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Journal articles on the topic 'IL-10 deficiency'

Author: Grafiati

Published: 1 April 2023

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1

Asadullah, K., K. Stephanek, M. Leupold, et al. "Relative IL-10 deficiency and effects of IL-10 therapy in psoriasis." Journal of Dermatological Science 16 (March 1998): S30. http://dx.doi.org/10.1016/s0923-1811(98)83173-3.

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2

Wan, Xin, Wen Juan Huang, Wen Chen, et al. "IL-10 Deficiency Increases Renal Ischemia-Reperfusion Injury." Nephron Experimental Nephrology 128, no. 1-2 (2014): 37–45. http://dx.doi.org/10.1159/000366130.

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3

Hennessy, A., H. L. Pilmore, L. A. Simmons, and D. M. Painter. "A Deficiency of Placental IL-10 in Preeclampsia." Journal of Immunology 163, no. 6 (1999): 3491–95. http://dx.doi.org/10.4049/jimmunol.163.6.3491.

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Abstract Accommodation of the fetoplacental unit in human pregnancy requires maternal immune tolerance to this “semiallograft”. Local antiplacental immunity is modified by synthesis of uncommon histocompatibility Ags (e.g., HLA-G), growth factors, and cytokines by the placenta. Placental interleukins have been identified in reproductive tissues, but their roles in adaptive maternal immunity and determining term pregnancy outcomes have not been fully clarified. This study examined the distribution of IL-10 and TNF-α staining in term placentas. Women with proteinuric hypertension (PE, n = 10) we

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4

Zigmond, Ehud, Biana Bernshtein, Gilgi Friedlander, et al. "Macrophage-Restricted Interleukin-10 Receptor Deficiency, but Not IL-10 Deficiency, Causes Severe Spontaneous Colitis." Immunity 40, no. 5 (2014): 720–33. http://dx.doi.org/10.1016/j.immuni.2014.03.012.

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5

Jones, Steven P., Steven D. Trocha, and David J. Lefer. "Cardioprotective actions of endogenous IL-10 are independent of iNOS." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 1 (2001): H48—H52. http://dx.doi.org/10.1152/ajpheart.2001.281.1.h48.

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Myocardial ischemia-reperfusion (I/R) is a well-known stimulus for acute inflammatory responses that promote cell death and impair pump function. Interleukin-10 (IL-10) is an endogenous, potent anti-inflammatory cytokine. Recently, it has been proposed that IL-10 inhibits inducible nitric oxide synthase (iNOS) activity after myocardial I/R and consequently exerts cardioprotective effects. However, whether this actually occurs remains unclear. To test this hypothesis, we utilized iNOS-deficient (−/−), IL-10 −/−, and IL-10/iNOS −/− mice to examine the potential mechanism of IL-10-mediated cardio

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6

Gunnett, Carol A., Donald D. Heistad, Daniel J. Berg, and Frank M. Faraci. "IL-10 deficiency increases superoxide and endothelial dysfunction during inflammation." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 4 (2000): H1555—H1562. http://dx.doi.org/10.1152/ajpheart.2000.279.4.h1555.

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Little is known about the role of interleukin-10 (IL-10), an anti-inflammatory cytokine, in blood vessels. We used IL-10-deficient mice (IL-10 −/−) to examine the hypothesis that IL-10 protects endothelial function after lipopolysaccharide (LPS) treatment. The responses of carotid arteries were studied in vitro 6 h after injection of a relatively low dose of LPS (10 μg ip). In IL-10 −/− mice, the maximum relaxation to ACh (3 μM) was 56 ± 6% (means ± SE) after LPS injection and 84 ± 4% after vehicle injection ( P < 0.05). Thus endothelium-dependent relaxation was impaired in carotid arteries

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7

Wang, B., L. Zhuang, H. Fujisawa, and D. N. Sauder. "Effect of IL-10 deficiency on the migration of epidermal Langerhans cells in IL-10 null mice." Journal of Dermatological Science 16 (March 1998): S90. http://dx.doi.org/10.1016/s0923-1811(98)83537-8.

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8

Zhang, Guag-Xian, Fang Zhou, Bogoljub Ciric, et al. "Ability of LPS to regulate expression of tolerance-related molecules on dendritic cells is blocked by IL-10 deficiency (48.18)." Journal of Immunology 188, no. 1_Supplement (2012): 48.18. http://dx.doi.org/10.4049/jimmunol.188.supp.48.18.

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Abstract Interleukin-10 (IL-10) is an anti-inflammatory cytokine that plays an important role in regulating the local inflammatory immune response, but regulatory mechanisms of this cytokine have not been fully elucidated. Here we demonstrate that IL-10 deficiency renders LPS treatment ineffective in regulating expression of CD40, CD80, CD86, B7-H2 and B7-DC on dendritic cells (DCs) and blocks up-regulation of IL-27. This inability to respond to LPS was found in both IL-10-/- bone marrow-derived and splenic DCs. Compared to wild type DCs, IL-10-/- DCs expressed similar levels of TLR4 and CD14,

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9

Pérez-de Puig, Isabel, Francesc Miró, Angélica Salas-Perdomo, et al. "IL-10 Deficiency Exacerbates the Brain Inflammatory Response to Permanent Ischemia without Preventing Resolution of the Lesion." Journal of Cerebral Blood Flow & Metabolism 33, no. 12 (2013): 1955–66. http://dx.doi.org/10.1038/jcbfm.2013.155.

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Stroke induces inflammation that can aggravate brain damage. This work examines whether interleukin-10 (IL-10) deficiency exacerbates inflammation and worsens the outcome of permanent middle cerebral artery occlusion (pMCAO). Expression of IL-10 and IL-10 receptor (IL-10R) increased after ischemia. From day 4, reactive astrocytes showed strong IL-10R immunoreactivity. Interleukin-10 knockout (IL-10 KO) mice kept in conventional housing showed more mortality after pMCAO than the wild type (WT). This effect was associated with the presence of signs of colitis in the IL-10 KO mice, suggesting tha

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10

Marco, Roberto Di, Ming Xiang, Paola Zaccone, et al. "Concanavalin A-induced Hepatitis in Mice is Prevented by Interleukin (IL)-10 and Exacerbated by Endogenous IL-10 Deficiency." Autoimmunity 31, no. 2 (1999): 75–83. http://dx.doi.org/10.3109/08916939908994050.

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11

Thaxton, Jessica E., Roberto Romero, and Surendra Sharma. "TLR9 Activation Coupled to IL-10 Deficiency Induces Adverse Pregnancy Outcomes." Journal of Immunology 183, no. 2 (2009): 1144–54. http://dx.doi.org/10.4049/jimmunol.0900788.

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12

Bristol, Ian J., Mark A. Farmer, Yingzi Cong, et al. "Heritable Susceptibility for Colitis in Mice Induced by IL-10 Deficiency." Inflammatory Bowel Diseases 6, no. 4 (2000): 290–302. http://dx.doi.org/10.1097/00054725-200011000-00006.

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13

Bristol, Ian J., Mark A. Farmer, Yingzi Cong, et al. "Heritable susceptibility for colitis in mice induced by IL-10 deficiency." Inflammatory Bowel Diseases 6, no. 4 (2000): 290–302. http://dx.doi.org/10.1002/ibd.3780060407.

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14

Li, Qing-Ya, Zhi-Zhong Guo, Jian Liang, et al. "Interleukin-10 Genotype Correlated to Deficiency Syndrome in Hepatitis B Cirrhosis." Evidence-Based Complementary and Alternative Medicine 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/298925.

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Traditional Chinese medicine (TCM) syndrome is an important basis for TCM diagnosis and treatment. As Child-Pugh classification as well as compensation and decompensation phase in liver cirrhosis, it is also an underlying clinical classification. In this paper, we investigated the correlation between single nucleotide polymorphisms (SNPs) of Interleukin-10 (IL-10) and TCM syndromes in patients with hepatitis B cirrhosis (HBC). Samples were obtained from 343 HBC patients in China. Three SNPs of IL-10 (−592A/C, −819C/T, and −1082A/G) were detected with polymerase chain-reaction-ligase detection

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15

Landuyt, Ashley E., Barbara J. Klocke, Lennard W. Duck, et al. "ICOS ligand and IL-10 synergize to promote host–microbiota mutualism." Proceedings of the National Academy of Sciences 118, no. 13 (2021): e2018278118. http://dx.doi.org/10.1073/pnas.2018278118.

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Genome-wide association studies have identified ICOSLG, which encodes the inducible costimulator ligand (ICOSLG or ICOSL) as a susceptibility locus for inflammatory bowel disease. ICOSL has been implicated in the enhancement of pattern recognition receptor signaling in dendritic cells, induction of IL-10 production by CD4 T cells, and the generation of high-affinity antibodies to specific antigens—all of which can potentially explain its involvement in gastrointestinal inflammation. Here, we show that murine ICOSL deficiency results in significant enrichment of IL-10–producing CD4 T cells part

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16

Rong, Heng-Mo, Xiao-Jun Qian, Chao Zhang, Ting Li, and Zhao-Hui Tong. "IL-17 Inversely Correlated with IL-10 via the STAT3 Gene in Pneumocystis-Infected Mice." Mediators of Inflammation 2019 (September 10, 2019): 1–12. http://dx.doi.org/10.1155/2019/6750861.

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Background. Pneumocystis pneumonia (PCP) remains a common opportunistic infection in immunosuppressed individuals. Current studies showed that multiple immune cells and cytokines took part in the host defense against Pneumocystis (PC). However, the roles of IL-17 and IL-10 in the development of PCP have not been elucidated. Methods. IL-10 and IL-17 levels in serum from PCP mice were detected via ELISA. The percentages of B10 cells, IL-10+ macrophages, and IL-10+ T cells in the lung from IL-17–/– PCP mice and Th17 cells and IL-17+γδT cells in IL-10–/– PCP mice were examined via flow cytometry.

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17

Roers, Axel, Lisa Siewe, Elke Strittmatter, et al. "T Cell–specific Inactivation of the Interleukin 10 Gene in Mice Results in Enhanced T Cell Responses but Normal Innate Responses to Lipopolysaccharide or Skin Irritation." Journal of Experimental Medicine 200, no. 10 (2004): 1289–97. http://dx.doi.org/10.1084/jem.20041789.

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Interleukin (IL)-10 is a regulator of inflammatory responses and is secreted by a variety of different cell types including T cells. T regulatory cells have been shown to suppress immune responses by IL-10–dependent, but also IL-10–independent, mechanisms. Herein, we address the role of T cell–derived IL-10 in mice with an inactivation of the IL-10 gene restricted to T cells generated by Cre/loxP-mediated targeting of the IL-10 gene. Splenocytes from this T cell–specific mutant secrete increased amounts of proinflammatory cytokines after activation in vitro compared with show enhanced contact

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18

Neven, Benedicte, Emilie Mamessier, Julie Bruneau, et al. "A Mendelian Predisposition to B Cell Lymphoma Caused by IL-10R2 Deficiency." Blood 120, no. 21 (2012): 5092. http://dx.doi.org/10.1182/blood.v120.21.5092.5092.

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Abstract Abstract 5092 Background The fact that monogenic interleukin (IL)-10 and IL-10 receptor deficiencies cause very early-onset, severe inflammatory bowel disease demonstrates the IL-10 pathway's crucial role in preventing microbiota-driven gut inflammation. However, no other severe complications of IL-10/IL-10R deficiencies have been reported to date. Methods A cohort of six patients with IL-10/IL-10R deficiency was retrospectively surveyed for phenotypic expression. The identification of a number of cases of lymphoma prompted an in-depth characterization of available biopsy material, wi

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19

Pini, Maria, Melissa E. Gove, Raja Fayad, Robert J. Cabay, and Giamila Fantuzzi. "Adiponectin deficiency does not affect development and progression of spontaneous colitis in IL-10 knockout mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 296, no. 2 (2009): G382—G387. http://dx.doi.org/10.1152/ajpgi.90593.2008.

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The goal of this study was to investigate the role of the adipokine adiponectin (APN) in development of spontaneous colitis in IL-10 knockout (KO) mice. To this aim, we generated double IL-10 APN KO mice and compared their disease development to that of single IL-10 KO mice. Both IL-10 KO and double IL-10 APN KO mice spontaneously developed colitis of comparable severity. No significant differences in inflammatory infiltrate or crypt elongation were observed in colonic tissue obtained from IL-10 KO and double IL-10 APN KO mice at either 12 or 20 wk of age. A comparable increase in circulating

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20

Lukic, Miodrag L., Hui-Rong Jiang, Zakeya Al Rasebi, et al. "Galectin-3 deficiency reduces the severity of experimental autoimmune encephalomyelitis (99.5)." Journal of Immunology 182, no. 1_Supplement (2009): 99.5. http://dx.doi.org/10.4049/jimmunol.182.supp.99.5.

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Abstract Galectin-3 (Gal-3) is a member of β-galactoside-binding lectin family and plays an important role in inflammatory. However, the precise role of Gal-3 in autoimmune diseases remains obscure. We have investigated the functional role of Gal-3 in experimental autoimmune encephalomyelititis (EAE) following immunization with myelin oligodendrocyte glycoprotein (MOG)35-55 peptide. Gal-3 deficient (Gal-3-/-) mice developed significantly milder EAE and markedly reduced leukocyte infiltration in the CNS compared with similarly treated wild-type (WT) mice. Gal-3-/- mice also contained fewer mono

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21

Lazarus, John J., Michelle J. Meadows, Robert E. Lintner, and R. Mark Wooten. "IL-10 Deficiency Promotes IncreasedBorrelia burgdorferiClearance Predominantly through Enhanced Innate Immune Responses." Journal of Immunology 177, no. 10 (2006): 7076–85. http://dx.doi.org/10.4049/jimmunol.177.10.7076.

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22

WHARY, M., B. SHEPPARD, J. CLINE, S. XU, and J. FOX. "IL-10 deficiency reduces Helicobacter pylori gastric colonization in C57BL/6 mice." Gastroenterology 120, no. 5 (2001): A99—A100. http://dx.doi.org/10.1016/s0016-5085(01)80488-1.

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23

Whary, Mark T., Barbara J. Sheppard, Jennifer Cline, Sandy Xu, and James G. Fox. "IL-10 deficiency reduces Helicobacter pylori gastric colonization in C57BL/6 mice." Gastroenterology 120, no. 5 (2001): A99—A100. http://dx.doi.org/10.1016/s0016-5085(08)80488-x.

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24

Sato, Yuichirou, Seiichi Takahashi, Yoshitaka Kinouchi, et al. "IL-10 deficiency leads to somatic mutations in a model of IBD." Carcinogenesis 27, no. 5 (2006): 1068–73. http://dx.doi.org/10.1093/carcin/bgi327.

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25

Hoffmann, Dirk, Johanna Sens, Sebastian Brennig, et al. "Genetic Correction of IL-10RB Deficiency Reconstitutes Anti-Inflammatory Regulation in iPSC-Derived Macrophages." Journal of Personalized Medicine 11, no. 3 (2021): 221. http://dx.doi.org/10.3390/jpm11030221.

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Patient material from rare diseases such as very early-onset inflammatory bowel disease (VEO-IBD) is often limited. The use of patient-derived induced pluripotent stem cells (iPSCs) for disease modeling is a promising approach to investigate disease pathomechanisms and therapeutic strategies. We successfully developed VEO-IBD patient-derived iPSC lines harboring a mutation in the IL-10 receptor β-chain (IL-10RB) associated with defective IL-10 signaling. To characterize the disease phenotype, healthy control and VEO-IBD iPSCs were differentiated into macrophages. IL-10 stimulation induced char

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26

Gaistruk, N. A., L. G. Dubas, A. N. Gaistruk, A. V. Melnik, and O. L. Liovkina. "Pathogenetic role of vitamin D deficiency and immune-inflammatory disorders in development of fetal distress in pregnant women with chronic hydramnion." Likarska sprava, no. 3-4 (June 30, 2020): 14–20. http://dx.doi.org/10.31640/jvd.3-4.2020(3).

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The role of vitamin D deficiency and immune-inflammatory disorders in the mechanisms of development of fetal distress in pregnant women with chronic polyhydramnios remains unexplored. Objective: to evaluate the role of vitamin D deficiency and associated immune inflammatory disorders in the development of fetal distress in pregnant women with chronic polyhydramnios. Materials and methods. Surveyed 30 women with a physiological course of pregnancy and 90 pregnant women with chronic polyhydramnios. In the serum, the level of the metabolite of vitamin D – 25(OH)D and the cytokines IL-10 and IL-6

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27

Bai, Xue-Feng, Jin-Qing Liu, Joseph Carl, Jr., et al. "Enhanced T cell proliferation, Th17 differentiation and unaltered IL-10 production lead to marginally enhanced development of experimental autoimmune encephalomyelitis in EBI3-deficient mice (114.12)." Journal of Immunology 186, no. 1_Supplement (2011): 114.12. http://dx.doi.org/10.4049/jimmunol.186.supp.114.12.

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Abstract Epstein-Barr virus-induced gene 3 (EBI3) encoded protein can form heterodimers with IL-27P28 and IL-12P35 to form IL-27 and IL-35. IL-27 and IL-35 may influence autoimmunity through inhibiting Th17 differentiation, and facilitating the inhibitory roles of Foxp3+ Treg cells, repectively. In this study we have evaluated the development of experimental autoimmune encephalomyelitis (EAE) in EBI3-deficient mice that lack both IL-27 and IL-35. We found that MOG peptide immunization resulted in marginally enhanced EAE development in EBI3-deficient C57BL6 and 2D2 TCR transgenic mice. EBI3-def

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Balto, Khaled, Hajime Sasaki, and Philip Stashenko. "Interleukin-6 Deficiency Increases Inflammatory Bone Destruction." Infection and Immunity 69, no. 2 (2001): 744–50. http://dx.doi.org/10.1128/iai.69.2.744-750.2001.

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ABSTRACT Periapical bone destruction occurs as a consequence of pulpal infection. In previous studies, we showed that interleukin-1 (IL-1) is the primary stimulator of bone destruction in this model. IL-6 is a pleiotropic cytokine that is induced in these infections and has both pro- and anti-inflammatory activities. In the present study, we determined the role of IL-6 in regulating IL-1 expression and bone resorption. The first molars of IL-6 knockouts (IL-6−/−) and wild-type mice were subjected to surgical pulp exposure and infection with a mixture of four common pulpal pathogens, includingP

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29

Yahia, Ramadan, Shereen M. Mohammed, Manal M. Hassanien, Shabaan H. Ahmed, and Helal F. Hetta. "Vitamin D as a Key Player in Modulating Rheumatoid Arthritis-derived Immune Response." Journal of Pure and Applied Microbiology 14, no. 4 (2020): 2453–65. http://dx.doi.org/10.22207/jpam.14.4.23.

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Rheumatoid arthritis (RA) is a systemic inflammatory disease with chronic nature of joints related to autoimmunity. Vitamin D was found to modulate cell growth, function of immune cells and anti-inflammatory action. The aims of that study were to investigate serum level of vitamin D and some cytokines and to identify the correlation between vitamin D and these cytokines in RA. Totally 40 RA patients without vitamin D supplement were involved in this study. Serum level of vitamin D, interleukin-6 (IL-6), IL-10, IL-35, C-reactive protein (CRP) and tumor necrosis factor α (TNF-α), all of them wer

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30

AVANZINI, M. "Specific synergic effect of IL-4 and IL-10 on in vitro IgA producction in IgA deficiency." Molecular Immunology 35, no. 11-12 (1998): 744. http://dx.doi.org/10.1016/s0161-5890(98)90424-2.

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31

Papoutsopoulou, Stamatia, Liam Pollock, Jonathan M. Williams, et al. "Interleukin-10 Deficiency Impacts on TNF-Induced NFkB Regulated Responses In Vivo." Biology 11, no. 10 (2022): 1377. http://dx.doi.org/10.3390/biology11101377.

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Interleukin-10 (IL-10) is an anti-inflammatory cytokine that has a major protective role against intestinal inflammation. We recently revealed that intestinal epithelial cells in vitro regulate NFkB-driven transcriptional responses to TNF via an autocrine mechanism dependent on IL-10 secretion. Here in this study, we investigated the impact of IL-10 deficiency on the NFkB pathway and its downstream targets in the small intestinal mucosa in vivo. We observed dysregulation of TNF, IkBa, and A20 gene and protein expression in the small intestine of steady-state or TNF-injected Il10-/- mice, compa

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32

Neven, Bénédicte, Emilie Mamessier, Julie Bruneau, et al. "A Mendelian predisposition to B-cell lymphoma caused by IL-10R deficiency." Blood 122, no. 23 (2013): 3713–22. http://dx.doi.org/10.1182/blood-2013-06-508267.

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Key Points Human inherited IL-10 receptor deficiency is associated with a very high risk of non-EBV–related diffuse large B-cell lymphoma. IL-10 signaling may be involved in the immune control of germinal center B-cell lymphoma.

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33

Kader, Muhamuda, Mounia Alaoui-El-Azher, Bhushan Kode, et al. "MyD88 suppresses IL-10 and IL-17 production in response to obligate intracellular Ehrlichia infection." Journal of Immunology 196, no. 1_Supplement (2016): 206.1. http://dx.doi.org/10.4049/jimmunol.196.supp.206.1.

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Abstract Ehrlichia is an obligate intracellular gram negative bacterium that target macrophages, and causes the potentially fatal human monocytic ehrlichiosis (HME). In murine models of fatal ehrlichiosis (FE), Ixodes ovatus Ehrlichia (IOE) inhibits autophagy, suppresses protective acquired immunity, and causes immunopathology and toxic shock syndrome. Innate Ehrlichia detection by TLR2 mediates host resistance, while NOD2 signaling confers host susceptibility to FE. Recently, we have shown that deficiency of type I interferon receptor (IFNaR) phenocopy NOD2 deficiency in IOE-infected mice, im

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Moriaitis, Andreas, Lita Freeman, Robert Shamburek, et al. "Elevated Interleukin-10 and “Disappearing HDL Syndrome” in Lymphoproliferative Disorders." Blood 124, no. 21 (2014): 4134. http://dx.doi.org/10.1182/blood.v124.21.4134.4134.

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Abstract BACKGROUND: Acquired severe HDL deficiency is relatively uncommon. It may occur with use of high doses of anabolic steroids or in severe liver diseases, which can lead to low LCAT activity and decreased apoA-I production. “Disappearing HDL Syndrome”*, a term first used by Goldberg and Mendez, refers to cases of severe HDL deficiency in patients that are not critically ill, sometimes long before the clinical or biochemical features of the underlying primary disease become evident. Disappearing HDL Syndrome can also result from an idiosyncratic reaction to medications, such as peroxisom

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Abston, Eric D., Michael J. Coronado, Adriana Bucek, et al. "TLR3 deficiency induces chronic inflammatory cardiomyopathy in resistant mice following coxsackievirus B3 infection: role for IL-4." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 304, no. 4 (2013): R267—R277. http://dx.doi.org/10.1152/ajpregu.00516.2011.

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Recent findings indicate that TLR3 polymorphisms increase susceptibility to enteroviral myocarditis and inflammatory dilated cardiomyopathy (iDCM) in patients. TLR3 signaling has been found to inhibit coxsackievirus B3 (CVB3) replication and acute myocarditis in mouse models, but its role in the progression from myocarditis to iDCM has not been previously investigated. In this study we found that TLR3 deficiency increased acute ( P = 5.9 × 10−9) and chronic ( P = 6.0 × 10−7) myocarditis compared with WT B6.129, a mouse strain that is resistant to chronic myocarditis and iDCM. Using left ventri

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36

Sun, Xiaofei, Monica Cappelletti, Yingju Li, Christopher L. Karp, Senad Divanovic, and Sudhansu K. Dey. "Cnr2 Deficiency Confers Resistance to Inflammation-Induced Preterm Birth in Mice." Endocrinology 155, no. 10 (2014): 4006–14. http://dx.doi.org/10.1210/en.2014-1387.

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Abstract Infection-induced inflammation, frequently associated with increased production of proinflammatory cytokines, is considered a significant contributor to preterm birth. A G protein-coupled cannabinoid receptor 2 (CB2), encoded by Cnr2, is expressed in various immune cells and was shown to modulate immune responses. We show here that Cnr2, but not Cnr1, deficient mice are resistant to lipopolysaccharide (LPS)-driven preterm birth and suppression of serum progesterone levels. After LPS challenge, Cnr2−/− mice exhibited increased serum levels of IL-10 with decreased IL-6 levels. These cha

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37

Moon, Sung, Jeong-Im Woo, Sejo Oh, Yoojin Lee, Okjin Ahn, and David Lim. "IL-10-mediated modulation of cochlear inflammation (P6228)." Journal of Immunology 190, no. 1_Supplement (2013): 115.10. http://dx.doi.org/10.4049/jimmunol.190.supp.115.10.

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Abstract Inflammatory response is commonly involved in the pathogenesis of various cochlear diseases such as acoustic trauma and cisplatin ototoxicity. Previously, we have demonstrated that the spiral ligament fibrocytes play a pivotal role in cochlear inflammation through secretion of chemokines such as CCL2 and CXCL2 in response to pro-inflammatory signals. In this study, we aim to determine molecular mechanism involved in negative modulation of cochlear inflammation. We found that IL-10 inhibits SLF’s CCL2 up-regulation and migration of THP-1 cells in response to SLF-derived molecules. The

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38

Jeong, Eui-Suk. "Role of IL-10 Deficiency in Pneumonia Induced by Corynebacterium kutscheri in Mice." Journal of Microbiology and Biotechnology 19, no. 4 (2009): 424–30. http://dx.doi.org/10.4014/jmb.0807.436.

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39

Tewari, N., SP Murphy, and S. Sharma. "1141635485 Genetic stress (IL-10 deficiency) and toxicant (PCB)-induced disruption of pregnancy." American Journal of Reproductive Immunology 55, no. 6 (2006): 408. http://dx.doi.org/10.1111/j.1600-0897.2006.00383_39.x.

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40

Kobbe, Philipp, Burkhard Stoffels, Joachim Schmidt, et al. "IL-10 deficiency augments acute lung but not liver injury in hemorrhagic shock." Cytokine 45, no. 1 (2009): 26–31. http://dx.doi.org/10.1016/j.cyto.2008.10.004.

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41

de Lemos Rieper, Carina, Pia Galle, Bente Klarlund Pedersen, and Morten Bagge Hansen. "A state of acquired IL-10 deficiency in 0.4% of Danish blood donors." Cytokine 51, no. 3 (2010): 286–93. http://dx.doi.org/10.1016/j.cyto.2010.06.009.

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42

Koh, Byunghee, and Mark H. Kaplan. "Etv5 promotes IL-10 production in Th2 cells." Journal of Immunology 196, no. 1_Supplement (2016): 58.15. http://dx.doi.org/10.4049/jimmunol.196.supp.58.15.

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Abstract The anti-inflammatory cytokine, IL-10, suppresses inflammatory responses at mucosal surfaces. Among T helper cell subsets, Th2 cells produce the highest concentrations. However, the transcription factors that regulate Il10 gene expression have not been completely defined. Etv5 is a member of the ETS transcription factor family that promotes production of IL-17 in Th17 cells and IL-9 in Th9 cells. To define the effects of Etv5 deficiency on cytokine expression in Th2 cells, T cells from CD4 specific Etv5 knockout (Etv5fl/flCD4-Cre+, termed Etv5 KO below) and littermate control (Etv5fl/

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Wang, Lei, Li Zhang, Xiaoxia Feng, et al. "The Functional Difference of Dendritic Cells in HBeAg Negative Chronic Hepatitis B Patients with Three Different Spleen Deficiency Syndromes and the Therapeutic Evaluation of Chinese Medicine Intervention Based on Syndrome Differentiation." Evidence-Based Complementary and Alternative Medicine 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/802402.

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Objective. To investigate the dendritic cells (DCs) maturity differences of HBeAg negative chronic hepatitis B (CHB) patients with different spleen deficiency (SD) syndromes and explore the role of syndrome differentiation in the therapeutic evaluation of Chinese medicine.Methods. 120 participants were recruited including three treatment groups in different SD syndrome categories as spleen deficiency with liver depression (SDLD), spleen deficiency with damp heat (SDDH), and spleen deficiency with kidney deficiency (SDKD) and one healthy control group; each group had 30 participants. Correspond

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Nguyen, Deanna, Jeremy Goettel, Marc-Andre Wurbel, et al. "Colitis in mice with WASP deficiency in innate immune cells is associated with impairment in IL-10 production (71.10)." Journal of Immunology 188, no. 1_Supplement (2012): 71.10. http://dx.doi.org/10.4049/jimmunol.188.supp.71.10.

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Abstract Colitis occurs in mice and some patients deficient in the Wiskott-Aldrich Syndrome protein (WASP), a hematopoietic-specific molecule that regulates the actin cytoskeleton. This colitis is lymphocyte-dependent, but severe disease is observed in chimeric mice with WT T cells and WASP KO innate immune cells, generated by transfer of WT CD4+ T cells into WASP/RAG DKO mice. Given the immunomodulatory function of IL-10, coupled with our findings that mixed bone marrow chimeras are free of colitis, we investigated whether alterations in IL-10 play a role in our colitis model. We found reduce

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Yang, Xi, Shuhe Wang, Yijun Fan, and Xiaobing Han. "IL-10 deficiency prevents IL-5 overproduction and eosinophilic inflammation in a murine model of asthma-like reaction." European Journal of Immunology 30, no. 2 (2000): 382–91. http://dx.doi.org/10.1002/1521-4141(200002)30:2<382::aid-immu382>3.0.co;2-l.

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Turner, Joanne, Joshua Cyktor, Bridget Carruthers, Rachel Kominsky, Paul Stromberg, and Gillian Beamer. "Deficiency in interleukin 10 reverses the susceptibility phenotype of CBA/J mice during infection with Mycobacterium tuberculosis. (43.23)." Journal of Immunology 188, no. 1_Supplement (2012): 43.23. http://dx.doi.org/10.4049/jimmunol.188.supp.43.23.

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Abstract Interleukin 10 is a known correlate of susceptibility to tuberculosis (TB) in man and similarly, elevated levels of IL-10 (either natural or induced) in mice can accelerate TB disease progression. The CBA/J mouse strain is a model that naturally produces abundant IL-10 and is also highly susceptible to infection with Mycobacterium tuberculosis (M.tb). We have generated CBA/J mice deficient in IL-10 (IL-10 KO) to determine the mechanisms of influence of IL-10 on TB disease progression in this highly susceptible mouse strain. In contrast to IL-10 KO on resistant mouse strain backgrounds

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Makris, A., B. Xu, B. Yu, C. Thornton, and A. Hennessy. "Placental Deficiency of Interleukin-10 (IL-10) in Preeclampsia and its Relationship to an IL10 Promoter Polymorphism." Placenta 27, no. 4-5 (2006): 445–51. http://dx.doi.org/10.1016/j.placenta.2005.05.003.

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Brufau, Gemma, Marion J. J. Gijbels, Ine M. J. Wolfs, et al. "Deleting myeloid IL-10 receptor signalling attenuates atherosclerosis in LDLR-/- mice by altering intestinal cholesterol fluxes." Thrombosis and Haemostasis 116, no. 09 (2016): 565–77. http://dx.doi.org/10.1160/th16-01-0043.

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SummaryInflammatory responses and cholesterol homeostasis are interconnected in atherogenesis. Interleukin (IL)-10 is an important anti-inflammatory cytokine, known to suppress atherosclerosis development. However, the specific cell types responsible for the atheroprotective effects of IL-10 remain to be defined and knowledge on the actions of IL-10 in cholesterol homeostasis is scarce. Here we investigated the functional involvement of myeloid IL-10-mediated atheroprotection. To do so, bone marrow from IL-10 receptor 1 (IL-10R1) wild-type and myeloid IL-10R1-deficient mice was transplanted to

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Yakovlev, A. T., T. F. Danilina, and V. F. Mikhalchenko. "Diagnostic information content of indicators of cytokine profile of gingival fluid in pregnant women with iron deficiency anemia." Parodontologiya 25, no. 4 (2020): 295–300. http://dx.doi.org/10.33925/1683-3759-2020-25-4-295-300.

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Relevance. Modern literature and clinical dental practice do not provide enough information about the value of local immunity parameters for early diagnosis of inflammatory periodontal diseases in pregnant women with iron deficiency anemia. Conventional anti-inflammatory medications used to treat inflammatory periodontal disease are frequently contraindicated during pregnancy. It is important to make a reasonable choice of safe medications, prevention methods, and treatment at early stages of inflammatory periodontal diseases in pregnant women with iron deficiency anemia. The aim of the presen

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Gunasekera, Dilini C., Amritha Ramakrishnan, Jinxia Ma, et al. "IL-22-deficiency mediates resolution of colitis in Il10 −/− mice." Journal of Immunology 198, no. 1_Supplement (2017): 201.4. http://dx.doi.org/10.4049/jimmunol.198.supp.201.4.

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Abstract The cytokines IL-10 and IL-22 play important, but presumably distinct roles in promoting intestinal homeostasis. Although the anti-inflammatory actions of IL-10 in the gut are well established, the role(s) of IL-22 remain unclear. Il10−/− mice develop chronic colitis characterized by rectal prolapse, colonic thickening and inflammatory infiltrates, including abundant Th17 cells. We have also observed a modest, but consistent elevation in IL-22 (mRNA and IL-22+CD4 T cells) in colons of Il10−/− mice. This is accompanied by an increased expression of IL-22-target bactericidal genes such

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