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Journal articles on the topic 'IL-10'

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Author: Grafiati

Published: 4 June 2021

Last updated: 11 March 2023

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1

Commins, Scott, John W. Steinke, and Larry Borish. "The extended IL-10 superfamily: IL-10, IL-19, IL-20, IL-22, IL-24, IL-26, IL-28, and IL-29." Journal of Allergy and Clinical Immunology 121, no. 5 (May 2008): 1108–11. http://dx.doi.org/10.1016/j.jaci.2008.02.026.

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2

Glocker, Erik-Oliver, Daniel Kotlarz, Christoph Klein, Neil Shah, and Bodo Grimbacher. "IL-10 and IL-10 receptor defects in humans." Annals of the New York Academy of Sciences 1246, no. 1 (December 2011): 102–7. http://dx.doi.org/10.1111/j.1749-6632.2011.06339.x.

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3

Wang, Min, Youji Hu, Ischiro Shima, and Mark E. Stearns. "IL-10/IL-10 Receptor Signaling Regulates TIMP-1 Expression." Cancer Biology & Therapy 1, no. 5 (September 13, 2002): 556–63. http://dx.doi.org/10.4161/cbt.1.5.222.

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4

Rennick, Donna M., and Madeline M. Fort. "XII. IL-10-deficient (IL-10−/−) mice and intestinal inflammation." American Journal of Physiology-Gastrointestinal and Liver Physiology 278, no. 6 (June 1, 2000): G829—G833. http://dx.doi.org/10.1152/ajpgi.2000.278.6.g829.

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Interleukin (IL)-10−/−mice spontaneously develop intestinal inflammation characterized by discontinuous transmural lesions affecting the small and large intestine and by dysregulated production of proinflammatory cytokines. The uncontrolled generation of IFN-γ-producing CD4+T cells (Th1 type) has been shown to play a causal role in the development of enterocolitis affecting these mutants. This article discusses studies of IL-10−/−mice that have investigated the role of enteric organisms in triggering intestinal disease, the mediators responsible for initiating and maintaining intestinal disease, the role IL-10 plays in the generation and/or function of regulatory cells, and the results of IL-10 therapy in experimental animal models of inflammatory bowel disease (IBD) and human patients with IBD.

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5

Jankovic, Dragana, and Giorgio Trinchieri. "IL-10 or not IL-10: that is the question." Nature Immunology 8, no. 12 (December 2007): 1281–83. http://dx.doi.org/10.1038/ni1207-1281.

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6

Mittal, Sharad K., Kyung-Jin Cho, Satoshi Ishido, and Paul A. Roche. "Interleukin 10 (IL-10)-mediated Immunosuppression." Journal of Biological Chemistry 290, no. 45 (September 25, 2015): 27158–67. http://dx.doi.org/10.1074/jbc.m115.682708.

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7

Ouyang, Wenjun, and Anne O’Garra. "IL-10 Family Cytokines IL-10 and IL-22: from Basic Science to Clinical Translation." Immunity 50, no. 4 (April 2019): 871–91. http://dx.doi.org/10.1016/j.immuni.2019.03.020.

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8

Conti, P., D. Kempuraj, S. Frydas, K. Kandere, W. Boucher, R. Letourneau, B. Madhappan, K. Sagimoto, S. Christodoulou, and T. C. Theoharides. "IL-10 subfamily members: IL-19, IL-20, IL-22, IL-24 and IL-26." Immunology Letters 88, no. 3 (September 2003): 171–74. http://dx.doi.org/10.1016/s0165-2478(03)00087-7.

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9

Mahmood Majeed, Hameed, and Malik Hadi Qadurie. "Evaluation Relationship between IL-10, IL-1α in Hepatocellular Carcinoma Patients." Diyala Journal For Pure Science 13, no. 3 (July 1, 2017): 103–12. http://dx.doi.org/10.24237/djps.1303.252b.

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10

Murray, Henry W., Christina M. Lu, Smita Mauze, Sherry Freeman, Andre L. Moreira, Gilla Kaplan, and Robert L. Coffman. "Interleukin-10 (IL-10) in Experimental Visceral Leishmaniasis and IL-10 Receptor Blockade as Immunotherapy." Infection and Immunity 70, no. 11 (November 2002): 6284–93. http://dx.doi.org/10.1128/iai.70.11.6284-6293.2002.

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ABSTRACT Interleukin-10 (IL-10) is thought to promote intracellular infection, including human visceral leishmaniasis, by disabling Th1 cell-type responses and/or deactivating parasitized tissue macrophages. To develop a rationale for IL-10 inhibition as treatment in visceral infection, Th1 cytokine-driven responses were characterized in Leishmania donovani-infected BALB/c mice in which IL-10 was absent or overexpressed or its receptor (IL-10R) was blockaded. IL-10 knockout and normal mice treated prophylactically with anti-IL-10R demonstrated accelerated granuloma assembly and rapid parasite killing without untoward tissue inflammation; IL-12 and gamma interferon mRNA expression, inducible nitric oxide synthase reactivity, and responsiveness to antimony chemotherapy were also enhanced in knockout mice. In IL-10 transgenic mice, parasite replication was unrestrained, and except for antimony responsiveness, measured Th1 cell-dependent events were all initially impaired. Despite subsequent granuloma assembly, high-level infection persisted, and antimony-treated transgenic mice also relapsed. In normal mice with established infection, anti-IL-10R treatment was remarkably active, inducing near-cure by itself and synergism with antimony. IL-10's deactivating effects regulate outcome in experimental visceral leishmaniasis, and IL-10R blockade represents a potential immuno- and/or immunochemotherapeutic approach in this infection.

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11

Asadullah, K., K. Stephanek, M. Leupold, D. Jasulaitis, H. Audring, H. D. Volk, W. D. Döcke, and W. Sterry. "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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12

NURDINA, MARIA S., and VITALII I. KUPAEV. "CORRELATION BETWEEN SERUM IL-17 AND IL-10 LEVEL AND ASTHMA CONTROL." Bulletin of Contemporary Clinical Medicine 10, no. 3 (March 2017): 35–38. http://dx.doi.org/10.20969/vskm.2017.10(3).35-38.

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13

Cannarile, L., G. Venditti, E. Ayroldi, D. V. Delfino, and G. Migliorati. "Dexamethasone Modulates IL-13 and IL-10 Expression." International Journal of Immunopathology and Pharmacology 10, no. 3 (September 1997): 175–82. http://dx.doi.org/10.1177/039463209701000302.

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Interleukin (IL-)-10 and IL-13 are Th2-cell-associated cytokines with a variety of biologic activities in immune and inflammatory responses. It is known that glucocorticoids (GCs) modulate inflammatory and immune functions. In fact, GCs are involved to regulate the transcription of cytokines which are relevant in chronic inflammation and cell-mediated immune response. In the present study we analyzed, in vitro, the effects of DEX on the expression of the IL-10 and IL-13 lymphokines in murine spleen and thymus cells. DEX-stimulation induced down-regulation of the expression of IL-10 and IL-13 mRNA. This effect was already evident 0.5 hr after treatment and persisted in time, in both resting and activated lymphocytes. These results suggest that GCs could have inhibitory effect on Th2 cytokine production.

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14

Zvenigorodska, Anna, and Veronica Dudnyk. "MP856GENE POLYMORPHISM OF IL-1B AND IL-10." Nephrology Dialysis Transplantation 32, suppl_3 (May 1, 2017): iii748. http://dx.doi.org/10.1093/ndt/gfx183.mp856.

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15

Vélez, C., D. Williamson, and M. Koncurat. "IL-1β, IL-2, IL-4 and IL-10 profile during porcine gestation." Placenta 51 (March 2017): 116. http://dx.doi.org/10.1016/j.placenta.2017.01.065.

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16

Shyh-Hwa, Liu, Tseng Wei-Ting, Lu Ming-Yu, Chang Hsiu-Luan, and Chaung Hso-Chi. "Association between interleukin-10 (IL-10) polymorphisms and IL-10 production of peripheral blood mononuclear cells." Molecular Immunology 51, no. 1 (May 2012): 39–40. http://dx.doi.org/10.1016/j.molimm.2012.03.004.

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17

Specht, Sabine, Lars Volkmann, Tom Wynn, and Achim Hoerauf. "Interleukin-10 (IL-10) Counterregulates IL-4-Dependent Effector Mechanisms in Murine Filariasis." Infection and Immunity 72, no. 11 (November 2004): 6287–93. http://dx.doi.org/10.1128/iai.72.11.6287-6293.2004.

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ABSTRACT Interleukin-10 (IL-10) was at first described as a Th2-associated cytokine, although more recent reports have shown that immunosuppression applies to both Th1 and Th2 cell responses, e.g., when produced by T regulatory cells. This concept when applied to human filariasis would argue that high parasite loads are associated with IL-10, while bona fide Th2 responses, mediated by IL-4, IL-5, and IL-13, are associated with parasite containment. To prove this relationship in a causal manner, we investigated the roles of IL-4 and IL-10 in a helminth infection model in which mice genetically deficient for IL-4, IL-10, or IL-4 plus IL-10 were infected with the rodent filaria Litomosoides sigmodontis. Compared to C57BL/6 wild-type and IL-10 knockout (KO) mice, IL-4 KO mice remained susceptible, exhibiting a remarkable number of live adult worms. Interestingly however, when the IL-10 gene was knocked out simultaneously with the IL-4 gene, the susceptibility of IL-4 KO mice was reversed. Although production of IFN-γ was increased in IL-4/IL-10 double-knockout mice, depletion of gamma interferon did not affect worm elimination, so it seems unlikely to be the major factor in mediating resistance in IL-4/IL-10 KO mice. Taken together, the results of this study add proof to the concept that has arisen for human filariasis that IL-10-dependent responses, which are associated with patency, are antagonistic to bona fide Th2 responses, which control parasite loads. The finding that knockout of IL-10 reversed a disease phenotype induced by knockout of IL-4 gives the first causal evidence of an antagonistic activity between IL-4 and IL-10 in an infection in vivo.

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18

Ramkumar, Hema L., De Fen Shen, Jingsheng Tuo, Rita M. Braziel, Sarah E. Coupland, Justine R. Smith, and Chi-Chao Chan. "IL-10 -1082 SNP and IL-10 in primary CNS and vitreoretinal lymphomas." Graefe's Archive for Clinical and Experimental Ophthalmology 250, no. 10 (May 25, 2012): 1541–48. http://dx.doi.org/10.1007/s00417-012-2037-1.

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19

Baranova, N. I., B. A. Molotilov, L. A. Ashchina, and N. A. Shkurova. "Role of IL-1β, TNF-α, IL-10, IL-17, and IL-4 gene polymorphisms in the pathogenesis of chronic rhinosinusitis with nasal polyps." Russian Medical Inquiry 6, no. 2 (2022): 57–61. http://dx.doi.org/10.32364/2587-6821-2022-6-2-57-61.

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Background: chronic rhinosinusitis with nasal polyps (CRSwNP) is a multifactorial disease, those mechanisms are not fully understood. A significant role of cytokines, e.g., interleukin (IL)-1β, tumor necrosis factor (TNF) α, IL-10, IL-17А, IL-4, and their genes, in the pathogenesis and predisposition to CRSwNP and treatment efficacy is established. Aim: to investigate IL-1β (Т-31С), TNF-α (G-308A), IL-10 (G-1082A), IL-17(G-197A), and IL-4 (С-589Т) gene polymorphisms and their role in CRSwNP pathogenesis. Patients and Methods: this open-label, prospective, randomized study enrolled 100 patients with CRSwNP. The control group included 72 healthy volunteers. DNA was isolated from the whole venous blood. IL-1β (Т-31С), TNF-α (G-308A), IL-10 (G-1082A), IL-17 (G-197A), and IL-4 (С-589Т) gene polymorphisms were assessed by the real-time polymerase chain reaction (PCR). Results: the analysis of IL-4 (С-589Т) gene polymorphism has demonstrated that 589С/С genotype is more common in CRSwNP patients compared to the controls (р=0.021, odds ratio/OR=1.248 [0.449–3.465]). The analysis of IL-10 (G-1082A) gene polymorphism has demonstrated that 1082А/A genotype is more common in CRSwNP patients compared to the controls (p=0.043, OR=1.027 [0.374–2.830]). The analysis of IL-17 (G-197A) gene polymorphism has demonstrated that 197A/А genotype is more common in CRSwNP patients than in the controls (p=0.046, OR=7.250 [0.863–2.532]). The analysis of TNF-α (G-308A) gene polymorphism has demonstrated that 308 G/G genotype is more common in CRSwNP patients compared to the controls (p=0.045, OR=1.789 [0.892–4.776]). Conclusion: the most relevant predictors of the increased risk of CRSwNP are 589С/С genotype of IL-4 gene, 1082А/A genotype of IL-10 gene, 197A/А genotype of IL-17 gene, and 308 G/G genotype of TNF-α gene. The analysis of essential cytokine gene polymorphisms, i.e., IL- 1β (Т-31С), TNF-α (G-308A), IL-10 (G-1082A), IL-17 (G-197A), and IL-4 (С-589Т), allows assessing genetic predisposition to CRSwNP. This technique is an important tool for predicting treatment efficacy. KEYWORDS: chronic rhinosinusitis with nasal polyps, cytokines, genotype, gene polymorphism, pathogenic mechanisms. FOR CITATION: Baranova N.I., Molotilov B.A., Ashchina L.A., Shkurova N.A. Role of IL-1β, TNF-α, IL-10, IL-17, and IL-4 gene polymorphisms in the pathogenesis of chronic rhinosinusitis with nasal polyps. Russian Medical Inquiry. 2022;6(2):57–61 (in Russ.). DOI: 10.32364/2587-6821-2022-6-2-57-61.

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20

M’Bondoukwé, Noé Patrick, Reinne Moutongo, Komi Gbédandé, Jacques Mari Ndong Ngomo, Tatiana Hountohotegbé, Rafiou Adamou, Jeanne Vanessa Koumba Lengongo, et al. "Circulating IL-6, IL-10, and TNF-alpha and IL-10/IL-6 and IL-10/TNF-alpha ratio profiles of polyparasitized individuals in rural and urban areas of gabon." PLOS Neglected Tropical Diseases 16, no. 4 (April 14, 2022): e0010308. http://dx.doi.org/10.1371/journal.pntd.0010308.

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Malaria, blood-borne filarial worms and intestinal parasites are all endemic in Gabon. This geographical co-distribution leads to polyparasitism and, consequently, the possibility of immune-mediated interactions among different parasite species. Intestinal protozoa and helminths could modulate antimalarial immunity, for example, thereby potentially increasing or reducing susceptibility to malaria. The aim of the study was to compare the cytokine levels and cytokine ratios according to parasitic profiles of the population to determine the potential role of co-endemic parasites in the malaria susceptibility of populations. Blood and stool samples were collected during cross-sectional surveys in five provinces of Gabon. Parasitological diagnosis was performed to detect plasmodial parasites, Loa loa, Mansonella perstans, intestinal helminths (STHs) and protozoan parasites. Nested PCR was used to detect submicroscopic plasmodial infection in individuals with negative blood smears. A cytometric bead array was used to quantify interleukin (IL)-6, IL-10 and tumour necrosis factor (TNF)-α in the plasma of subjects with different parasitological profiles. Median IL-6 and IL-10 levels and the median IL-10/TNF-α ratio were all significantly higher among individuals with Plasmodium (P.) falciparum infection than among other participants (p<0.0001). The median TNF-α level and IL-10/IL-6 ratio were higher in subjects with STHs (p = 0.09) and P. falciparum-intestinal protozoa co-infection (p = 0.04), respectively. IL-6 (r = -0.37; P<0.01) and IL-10 (r = -0.37; P<0.01) levels and the IL-10/TNF-α ratio (r = -0.36; P<0.01) correlated negatively with age. Among children under five years old, the IL-10/TNF-α and IL-10/IL-6 ratios were higher in those with intestinal protozoan infections than in uninfected children. The IL-10/TNF-α ratio was also higher in children aged 5–15 years and in adults harbouring blood-borne filariae than in their control counterparts, whereas the IL-10/IL-6 ratio was lower in those aged 5–15 years with filariae and intestinal parasites but higher in adults with intestinal parasitic infections. Asymptomatic malaria is associated with a strong polarization towards a regulatory immune response, presenting high circulating levels of IL-10. P. falciparum/intestinal protozoa co-infections were associated with an enhanced IL-10 response. Immunity against malaria could differ according to age and carriage of other parasites. Helminths and intestinal protozoa can play a role in the high susceptibility to malaria currently observed in some areas of Gabon, but further investigations are necessary.

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21

Oral, Haluk B, Sergei V Kotenko, Mustafa Yılmaz, Orlando Mani, Judith Zumkehr, Kurt Blaser, Cezmi A Akdis, and Mübeccel Akdis. "Regulation of T cells and cytokines by the interleukin-10 (IL-10)-family cytokines IL-19, IL-20, IL-22, IL-24 andIL-26." European Journal of Immunology 36, no. 2 (February 2006): 380–88. http://dx.doi.org/10.1002/eji.200425523.

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22

Zhang, Guicheng, Maria Nelia Manaca, Michelle McNamara-Smith, Alfredo Mayor, Augusto Nhabomba, Tamara Katherine Berthoud, Siew-Kim Khoo, et al. "Interleukin-10 (IL-10) Polymorphisms Are Associated with IL-10 Production and Clinical Malaria in Young Children." Infection and Immunity 80, no. 7 (May 7, 2012): 2316–22. http://dx.doi.org/10.1128/iai.00261-12.

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ABSTRACTThe role of interleukin-10 (IL-10) in malaria remains poorly characterized. The aims of this study were to investigate (i) whether genetic variants of the IL-10 gene influence IL-10 production and (ii) whether IL-10 production as well as the genotypes and haplotypes of the IL-10 gene in young children and their mothers are associated with the incidence of clinical malaria in young children. We genotyped three IL-10 single nucleotide polymorphisms in 240 children and their mothers from a longitudinal prospective cohort and assessed the IL-10 production by maternal peripheral blood mononuclear cells (PBMCs) and cord blood mononuclear cells (CBMCs). Clinical episodes ofPlasmodium falciparummalaria in the children were documented until the second year of life. The polymorphism IL-10 A-1082G (GCC haplotype of three SNPs in IL-10) in children was associated with IL-10 production levels by CBMC cultured withP. falciparum-infected erythrocytes (P= 0.043), with the G allele linked to low IL-10 production capacity. The G allele in children was also significantly associated with a decreased risk for clinical malaria infection in their second year of life (P= 0.016). Furthermore, IL-10 levels measured in maternal PBMCs cultured with infected erythrocytes were associated with increased risk of malaria infection in young children (P< 0.001). In conclusion, IL-10 polymorphisms and IL-10 production capacity were associated with clinical malaria infections in young children. High IL-10 production capacity inherited from parents may diminish immunological protection againstP. falciparuminfection, thereby being a risk for increased malaria morbidity.

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23

Hansen, Emily S., Velinka Medić, Joseph Kuo, Thomas F. Warner, Ronald F. Schell, and Dean T. Nardelli. "Interleukin-10 (IL-10) Inhibits Borrelia burgdorferi-Induced IL-17 Production and Attenuates IL-17-Mediated Lyme Arthritis." Infection and Immunity 81, no. 12 (September 16, 2013): 4421–30. http://dx.doi.org/10.1128/iai.01129-13.

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ABSTRACTPrevious studies have shown that cells and cytokines associated with interleukin-17 (IL-17)-driven inflammation are involved in the arthritic response toBorrelia burgdorferiinfection. Here, we report that IL-17 is a contributing factor in the development of Lyme arthritis and show that its production and histopathological effects are regulated by interleukin-10 (IL-10). Spleen cells obtained fromB. burgdorferi-infected, “arthritis-resistant” wild-type C57BL/6 mice produced low levels of IL-17 following stimulation with the spirochete. In contrast, spleen cells obtained from infected, IL-10-deficient C57BL/6 mice produced a significant amount of IL-17 following stimulation withB. burgdorferi. These mice developed significant arthritis, including erosion of the bones in the ankle joints. We further show that treatment with antibody to IL-17 partially inhibited the significant hind paw swelling and histopathological changes observed inB. burgdorferi-infected, IL-10-deficient mice. Taken together, these findings provide additional evidence of a role for IL-17 in Lyme arthritis and reveal an additional regulatory target of IL-10 following borrelial infection.

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24

Wande, I. Nyoman, Endang Retnowati, and Juli Soemarsono. "KADAR INTERLEUKIN 10 (IL-10) MALARIA DAN ANEMIA." INDONESIAN JOURNAL OF CLINICAL PATHOLOGY AND MEDICAL LABORATORY 18, no. 1 (October 14, 2016): 4. http://dx.doi.org/10.24293/ijcpml.v18i1.767.

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Anaemia is an important complication of malaria, and its pathogenesis is not well understood. High level of the Th2 cytokine (such as IL-10), which counteract the Th1 cytokine, might prevent the development of severe malarial anaemia. The purpose of this study was to know the comparation between the plasma level of IL-10 in malaria patients with anaemia and without anaemia. The plasma level of IL-10 was examined in 16 malaria patients with anaemia and 16 malaria caused by P. falciparum patients without anaemia samplestaken from patients at the primary health centres in West Lombok and Centre Lombok during March until July 2008. The samples were measured using ELISA. The concentration of haemoglobin (Hb) was measured using hematological analyzer. The anaemia concentration of Hb is <11 g/dL. The results were analyzed using two (2) sample t test with SPSS ver.13.The plasma level of IL-10 in malaria patients caused by P. falciparum with anaemia was 8.81(3.04) [mean(SD)] pg/mL where as the plasma level of IL-10 in malaria patients without anaemia was 47.99(25.26) pg/mL. The mean of IL-10 level in malaria falciparum patients with anaemia was significantly lower than that of malaria patients caused by P. falciparum without anaemia (p=0.000).

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25

Furukawa, Yutaka, Gerold Becker, Jennifer L. Stinn, Koichi Shimizu, Peter Libby, and Richard N. Mitchell. "Interleukin-10 (IL-10) Augments Allograft Arterial Disease." American Journal of Pathology 155, no. 6 (December 1999): 1929–39. http://dx.doi.org/10.1016/s0002-9440(10)65512-5.

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26

Salwen, S. A., T. Sato, K. Masuoka, G. Inoue, M. J. Mastrangelo, and D. Berd. "INTERLEUKIN-10 (IL-10) PRODUCTION BY MELANOMA CELLS." Journal of Immunotherapy 18, no. 2 (August 1995): 129. http://dx.doi.org/10.1097/00002371-199508000-00014.

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27

McIntosh, Christine M., and Maria‐Luisa Alegre. "Teamwork by IL ‐10+ and IL ‐35 + T regs." American Journal of Transplantation 19, no. 8 (July 25, 2019): 2147. http://dx.doi.org/10.1111/ajt.15511.

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28

Cicuttini, F. M., K. A. Byron, D. Maher, A. M. Wootton, K. D. Muirden, and J. A. Hamilton. "Serum IL-4, IL-10 and IL-6 levels in inflammatory arthritis." Rheumatology International 14, no. 5 (January 1995): 201–6. http://dx.doi.org/10.1007/bf00262298.

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29

Steensberg, Adam, Christian P. Fischer, Charlotte Keller, Kirsten Møller, and Bente Klarlund Pedersen. "IL-6 enhances plasma IL-1ra, IL-10, and cortisol in humans." American Journal of Physiology-Endocrinology and Metabolism 285, no. 2 (August 2003): E433—E437. http://dx.doi.org/10.1152/ajpendo.00074.2003.

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The purpose of the present study was to test the hypothesis that a transient increase in plasma IL-6 induces an anti-inflammatory environment in humans. Therefore, young healthy volunteers received a low dose of recombinant human (rh)IL-6 or saline for 3 h. Plasma IL-6 levels during rhIL-6 infusion were ∼140 pg/ml, corresponding to the levels obtained during strenuous exercise. The infusion of rhIL-6 did not induce enhanced levels of the proinflammatory cytokine TNF-α but enhanced the plasma levels of the two anti-inflammatory cytokines IL-1 receptor agonist (IL-1ra) and IL-10 compared with saline infusion. In addition, C-reactive protein increased 3 h post-rhIL-6 infusion and was further elevated 16 h later compared with saline infusion. rhIL-6 induced increased levels of plasma cortisol and, consequently, an increase in circulating neutrophils and a decrease in the lymphocyte number without effects on plasma epinephrine, body temperature, mean arterial pressure, or heart rate. In conclusion, this study demonstrates that physiological concentrations of IL-6 induce an anti-inflammatory rather than an inflammatory response in humans and that IL-6, independently of TNF-α, enhances the levels not only of IL-1ra but also of IL-10. Furthermore, IL-6 induces an increase in cortisol and, consequently, in neutrocytosis and late lymphopenia to the same magnitude and with the same kinetics as during exercise, suggesting that muscle-derived IL-6 has a central role in exercise-induced leukocyte trafficking.

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30

Knutsen, A. P., B. Kariuki, and M. R. Shah. "IL-4Ra, IL-13 and IL-10 Polymorphisms in Allergic Bronchopulmonary Aspergillosis." Journal of Allergy and Clinical Immunology 119, no. 1 (January 2007): S241. http://dx.doi.org/10.1016/j.jaci.2006.12.311.

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31

Konenkov, Konenkov V. I., Koroleva E. G. Koroleva, Orlov N. B. Orlov, Prokof’ev V. F. Prokof’ev, Shevchenko A. V. Shevchenko, Novikov A. M. Novikov, Dergacheva T. I. Dergacheva, and Ostanin A A. Ostanin A. "Anti-inflammatory activity of serum cytokines (IL-4, IL-10, IL-13) and the natural IL-1β receptor antagonist (IL-1Ra) in women with uterine myoma." Akusherstvo i ginekologiia 10_2018 (October 31, 2018): 80–85. http://dx.doi.org/10.18565/aig.2018.10.80-85.

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32

Guida, Pier Luigi. "Il PM compie 10 anni." PROJECT MANAGER (IL), no. 40 (November 2019): 4. http://dx.doi.org/10.3280/pm2019-040001.

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33

Azizieh, F. Y., and R. Raghupathy. "IL-10 and pregnancy complications." Clinical and Experimental Obstetrics & Gynecology 44, no. 2 (April 10, 2017): 252–58. http://dx.doi.org/10.12891/ceog3456.2017.

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34

Sabat, Robert. "IL-10 family of cytokines." Cytokine & Growth Factor Reviews 21, no. 5 (October 2010): 315–24. http://dx.doi.org/10.1016/j.cytogfr.2010.11.001.

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35

Yin, Zhinan, Gul Bahtiyar, Na Zhang, Lanzhen Liu, Ping Zhu, Marie E. Robert, Jennifer McNiff, Michael P. Madaio, and Joe Craft. "IL-10 Regulates Murine Lupus." Journal of Immunology 169, no. 4 (August 15, 2002): 2148–55. http://dx.doi.org/10.4049/jimmunol.169.4.2148.

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36

Minton, Kirsty. "IL-10 targets macrophage metabolism." Nature Reviews Immunology 17, no. 6 (May 26, 2017): 345. http://dx.doi.org/10.1038/nri.2017.57.

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37

Kugelberg, Elisabeth. "Opposing effects of IL-10." Nature Reviews Immunology 14, no. 6 (May 23, 2014): 357. http://dx.doi.org/10.1038/nri3693.

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38

DeWitt, Natalie. "A synthetic IL-10 mimic." Nature Biotechnology 17, no. 3 (March 1999): 214. http://dx.doi.org/10.1038/6942.

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39

Otsumi, Takemi, Kenichiro Yata, Haruko Sakaguchi, Masako Uno, Tomohiro Fujii, Hideho Wada, Takashi Sugihara, and Ayako Ueki. "IL-10 in Myeloma Cells." Leukemia & Lymphoma 43, no. 5 (January 2002): 969–74. http://dx.doi.org/10.1080/10428190290021579.

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40

Bromberg, Jonathan S. "IL-10 immunosuppression in transplantation." Current Opinion in Immunology 7, no. 5 (October 1995): 639–43. http://dx.doi.org/10.1016/0952-7915(95)80070-0.

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41

Chu, Charles C., Stephanie T. Reese, Leslie O. Goodwin, Dorothy Guzowski, Alamelu Chandrasekaran, Craig Gawel, Wentian Li, et al. "Is Elevated Serum IL-10 in B-CLL Associated with IL-10 Promoter Polymorphisms?." Blood 106, no. 11 (November 16, 2005): 1198. http://dx.doi.org/10.1182/blood.v106.11.1198.1198.

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Abstract Interleukin-10 (IL-10), a cytokine that regulates inflammation, may play an important role in B-cell chronic lymphocytic leukemia (B-CLL), because of the reported association of high serum IL-10 levels with a lower prognosis of survival. Using the Bio-Plex protein array system, we confirmed that B-CLL patients exhibit higher median IL-10 levels (3.54 pg/ml, n=50) as compared to controls (1.28 pg/ml, n=33) (p<0.0001). We are in the midst of determining B-CLL VH gene mutation status and IL-10 levels. To determine if elevated IL-10 levels are due to inherent genetic polymorphisms, we examined three single nucleotide polymorphisms (SNPs) in the proximal end of the promoter region of the IL-10 gene (-1082 A/G, −819 T/C, and −592 A/C) that may affect IL-10 transcription levels. DNA from an overlapping set of 54 B-CLL patients and 48 normals was genotyped using the Transgenomic WAVE system. The difference in allele frequencies at a single locus showed no trend towards significance between groups using the Pearsons chi-square test and Odds Ratios (OR) with 95% Confidence Intervals (CI) for each SNP (-1082 (p = 0.686, OR = 1.122, CI = 0.641–1.966), −819 (p = 0.844, OR = 1.062, CI = 0.585–1.926) and −592 (p = 0.720, OR = 1.116, CI = 0.613–2.031)). B-CLL cases and normal subjects showed no significant departure from Hardy-Weinberg equilibrium in single locus genotype frequencies. Differences in single locus genotype frequencies between B-CLL cases and controls showed no significant differences for each SNP (−1082 (p = 0.600, OR = 1.366, CI = 0.425–4.389), −819 (p = 0.638, OR = 0.727, CI = 0.192–2.749), and −592 (p = 0.638, OR = 0.727, CI = 0.192–2.749)). The haplotype frequencies were calculated using maximum likelihood method based on the observed genotypes. The differences in maximum likelihood haplotype frequencies, between the B-CLL cases and controls, were insignificant (p = 0.754). The haplotype pair genotype frequency differences between the B-CLL cases and controls were also insignificant (p = 0.921). In conclusion, the allele, genotype, and haplotype frequencies of IL-10 SNPs −1082, −819, and −592 show no trend towards significance overall. This suggests that these promoter SNPs do not contribute to elevated serum IL-10 in B-CLL. However, a suggestion of association with VH gene mutation status is being further investigated with a larger sample size.

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42

Körholz, Dieter, Ursula Banning, Halvard Bönig, Markus Grewe, Marion Schneider, Christine Mauz-Körholz, Anne Klein-Vehne, Jean Krutmann, and Stephan Burdach. "The Role of Interleukin-10 (IL-10) in IL-15–Mediated T-Cell Responses." Blood 90, no. 11 (December 1, 1997): 4513–21. http://dx.doi.org/10.1182/blood.v90.11.4513.

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Abstract Interleukin-15 (IL-15) is a potent T-cell stimulating factor, which has recently been used for pre-clinical in vivo immunotherapy. Here, the IL-15 effect on CD3-stimulated peripheral human T cells was investigated. IL-15 induced a significant T-cell proliferation and upregulated CD25 expression. IL-15 significantly enhanced T-cell production of interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), and IL-10. Between 10- and 100-fold greater concentrations of IL-15 were necessary to reach a biological effect equivalent to that of IL-2. Blockade of IL-2 binding to the high-affinity IL-2 receptor did not affect the IL-15 effects, suggesting that IL-15 did not act by inducing endogenous IL-2. Exogenously administered IL-10 significantly reduced the IL-15 and IL-2–mediated IFN-γ and TNF-α production, whereas T-cell proliferation and CD25 expression were not affected. The inhibitory effects of exogenously administered IL-10 on T-cell cytokine production appeared indirect, and are likely secondary to decreased IL-12 production by accessory cells. Inhibition of endogenous IL-10 binding to the IL-10 receptor significantly increased IFN-γ and TNF-α release from T cells. These data suggest that endogenous IL-10 can regulate activated T-cell production of IFN-γ and TNF-α via a paracrine negative feedback loop. The observations of this study could be of relevance for the therapeutic use of IL-15 in vivo.

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43

Körholz, Dieter, Ursula Banning, Halvard Bönig, Markus Grewe, Marion Schneider, Christine Mauz-Körholz, Anne Klein-Vehne, Jean Krutmann, and Stephan Burdach. "The Role of Interleukin-10 (IL-10) in IL-15–Mediated T-Cell Responses." Blood 90, no. 11 (December 1, 1997): 4513–21. http://dx.doi.org/10.1182/blood.v90.11.4513.4513_4513_4521.

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Abstract:

Interleukin-15 (IL-15) is a potent T-cell stimulating factor, which has recently been used for pre-clinical in vivo immunotherapy. Here, the IL-15 effect on CD3-stimulated peripheral human T cells was investigated. IL-15 induced a significant T-cell proliferation and upregulated CD25 expression. IL-15 significantly enhanced T-cell production of interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), and IL-10. Between 10- and 100-fold greater concentrations of IL-15 were necessary to reach a biological effect equivalent to that of IL-2. Blockade of IL-2 binding to the high-affinity IL-2 receptor did not affect the IL-15 effects, suggesting that IL-15 did not act by inducing endogenous IL-2. Exogenously administered IL-10 significantly reduced the IL-15 and IL-2–mediated IFN-γ and TNF-α production, whereas T-cell proliferation and CD25 expression were not affected. The inhibitory effects of exogenously administered IL-10 on T-cell cytokine production appeared indirect, and are likely secondary to decreased IL-12 production by accessory cells. Inhibition of endogenous IL-10 binding to the IL-10 receptor significantly increased IFN-γ and TNF-α release from T cells. These data suggest that endogenous IL-10 can regulate activated T-cell production of IFN-γ and TNF-α via a paracrine negative feedback loop. The observations of this study could be of relevance for the therapeutic use of IL-15 in vivo.

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44

Visser, Jeroen, Anette van Boxel-Dezaire, Dion Methorst, Tibor Brunt, E. Ronald de Kloet, and Lex Nagelkerken. "Differential Regulation of Interleukin-10 (IL-10) and IL-12 by Glucocorticoids In Vitro." Blood 91, no. 11 (June 1, 1998): 4255–64. http://dx.doi.org/10.1182/blood.v91.11.4255.

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Abstract Antigen-presenting cells are thought to modulate the development of Th1 and Th2 cells by the secretion of interleukin-10 (IL-10) and IL-12. Because glucocorticoids (GC) favor the development of Th2 responses, we determined whether dexamethasone (DEX) and hydrocortisone (HC) have differential effects on lipopolysaccharide-induced IL-10 and IL-12 production in whole-blood cultures. Significant inhibition of IL-12(p40) and IL-12(p70) was found with 10−8 mol/L and 10−9 mol/L DEX respectively, whereas IL-10 was relatively insensitive or even stimulated. Accordingly, the expression of IL-12(p40) and IL-12(p35) mRNA was more sensitive to DEX than IL-10 mRNA. The glucocorticoid receptor (GR) antagonist RU486 enhanced IL-12 production and largely abrogated the inhibition of IL-12 by GC, indicating that this suppression was mainly GR-mediated. High concentrations of RU486 were inhibitory for IL-10, suggesting that GC may exert a positive effect on IL-10. In the presence of neutralizing anti–IL-10 antibodies, DEX was still capable of IL-12 suppression whereas RU486 still enhanced IL-12 production, indicating that GC do not modulate IL-12 via IL-10 exclusively. Taken together these results indicate that GC may favor Th2 development by differential regulation of IL-10 and IL-12.

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45

Visser, Jeroen, Anette van Boxel-Dezaire, Dion Methorst, Tibor Brunt, E. Ronald de Kloet, and Lex Nagelkerken. "Differential Regulation of Interleukin-10 (IL-10) and IL-12 by Glucocorticoids In Vitro." Blood 91, no. 11 (June 1, 1998): 4255–64. http://dx.doi.org/10.1182/blood.v91.11.4255.411a03_4255_4264.

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Abstract:

Antigen-presenting cells are thought to modulate the development of Th1 and Th2 cells by the secretion of interleukin-10 (IL-10) and IL-12. Because glucocorticoids (GC) favor the development of Th2 responses, we determined whether dexamethasone (DEX) and hydrocortisone (HC) have differential effects on lipopolysaccharide-induced IL-10 and IL-12 production in whole-blood cultures. Significant inhibition of IL-12(p40) and IL-12(p70) was found with 10−8 mol/L and 10−9 mol/L DEX respectively, whereas IL-10 was relatively insensitive or even stimulated. Accordingly, the expression of IL-12(p40) and IL-12(p35) mRNA was more sensitive to DEX than IL-10 mRNA. The glucocorticoid receptor (GR) antagonist RU486 enhanced IL-12 production and largely abrogated the inhibition of IL-12 by GC, indicating that this suppression was mainly GR-mediated. High concentrations of RU486 were inhibitory for IL-10, suggesting that GC may exert a positive effect on IL-10. In the presence of neutralizing anti–IL-10 antibodies, DEX was still capable of IL-12 suppression whereas RU486 still enhanced IL-12 production, indicating that GC do not modulate IL-12 via IL-10 exclusively. Taken together these results indicate that GC may favor Th2 development by differential regulation of IL-10 and IL-12.

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46

Zhu, Lei, Tingting Shi, Chengdi Zhong, Yingde Wang, Michael Chang, and Xiuli Liu. "IL-10 and IL-10 Receptor Mutations in Very Early Onset Inflammatory Bowel Disease." Gastroenterology Research 10, no. 2 (2017): 65–69. http://dx.doi.org/10.14740/gr740w.

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47

Myers, Daniel D., Angela E. Hawley, Diana M. Farris, Amy M. Chapman, Shirley K. Wrobleski, Peter K. Henke, and Thomas W. Wakefield. "Cellular IL-10 is more effective than viral IL-10 in decreasing venous thrombosis." Journal of Surgical Research 112, no. 2 (June 2003): 168–74. http://dx.doi.org/10.1016/s0022-4804(03)00144-6.

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48

Kamanaka, Masahito, Sean Kim, Yisong Wan, and Richard Flavell. "Visualization of Il-10 Expressing Lymphocytes and Suppression of Intestinal Inflammation By Il-10." Clinical Immunology 119 (January 2006): S43—S44. http://dx.doi.org/10.1016/j.clim.2006.04.410.

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49

Hsueh, Yu-Hsin, Hung-Wen Chen, Bi-Jhen Syu, Chia-I. Lin, Patrick S. C. Leung, M. Eric Gershwin, and Ya-Hui Chuang. "Endogenous IL-10 maintains immune tolerance but IL-10 gene transfer exacerbates autoimmune cholangitis." Journal of Autoimmunity 95 (December 2018): 159–70. http://dx.doi.org/10.1016/j.jaut.2018.09.009.

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50

Colino, Jesus. "Caveats Regarding the Use of IL-10 and IL-10 Antagonist as Immunotherapeutic Factors." Letters in Drug Design & Discovery 4, no. 7 (October 1, 2007): 487–95. http://dx.doi.org/10.2174/157018007781788552.

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