD, there was an upregulation of inflammatory and lipid metabolism pathways. IL32 was the most robustly upregulated gene in the severe NAFLD group (adjusted p=1×10−6), and its expression correlated with steatosis severity, both in I148M variant carriers and non-carriers. In 77 severely obese, and in a replication cohort of 160 individuals evaluated at the hepatology service, circulating IL32 levels were associated with both NAFLD and severe NAFLD independently of aminotransferases (p<0.01 for both). A linear combination of IL32-ALT-AST showed a better performance than ALT-AST alone in NAFLD diagnosis (area under the curve=0.92 vs 0.81, p=5×10−5).ConclusionHepatic IL32 is overexpressed in NAFLD, correlates with hepatic fat and liver damage, and is detectable in the circulation, where it is independently associated with the presence and severity of NAFLD.
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Gautam, Anuradha, and Bhaswati Pandit. "IL32: The multifaceted and unconventional cytokine." Human Immunology 82, no. 9 (September 2021): 659–67. http://dx.doi.org/10.1016/j.humimm.2021.05.002.

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Logan, Jeongok G., Sijung Yun, Yongde Bao, Emily Farber, and Charles R. Farber. "RNA-sequencing analysis of differential gene expression associated with arterial stiffness." Vascular 28, no. 5 (May 6, 2020): 655–63. http://dx.doi.org/10.1177/1708538120922650.

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Objectives Arterial stiffness is recognized as an important predictor of cardiovascular disease morbidity and mortality, independent of traditional cardiovascular disease risk factors. Given that arterial tissue is not easily accessible, most gene expression studies on arterial stiffness have been conducted on animals or on patients who have undergone by-pass surgeries. In order to obtain a deeper understanding of early changes of arterial stiffness, this study compared transcriptome profiles between healthy adults with higher and lower arterial stiffness. Methods The sample included 20 healthy female adults without cardiovascular disease. Arterial stiffness was measured by carotid-femoral pulse wave velocity, the “gold-standard” measure of central arterial stiffness. Peripheral blood samples collected to PAXgene™ RNA tubes were used for RNA sequencing (RNA-seq). The potential confounding effects of age, body mass index, and mean arterial pressure were controlled for in RNA-seq analysis. To validate RNA-seq results, quantitative real-time PCR (qRT-PCR) was performed for six selected genes. Results The findings demonstrated that genes including CAPN9, IL32, ERAP2, RAB6B, MYBPH, and miRNA626 were down-regulated, and that MOCS1 gene was up-regulated among the people with higher arterial stiffness. Real-time PCR showed that the changes of CAPN9, IL32, ERAP2, and RAB6B were in concordance with RNA-seq data, and confirmed the validity of the gene expression profiles obtained by RNA-seq analysis. Conclusions Previous studies have suggested the potential roles of CAPN9, IL32, and ERAP2 in structural changes of the arterial wall through up-regulation of metalloproteinases. However, the current study showed that CAPN9, IL32, and ERAP2 were down-regulated in the individuals with higher arterial stiffness, compared with those with lower arterial stiffness. The unexpected directions of expression of these genes may indicate an effort to maintain vascular homeostasis during increased arterial stiffness among healthy individuals. Further studies are guaranteed to investigate the roles of CAPN9, IL32, and ERAP2 in regulating arterial stiffness in people with and without cardiovascular disease.
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Diakowska, Dorota, and Małgorzata Krzystek-Korpacka. "Local and Systemic Interleukin-32 in Esophageal, Gastric, and Colorectal Cancers: Clinical and Diagnostic Significance." Diagnostics 10, no. 10 (October 4, 2020): 785. http://dx.doi.org/10.3390/diagnostics10100785.

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Little is known on clinical and diagnostic relevance of interleukin-32 in gastrointestinal tract (GIT) cancers. We determined its mRNA (n = 52) and protein (n = 63) expression in paired (tumor-normal) samples from esophageal squamous cell carcinoma (ESCC) and gastric (GC) and colorectal cancer (CRC) patients, with reference to cancer-associated genes, and quantified circulating interleukin-32 in 70 cancer patients and 28 controls. IL32 expression was significantly upregulated solely in ESCC, reflecting T stage in non-transformed tumor-adjacent tissue. Fold-change in IL32 and IL-32 was higher in left-sided CRC, owing to high interleukin expression in non-transformed right-sided colonic mucosa. IL32 was independently and positively associated with Ki67, HIF1A, and ACTA2 and negatively with TJP1 in tumors and with IL10Ra and BCLxL in non-transformed tumor-adjacent tissue. IL-32 protein was significantly upregulated in colorectal tumors. In ESCC, advanced stage and lymph node metastasis were associated with significant IL-32 upregulation. Circulating interleukin was significantly elevated in cancer patients, more so in ESCC and GC than CRC. As biomarker, IL-32 detected gastroesophageal cancers with 99.5% accuracy. In conclusion, IL-32 is upregulated in GIT cancers at local and systemic level, reflecting hypoxia and proliferative and invasive/metastatic capacity in tumors and immunosuppressive and antiapoptotic potential in non-transformed mucosa, while being an accurate biomarker of gastroesophageal cancers.
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Ramirez-Carracedo, Rafael, Laura Tesoro, Ignacio Hernandez, Javier Diez-Mata, David Piñeiro, Macarena Hernandez-Jimenez, Jose Luis Zamorano, and Carlos Zaragoza. "Targeting TLR4 with ApTOLL Improves Heart Function in Response to Coronary Ischemia Reperfusion in Pigs Undergoing Acute Myocardial Infarction." Biomolecules 10, no. 8 (August 9, 2020): 1167. http://dx.doi.org/10.3390/biom10081167.

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Toll-like receptor 4 (TLR4) contributes to the pathogenesis of coronary ischemia/reperfusion (IR). To test whether the new TLR4 antagonist, ApTOLL, may prevent coronary IR damage, we administered 0.078 mg/kg ApTOLL or Placebo in pigs subjected to IR, analyzing the levels of cardiac troponins, matrix metalloproteinases, pro-, and anti-inflammatory cytokines, heart function, and tissue integrity over a period of 7 days after IR. Our results show that ApTOLL reduced cardiac troponin-1 24 h after administration, improving heart function, as detected by a significant recovery of the left ventricle ejection fraction (LVEF) and the shortening fraction (FS) cardiac parameters. The extension of necrotic and fibrotic areas was also reduced, as detected by Evans blue/2,3,5-triphenyltetrazolium chloride (TTC) staining, Hematoxylin/Eosine, and Masson Trichrome staining of heart sections, together with a significant reduction in the expression of the extracellular matrix-degrading, matrix metalloproteinase 9. Finally, the expression of the following cytokines, CCL1, CCL2, MIP1-A-B, CCL5, CD40L, C5/C5A, CXCL1, CXCL10, CXCL11, CXCL12, G-CSF, GM-CSF, ICAM-1, INF-g, IL1-a, ILI-b, IL-1Ra, IL2, IL4, IL5, IL6, IL8, IL10, IL12, IL13, IL16, IL17-A, IL17- E, IL18, IL21, IL27, IL32, MIF, SERPIN-E1, TNF-a, and TREM-1, were also assayed, detecting a pronounced decrease of pro-inflammatory cytokines after 7 days of treatment with ApTOLL. Altogether, our results show that ApTOLL is a promising new tool for the treatment of acute myocardial infarction (AMI).
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Poma, Anello Marcello, Angelo Genoni, Francesco Broccolo, Maria Denaro, Alberto Pugliese, Fulvio Basolo, and Antonio Toniolo. "Immune Transcriptome of Cells Infected with Enterovirus Strains Obtained from Cases of Type 1 Diabetes." Microorganisms 8, no. 7 (July 12, 2020): 1031. http://dx.doi.org/10.3390/microorganisms8071031.

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Enterovirus (EV) infection of insulin-producing pancreatic beta cells is associated with type 1 diabetes (T1D), but little is known about the mechanisms that lead the virus to cause a persistent infection and, possibly, to induce beta cell autoimmunity. A cell line susceptible to most enterovirus types was infected with EV isolates from cases of T1D and, for comparison, with a replication-competent strain of coxsackievirus B3. The transcription of immune-related genes and secretion of cytokines was evaluated in infected vs. uninfected cells. Acutely infected cells showed the preserved transcription of type I interferon (IFN) pathways and the enhanced transcription/secretion of IL6, IL8, LIF, MCP1, and TGFB1. On the other hand, infection by defective EV strains obtained from diabetic subjects suppressed IFN pathways and the transcription of most cytokines, while enhancing the expression of IL8, IL18, IL32, and MCP1. IL18 and IL32 are known for their pathogenic role in autoimmune diabetes. Thus, the cytokine profile of AV3 cells infected by diabetes-derived EV strains closely matches that observed in patients at the early stages of T1D. The concordance of our results with clinically verified information reinforces the hypothesis that the immune changes observed in type 1 diabetic patients are due to a hardly noticeable virus infection.
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Wang, Anna, Hongyan Guo, and Zaiqiu Long. "Integrative Analysis of Differently Expressed Genes Reveals a 17-Gene Prognosis Signature for Endometrial Carcinoma." BioMed Research International 2021 (July 14, 2021): 1–18. http://dx.doi.org/10.1155/2021/4804694.

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Endometrial carcinoma (EC) is the fifth widely occurring malignant neoplasm among women all over the world. However, there is still lacking efficacy indicators for EC’s prognosis. Here, we analyzed two databases including an RNA-sequencing-based TCGA dataset and a microarray-based GSE106191. After normalizing the raw data, we identified 114 common genes with upregulation and 308 common genes with downregulation in both the TCGA and GSE106191 databases. Bioinformatics analysis showed that the differently expressed genes in EC were related to the IL17 signaling pathway, PI3K-Akt signaling pathway, and cGMP-PKG signaling pathway. Furthermore, we performed the least absolute shrinkage and selection operator (LASSO) Cox regression analysis and generated a signature featuring 17 prognosis-related genes (MAL2, ANKRD22, METTL7B, IL32, ERFE, OAS1, TRPC1, SRPX, RAPGEF4, PSD3, SIMC1, TRPC6, WFS1, PGR, PAMR1, KCNK6, and FAM189A2) and found that it could predict OS in EC patients. The further analysis showed that OAS1, MAL2, ANKRD22, METTL7B, and IL32 were significantly upregulated in EC samples after comparison with normal samples. However, TRPC1, SRPX, RAPGEF4, PSD3, SIMC1, TRPC6, WFS1, PGR, PAMR1, KCNK6, and FAM189A2 were significantly downregulated in EC samples in comparison with normal samples. And correlation analysis showed that our results showed that the expressions of 17 prognosis-related hub genes were significantly correlated based on Pearson correlation. We here offer a newly genetic biomarker for the prediction of EC patients’ prognosis.
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Dissertations / Theses on the topic "IL32"

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Daga, Sergio. "CRISPR/Cas9 gene therapy on urine-derived-podocyte-lineage cells and novel biomarker identification: new perspectives in Alport Syndrome (ATS)." Doctoral thesis, Università di Siena, 2019. http://hdl.handle.net/11365/1072659.

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Alport syndrome (ATS) is an inherited genetic disorder characterized by glomerular basement membrane (GBM) abnormalities up to end-stage renal disease. Usually, in the most severe forms nephropathy is associated with involvement of eyes and ears because of COL4 chains expression being restricted to kidney, ear and eye. Podocytes, key component of the glomerular structure, are the only cells in the kidney able to produce the COLIVα3-α4-α5 heterotrimer and thus, they are extensively defined as key-players in the pathogenesis of the renal disease. We have demonstrated how it is possible to isolate podocyte-lineage cells from urines of ATS patients and healthy carriers, providing an easily available cell system closer to podocytes’ physiological conditions. Our cellular model represents a novel tool and it turned out to be useful not only to characterize the effect of spliceogenic intronic variants but also to identify the presence of cryptic mosaicism confined to the involved tissue and undetectable on peripheral blood samples. This finding dramatically increases the possibility to implement, theoretically with no limits, the molecular genetic test that we can offer to patients. On the basis of the RNA-Seq data analysis, we have investigated the involvement of IL-32 in ATS. Being convinced about the fundamental role of IL-32 in ATS, and confirming the real involvement of the IL-32/IL-6/IL-8 pathway in podocytes, we performed the most sensitive ELISA assay to detect IL-32 release into urines of ATS patients. Although no such generous amounts of IL-32 were found in the urines, the values found are reported as sufficient to define a peculiar activation of the IL-32 pathway and more in general inflammatory pathway definitely related to the disease. At the end, we have explored the innovative gene therapy approach, that we hope will be definitive in the treatment of the disease, directly on the affected cells isolated from patients, exploring the possibility of reverting collagen IV causative mutations in ATS injured podocytes. With this work and with the achieved results we have demonstrated that gene therapy through gene editing approach is not anymore an unexplored frontier, but it can become an increasingly convincing reality. Although preliminary, the achieved results demonstrate how it is possible to obtain a partial recovery of the causative COL4A3 and COL4A5 mutations, unbalancing the heterozygous state towards the wild type condition. All the results taken together will be fundamental to open new frontiers of management and treatment of the disorder, also in preclinical model, like in dog model through the use of easy-deliverable AAVs system.
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CARDILLO, MARTINA. "Expression of IL12 and IL23 receptors and cytokines in Chronic Lymphocytic Leukemia and normal B cells." Doctoral thesis, Università degli studi di Genova, 2021. http://hdl.handle.net/11567/1044948.

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The mechanisms of clonal expansion of CLL are only partially understood. Several interactions of neoplastic cells with accessory cells and cytokines potentially sustaining neoplastic B cell clone survival and proliferation have been described. Recently, a paracrine/autocrine loop has been reported, involving the upregulation of the IL23R complex and IL23 secretion by CLL cells. This loop drives CLL cell clonal expansion in vitro and in xenografted NSG mice. Furthermore, in situ observations on tissue sections demonstrate that infiltrating IL23 secreting CLL cells interact with macrophages and CD40L expressing T cells. Although inducible in vitro by co-culturing CLL cells with T cells or CD40L expressing cells, the IL23 loop is not observed following stimulation of CLL cells via surface Ig or contact with nurse like cells or bone marrow stromal cells. In this study, we investigated whether the IL23 loop could be induced following Toll-like receptor 9 (TLR9) engagement which influences leukemic cell survival, activation proliferation albeit in a heterogeneous manner. In addition, we explored the possible existence of an autocrine/paracrine loop mediated by IL12 which shares similarities and surface receptors with IL23 although with a likely opposite outcome in term of the possibility to sustain leukemic cell growth . IL23R and IL12R complexes (IL23R/IL12Rβ1, IL12β2/IL12Rβ1) expression were evaluated by flow-cytometry following stimulation with CpG oligodeoxynucleotide (ODN) that binds the TLR9 on CLL, showing that CLL cells are able to express the IL23R complex on membrane and, at lower extent, the IL12R complex. These receptors were assessed also in normal B cells by flow cytometry after 72h of stimulation with CpG and CpG+IL15. In this setting, normal B cells were less capable of IL23R complex expression compared to CLL cells. A further striking difference observed was related to the limited expression of IL12Rß2 receptor chain in stimulated CLL cells compared to normal B cells. Supernatants of CLL cells and normal B cells were both tested for the production of these cytokines after stimulation. The results showed a low level of IL23p19 secretion for both CLL cells and normal B cells, which is significant after CD40L stimulation (used as positive control), and a higher production of IL12p70 which is more pronounced in normal B cells compared to CLL. In another series of tests, CLL cells were stimulated with CpG for 72h, and subsequently exposed to IL12 or IL23. Exposure to IL12 and IL23 induced the expression of pSTAT1 and pSTAT3. Collectively our data corroborate the notion that IL23R complex act as a pro-survival factor for CLL cells. In contrast, the restricted IL12R complex expression in CLL cells compared to normal B cells indicated that the suppression of the expression of this receptor may favor the survival of the leukemic clones. The possibility of a reciprocal competition of the shared receptor chains is discussed.
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Pienaar, Sandra Margaret. "Tuberculosis and genes of the IL12/IL23/IFNγ pathway: Exploring functional significance of novel mutations in the IL12p40 promoter." Doctoral thesis, University of Cape Town, 2014. http://hdl.handle.net/11427/9534.

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The aim of this work was to screen the IL12p40 gene promoter for association with TB disease. Initially a subcohort of children (TB cases and healthy controls) from a TB-endemic area was screened for DNA changes by the WAVE method. Thereafter, the entire paediatric cohort and a cohort of healthy adult controls were screened by Amplification Refractory Mutation System PCR. Functional testing was done by reporter assay and immunological phenotype was investigated by measurement of cytokines levels and cytokine receptor expression. WAVE screening identified two heterozygous SNPs, -1523 A/G and -1564 C/T. Statistical analysis showed that -1523 A/G may be protective against TB disease (p=0.02). This possibility was supported by the location of -1523 A/G occurring within a GTATA sequence reported to bind nuclear proteins. Specific ARMS-PCR assays were then designed for screening of additional paediatric subjects and healthy adult controls for these SNPs. Analysis of the larger group, showed that -1564 C/T may contribute to susceptibility to TB disease (p=0.03) Exploring functional relevance, normal and mutant promoter fragments were PCR amplified, using uniquely adapted primers that included restriction sites corresponding to those in the multiple cloning site of an expression vector, facilitating cloning. A truncated promoter and one with essential regions deleted, were created as negative controls. These five promoter fragments were cloned into the expression vector and functional differences tested by reporter. No significant functional differences between variant and normal promoter fragments were observed. A predictive immune phenotype was investigated by measurement of IFNγ, TNFα and IL12p70 cytokine levels and IL12βR1 receptor expression. While distinct patterns of cytokine responses were seen, these did not predict genotype. These results show that the IL12p40 gene promoter is highly conserved and sequence variants may be just one of many factors contributing to TB susceptibility.
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Perri, Graziela. "Presença de IL33 em amostras de carcinoma espinocelular." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/25/25149/tde-30032017-213204/.

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O carcinoma espinocelular (CEC) é a segunda forma de neoplasia cutânea mais prevalente. Os mecanismos exatos envolvidos na progressão desse tipo de tumor ainda não estão elucidados. Estudos recentes têm mostrado que a citocina IL33 é uma citocina reguladora da resposta imune adaptativa, principalmente como potente indutor do perfil Th2. Juntamente com seu receptor ST2, apresenta-se com os níveis elevados em alguns tipos de câncer, corroborando para a evidência de que essa citocina contribui para a carcinogênese. Baseado nessas informações, testamos a hipótese de que a presença de IL33 em carcinoma espinocelular, poderia estar relacionada a um melhor prognóstico. Neste estudo foram utilizadas amostras de carcinoma espinocelular, em diferentes gradações de malignidade tumoral (Grau I, Grau II e Grau III). Os resultados mostraram um infiltrado inflamatório mais intenso em tumores com Grau I e II. Imunorreatividade para IL33 foi observada em tumores de Grau I e II tanto por células epiteliais como por células do infiltrado inflamatório. A análise por microscopia confocal evidenciou que um grande número de células TCD4+ e TCD8+ que expressavam IL33 foi observado em tumores de Grau II. Esses resultados indicam a presença de um intenso infiltrado inflamatório e expressão de IL33 em amostras de carcinoma espinocelular com níveis menores de malignidade tumoral.
Squamous cell carcinoma (SCC) is the second most common form of cutaneous neoplasm. The exact mechanisms involved in the progression of this type of tumor have not yet been elucidated. Recent studies have shown that the cytokine IL33 is a cytokine regulating the adaptive immune response, mainly as a potent inducer of Th2 profile. Together with its ST2 receptor, its presents with elevated levels in some types of cancer, corroborating to evidence that this cytokine contributes to carcinogenesis. Based on this information, we tested the hypothesis that the presence of IL33 in squamous cell carcinoma could be related to a better prognosis. In this study, squamous cell carcinoma samples were used in three different gradations of tumor malignancy (Grade I, Grade II and Grade III). The results showed that a more intense inflammatory infiltrate in Grade I and II tumors. Immunoreactivity for IL33 was observed in Grade I and Grade II tumor, by epithelial cells and by inflammatory infiltrate cells. The analysis by confocal microscopy evidenced that a great number of TCD8+ and TCD4+ cells expressing IL33 was observed in grade II tumors. These results indicate the presence of an intense inflammatory infiltrate and expression of IL33 in samples of squamous cell carcinoma with lower levels of tumor malignancy.
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Ruiz, Castilla Mireia. "Paper de l’eix IL33/ST2 en el pacient cremat." Doctoral thesis, Universitat Autònoma de Barcelona, 2018. http://hdl.handle.net/10803/665727.

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La lesió per cremada s’ha associat a l’augment de la concentració de molts mediadors inflamatoris. Aquests mediadors són importants en la fisiopatologia de la cremada, contribuint a la disfunció orgànica i l’aparició de complicacions sèptiques. També són útils en l’establiment del pronòstic i són importants en la fisiopatologia de situacions concretes com la cicatrització o la lesió per inhalació de fums. En conseqüència, alguns d’aquests biomarcadors també podrien ser considerats com a possibles dianes terapèutiques. Igualment, com que els tractaments també poden afectar els processos biològics, els biomarcadors poden ser útils per guiar l’ús de determinats tractaments i podrien ajudar a explicar perquè alguns tractaments no són útils a l’hora de millorar el pronòstic de determinats pacients. Per tant, la investigació en biomarcadors és una característica principal de la medicina translacional d’aquesta àrea de coneixement. La present tesi té l’objectiu de valorar la utilitat en la determinació del pronòstic dels pacients cremats dels biomarcadors implicats en l’eix IL33/ST2. De fet, es tracta del primer article que analitza la significació pronòstica d’aquests biomarcadors en pacients cremats i els resultats obtinguts demostren la relació existent entre la concentració de la fracció soluble de la proteïna supressió de la tumorigenicitat 2 (sST2) i la mortalitat d’aquests pacients. A més a més, nivells elevats de sST2 també es van associar a una major incidència de complicacions infeccioses i de disfunció orgànica, suggerint que podria tenir un paper significatiu en la gènesi de la disfunció orgànica associada a la cremada. Per tots aquests motius, la mesura de la concentració de sST2 podria, en un futur, ajudar en el procés de presa de decisions sobre el tractament indicat en cada pacient ja que ens permetria saber quins són els pacients amb més alt risc de patir una mala evolució i que, per tant, es podrien beneficiar d’un tractament més agressiu.
Several inflammatory mediators have been shown to be increased after burn injury. They may be important in burn pathophysiology, contributing to organ dysfunction and sepsis apparition, and they may also predict outcomes. Moreover, they have been involved in pathophysiology of some special processes, such as inhalation injury or wound healing. Consequently, some biomarkers have been described as potential therapeutic targets. Importantly, as therapeutic interventions may also affect biological processes, biomarkers may be a useful tool to guide some treatments and may also explain why some treatments succeed or fail in improving outcomes. Therefore, investigation into biomarkers in severe burn patients is a key feature of translational medicine in this area of knowledge. Our aim was to analyze whether plasma levels of biomarkers involved in the IL33/ST2 axis might help to predict mortality in burn patients. This is the first study to show the prognostic significance of plasma levels of sST2 after burn injury. Indeed, higher plasma concentrations of sST2 were consistently associated with a higher risk of death, even after adjusting for different potential confounding. Moreover, higher levels of sST2 were also observed in burn patients who developed any infectious complication during their stay in the Burns Unit as well as in patients who presented MODS. In conclusion, the results of this study suggest that plasma sST2 levels predict mortality in burn patients and may be useful to help or guide physicians in the bedside decision-making process during patient management.
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Verma, Akash. "Unraveling the IL4-IL33 Nexus in Histoplasma Capsulatum Infection." University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1406898828.

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Ferrasi, Adriana Camargo [UNESP]. "Transcript finishing initiative: contribuição do laboratório IL2." Universidade Estadual Paulista (UNESP), 2003. http://hdl.handle.net/11449/87745.

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Made available in DSpace on 2014-06-11T19:23:00Z (GMT). No. of bitstreams: 0 Previous issue date: 2003-02-25Bitstream added on 2014-06-13T20:49:45Z : No. of bitstreams: 1 ferrasi_ac_me_rcla.pdf: 2629180 bytes, checksum: c178eeb179f2c77ab45bfcddeb648f51 (MD5)
O principal objetivo na análise de um genoma é a identificação gênica. Várias ferramentas computacionais estão disponíveis para este propósito e são baseadas em similaridade (BLAST e BLAT) ou em predição de genes (Genscan e Fgenes). Entretanto, estes programas estão se mostrando ineficientes para detectar e caracterizar todos os genes presentes no genoma humano. A importância das informações de cDNAs tem sido reconhecida desde o início do Projeto Genoma Humano, entretanto, o seqüenciamento em larga escala de cDNAs completos ainda requer técnicas avançadas tais como a produção de bibliotecas de cDNAs enriquecidas por transcritos grandes e raros. O seqüenciamento parcial de etiquetas de seqüências expressas (ESTs) foi desenvolvido como uma técnica alternativa para gerar, em larga escala, vários tipos de cDNAs. Atualmente, a maioria das informações de cDNAs no GenBank são representadas por ESTs convencionais 3þ e 5þ e ORESTES (provenientes das porções centrais dos transcritos). Baseados nos bancos de dados gerados pelo alinhamento de todas essas seqüências com as seqüências genômicas humanas disponíveis foi proposta a estratégia transcript finishing para a caracterização e validação de novos genes humanos, como parte do consórcio entre FAPESP e Instituto Ludwig de Pesquisa sobre o Câncer. O projeto Transcript Finishing Initiative está sendo realizado por uma rede de 31 diferentes grupos de pesquisa do Estado de São Paulo. Foram selecionados pela coordenação do projeto, 602 transcritos e destes 300 (50%) foram validados. Destes transcritos, 20 foram atribuídos ao laboratório validador IL2, e destes, 11 (55%) foram validados. Utilizando ferramentas de bioinformática, o laboratório IL2 realizou uma anotação preliminar dos consensos de seus transcritos validados (disponibilizados pela coordenação do projeto)... .
A fundamental task in analyzing genome is gene identification. This is relatively straightforward for compact genome but much more challenging for complex genomes. Some computational tools are available for this purpose, but they are bases on similarity (BLAST) or prediction analysis (Genscan and Fgenes). However, these programs are inefficient to detect and characterize all genes present in the genome. The importance of cDNA information has been recognized since the beginning of the Human Genome Project, however cost-effective and hightroughput sequencing of full-length cDNA still requires technical advances such as the production of cDNA libraries enriched for large and rare transcripts. Partial sequencing of expressed sequences (EST) has been developed as an alternative approach for the generation, in large-scale, of several kinds of cDNAs. Currently, the vast majority of cDNA data in the GenBank is represented both by conventional 5þand 3þexpressed sequence tags (ESTs) and by ORESTES (open reading frame ESTs), which is derived from central portions of the transcripts. Based on a database generated through alignment of all of these sequences to the available human genomic sequences, have been proposed the transcript finishing strategy for characterization and validation of new human genes, as part of the FAPESP-LICR Transcript Finishing Initiative. The strategy utilizes the ORESTES scaffold EST sequence to build primers for reverse transcription (RT) - PCR reactions in order to bridge gaps, thereby confirming the membership of ESTs to a common transcript and providing information on the intervening sequence (validation strategy). The FAPESP-LICR Transcript Finishing Initiative is being pursed by a network of 31 different research groups from the State of São Paulo (The Transcript Finishing Consortium) coordinated by 2 different laboratories... (Complete abstract click electronic address below).
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Ferrasi, Adriana Camargo. ""Transcript finishing initiative" : contribuição do laboratório IL2 /." Rio Claro : [s.n.], 2003. http://hdl.handle.net/11449/87745.

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Orientador: Maria Inês de Moura Campos Pardini
Banca: Maurício Bacci Junior
Banca: Magaly Machado Sales
Resumo: O principal objetivo na análise de um genoma é a identificação gênica. Várias ferramentas computacionais estão disponíveis para este propósito e são baseadas em similaridade (BLAST e BLAT) ou em predição de genes (Genscan e Fgenes). Entretanto, estes programas estão se mostrando ineficientes para detectar e caracterizar todos os genes presentes no genoma humano. A importância das informações de cDNAs tem sido reconhecida desde o início do Projeto Genoma Humano, entretanto, o seqüenciamento em larga escala de cDNAs completos ainda requer técnicas avançadas tais como a produção de bibliotecas de cDNAs enriquecidas por transcritos grandes e raros. O seqüenciamento parcial de etiquetas de seqüências expressas (ESTs) foi desenvolvido como uma técnica alternativa para gerar, em larga escala, vários tipos de cDNAs. Atualmente, a maioria das informações de cDNAs no GenBank são representadas por ESTs convencionais 3þ e 5þ e ORESTES (provenientes das porções centrais dos transcritos). Baseados nos bancos de dados gerados pelo alinhamento de todas essas seqüências com as seqüências genômicas humanas disponíveis foi proposta a estratégia "transcript finishing" para a caracterização e validação de novos genes humanos, como parte do consórcio entre FAPESP e Instituto Ludwig de Pesquisa sobre o Câncer. O projeto "Transcript Finishing Initiative" está sendo realizado por uma rede de 31 diferentes grupos de pesquisa do Estado de São Paulo. Foram selecionados pela coordenação do projeto, 602 transcritos e destes 300 (50%) foram validados. Destes transcritos, 20 foram atribuídos ao laboratório validador IL2, e destes, 11 (55%) foram validados. Utilizando ferramentas de bioinformática, o laboratório IL2 realizou uma anotação preliminar dos consensos de seus transcritos validados (disponibilizados pela coordenação do projeto)... (Resumo completo, clicar acesso eletrônico abaixo).
Abstract: A fundamental task in analyzing genome is gene identification. This is relatively straightforward for compact genome but much more challenging for complex genomes. Some computational tools are available for this purpose, but they are bases on similarity (BLAST) or prediction analysis (Genscan and Fgenes). However, these programs are inefficient to detect and characterize all genes present in the genome. The importance of cDNA information has been recognized since the beginning of the Human Genome Project, however cost-effective and hightroughput sequencing of full-length cDNA still requires technical advances such as the production of cDNA libraries enriched for large and rare transcripts. Partial sequencing of expressed sequences (EST) has been developed as an alternative approach for the generation, in large-scale, of several kinds of cDNAs. Currently, the vast majority of cDNA data in the GenBank is represented both by conventional 5þand 3þexpressed sequence tags (ESTs) and by ORESTES (open reading frame ESTs), which is derived from central portions of the transcripts. Based on a database generated through alignment of all of these sequences to the available human genomic sequences, have been proposed the transcript finishing strategy for characterization and validation of new human genes, as part of the FAPESP-LICR Transcript Finishing Initiative. The strategy utilizes the ORESTES scaffold EST sequence to build primers for reverse transcription (RT) - PCR reactions in order to bridge gaps, thereby confirming the membership of ESTs to a common transcript and providing information on the intervening sequence (validation strategy). The FAPESP-LICR Transcript Finishing Initiative is being pursed by a network of 31 different research groups from the State of São Paulo (The Transcript Finishing Consortium) coordinated by 2 different laboratories... (Complete abstract click electronic address below).
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Nicol, Louise Maureen Marie. "Investigating differential T cell polarization in the two pathological forms of sheep paratuberculosis." Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/22855.

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Paratuberculosis is a chronic enteropathy of ruminants that presents as two distinct disease forms in sheep; paucibacillary (or tuberculoid) and multibacillary (or lepromatous) disease. The immunopathology of paucibacillary and multibacillary sheep paratuberculosis has been linked to inflammatory Th1/Th17 cell and Th2/macrophage responses respectively. IL23 and IL25 are key to the development of these responses by interaction with their complex receptors, IL23R/IL12RB1 and IL17RA/IL17RB. Furthermore, the polarization of T cells and the development of appropriate immune responses is controlled by the master regulator transcription factor; T-bet, GATA3, RORγt and RORα. In humans, variations in the structure, sequence and/or expression of the genes encoding these proteins have been implicated in the different pathological forms of tuberculosis and leprosy, and gastrointestinal inflammatory disorders such as Crohn’s disease. In the current study, sequencing has identified multiple transcript variants of sheep IL23R, IL12RB1 and IL17RB and a single IL17RA transcript. RT-qPCR assays were developed for the cytokine receptor variants identified in this study and known transcript variants of the transcription factor genes. Expression levels were compared in the ileo cecal lymph node of paucibacillary or multibacillary paratuberculosis diseased sheep. Of the cytokine receptors; the IL12RB1v3 variant, which lacks the receptor activation motif, was differentially expressed and was significantly increased in multibacillary disease; this may contribute to high Th2 responses. Full length IL17RB was differentially expressed and was significantly increased in multibacillary pathology, which may also contribute to Th2 polarization. IL17RA was significantly increased in paucibacillary disease. The contrast between the IL17RA and IL17RB results may indicate that, in addition to Th1 cells, Th17 T cells are also involved in paucibacillary pathology. Of the transcription factor transcripts; full length TBX21 (T-bet) was differentially expressed and was significantly increased in paucibacillary disease; this may explain increased Th1 responses in these sheep. Full length GATA3 was significantly increased in paucibacillary compared to multibacillary sheep, suggesting a loss of Th2 responses in late-stage multibacillary pathology. RORAv1 variant was differentially expressed and was significantly increased in paucibacillary pathology, indicating a role of Th17 T cells in paucibacillary pathology.
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Geremia, Alessandra. "The role of the IL23/IL17 pathway in inflammatory bowel disease." Thesis, University of Oxford, 2011. http://ora.ox.ac.uk/objects/uuid:f39c2ab5-098e-45d8-a800-e4c4bc7ae85f.

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The aetiology of IBD is unknown, but available evidence suggests that an aberrant immune response towards the commensal microbial flora is responsible for intestinal inflammation in genetically susceptible individuals. Studies from animal models of intestinal inflammation have greatly advanced our understanding of the immunological basis of IBD. However, translation of results from animal research into human studies is essential in order to improve treatment options and patient quality of life. In this thesis we present the successful introduction of translational studies on human tissue in our laboratory. In particular, we evaluated the role of the IL23/IL17 pathway in the human immune response and its role in IBD. IL23-driven inflammation has been primarily linked to its activity on Th-17 cells; however, work from our laboratory has identified a novel population of IL23-responsive ILC, which are responsible for innate colitis in mice. Here we have analyzed the role of IL23-responsive innate cells in IBD. Our results show increased expression of Th-17 signature genes amongst intestinal CD3- cells in patients with IBD. Furthermore, we observed a marked and selective increase in IL17 producing CD56- ILC in the inflamed intestine of patients with CD. ILC may contribute to intestinal inflammation through secretion of cytokines, such as IL17A and IL17F, and recruitment of other inflammatory cells, representing a novel tissue-specific target for the treatment of IBD. In addition, we present here our preliminary data on the characterization of human intestinal and systemic DC populations. In particular, we aimed to evaluate if in the context of the intestinal microenvironment DC develop specific regulatory features, as observed in murine CD103+ DC. We show that human intestinal DC populations exhibit specific regulatory properties, such as expression of genes associated with TGF-β and RA activity. Furthermore, CD103+ DC are present in the human gut and are characterized by tolerogenic markers. Remarkably, patients with IBD have reduced frequencies of intestinal CD103+ DC, which display a more pro-inflammatory phenotype. Alteration in DC subset composition and functional activity may result in a distort balance between immune effector and regulatory responses, promoting the development of intestinal inflammation.
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Books on the topic "IL32"

1

Universität Stuttgart. Institut für Leichte Flächentragwerke. IL39: Ungeplante siedlungen : charakteristische merkmale - wegesystem, flächenteilung = IL39 : non-planned settlements : characteristic features - path system, surface subdivision. Edited by Schaur Eda. Stuttgart: Institut für leichte Flächentragwerke, 1992.

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Helmcke, Johann-Gerhard. IL38: Diatomeen II : Schalen in Natur und Technik = IL38 : Diatoms I I : Shells in nature and technics III. Stuttgart: Institut für Leichte Flächentragwerke, Universität Stuttgart, 2004.

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-Th, Raepsaet-Charlier M., and Deman A, eds. Nouveau recueil des inscriptions latines de Belgique (ILB2). Bruxelles: Editions Latomus, 2002.

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Zhang, Nan. Role of IL2-induced tyrosine phosphorylation in T cell proliferation. Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1991.

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Flächentragwerke, Universität Stuttgart Institut für Leichte. IL35: Pneu und knochen : Johann-Gerhard Helmcke gewidmet(3/5/1908 - 18/7/1993 = IL35 : pneu and bone : dedicated to Johann-Gerhard Helmcke 3/5/1908 - 18/7/1993. Stuttgart: The Institute, 1995.

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Otto, Frei. IL23: Konstruktion : form, kraft, masse 3 : ein vorschlag zur ordnung und beschreibung von konstruktionen von Frei Otto = Structure : form, force, mass 3 : a proposal for the classification and description of structures by Frei Otto. Stuttgart: Institut fur leichte flachentragwerke, 1992.

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Tomlow, Jos. IL34: Das Modell : Antoni Gaudis Hängemodell und seine Rekonstruktion - neue Erkenntnisse zum Entwurf für die Kirche derColonia Güell = The model : Antoni Gaudi's hanging model and its reconstruction - new light on the design of the church of Colonia Güell. Stuttgart: Institut für leichte Flächentragwerke, 1989.

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Ilr2 - Hungry Bugs. ticktock Media Ltd, 2009.

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Ilyushin Il2. Midland Publishing, 2010.

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Ilr2 Fh - Amazing Planes. TickTock Books, 2008.

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Book chapters on the topic "IL32"

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Bleackley, R. Chris, Corrinne G. Lobe, Calliopi Havele, Jennifer Shaw, Bill Pohajdak, and Mark Redmond. "Life after IL2." In Molecular Basis of Lymphokine Action, 233–44. Totowa, NJ: Humana Press, 1987. http://dx.doi.org/10.1007/978-1-4612-4598-8_22.

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Blaise, D., A. M. Stoppa, M. Attal, J. Reiffers, J. Fleury, M. Michallet, E. Archimbaud, R. Bouabdallah, J. A. Gastaut, and D. Maraninchi. "IL2 in Acute Leukemia." In Acute Leukemias V, 274–78. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-78907-6_46.

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Maloy, Kevin J. "The IL23-Th17 Axis in Intestinal Inflammation." In Molecular Genetics of Inflammatory Bowel Disease, 219–40. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-8256-7_11.

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Hombach, Andreas A., and Hinrich Abken. "Antibody-IL2 Fusion Proteins for Tumor Targeting." In Antibody Engineering, 611–26. Totowa, NJ: Humana Press, 2012. http://dx.doi.org/10.1007/978-1-61779-974-7_34.

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Sparkes, B. G., J. A. Teodorczyk-Injeyan, W. J. Peters, and R. E. Falk. "Mediators Affecting IL2 Function in Burn Immunosuppression." In Lipid Mediators in the Immunology of Shock, 337–47. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-0919-2_37.

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Xu, Hui, and Meihong Deng. "Identification of ILC2 in the Lung Using Flow Cytometry." In Methods in Molecular Biology, 161–68. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1488-4_14.

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Dibra, Denada, and Shulin Li. "Role of IL12 Family in Regulation of Antitumor Immune Response." In Targeted Cancer Immune Therapy, 3–18. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0170-5_1.

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Wolowczuk, Isabelle, Benjamin Pariente, Matthieu Allez, and Mathias Chamaillard. "IL17 and/or IL22 as Potential Target(s) for Crohn’s Disease." In IL-17, IL-22 and Their Producing Cells: Role in Inflammation and Autoimmunity, 273–85. Basel: Springer Basel, 2012. http://dx.doi.org/10.1007/978-3-0348-0522-3_20.

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Ochoa, A. C., G. Gromo, S. L. Wee, and F. H. Bach. "Regulation of Lytic Function by Recombinant IL2 and Antigen." In Current Topics in Microbiology and Immunology, 155–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 1986. http://dx.doi.org/10.1007/978-3-642-71152-7_19.

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Paetkau, Verner, Jennifer Shaw, John Elliott, Bill Pohajdak, and Karen Meerovitch. "Regulation of IL2 and Related Genes at the mRNA Level." In Molecular Basis of Lymphokine Action, 181–91. Totowa, NJ: Humana Press, 1987. http://dx.doi.org/10.1007/978-1-4612-4598-8_17.

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Conference papers on the topic "IL32"

1

Truglia, S., C. Alessandri, F. Ciccia, A. Rizzo, T. Colasanti, F. Miranda, FR Spinelli, et al. "OP0299 Serum and glomerular expression of IL32 in lupus nephritis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.5277.

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Smirnova, Svetlana, Marina Smolnikova, and Sergey Tereshchenko. "IL13, IL31 and IL33 gene polymorphisms in moderate-to-severe asthma in Siberian children." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.2044.

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Morante, Roser, and Bertjan Busser. "ILK2." In the 4th International Workshop. Morristown, NJ, USA: Association for Computational Linguistics, 2007. http://dx.doi.org/10.3115/1621474.1621512.

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Portelli, Michael, Matthew Edwards, Maria Ketelaar, Cheng-Jian Xu, Joshua Hoffman, David Mayhew, Ian Hall, et al. "IL33 receptor activation is IL33 isoform and receptor genotype specific." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa5403.

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Van Geffen, E., A. van Caam, C. Thudium, A. C. Bay-Jensen, E. Blaney Davidson, and P. van der Kraan. "AB0092 Il37 inhibits proteoglycan loss in human oa cartilage: link between il37 and mmp3." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.6332.

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Caam, Arjan van, Ellen van Geffen, Joyce Aarts, Elly Vitters, Esmeralda Blaney Davidson, and Peter van der Kraan. "FRI0526 IL37 AMELIORATES EXPERIMENTAL MURINE OSTEOARTHRITIS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.7483.

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Goldsteen, Pien A., L. Van Der Koog, L. E. M. Kistemaker, Y. S. Prakash, B. Ditz, M. Van Den Berge, G. H. Koppelman, M. C. Nawijn, A. M. Dolga, and R. Gosens. "IL33 regulates airway neuronal plasticity in vitro." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.5035.

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Faiz, A., F. S. Boedijono, W. Timens, M. Nawijn, P. M. Hansbro, R. Mahbub, M. D. Johansen, et al. "The regulation of IL33 following smoking cessation." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.3314.

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Howard, C., D. C. Decker, K. M. Blaine, I. A. Swanson, D. F. Camacho, M. Nobrega, and A. I. Sperling. "Negative Human IL33 Regulation in Lung Endothelium During Allergic Inflammation Is Dependent on a 5kB Upstream Region in the IL33 Locus." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1054.

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Lajunen, Taina K., Jouni J. K. Jaakkola, and Maritta S. Jaakkola. "Interleukin 33(IL33) polymorphisms associate with incident adult-onset asthma." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.oa1457.

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