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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 (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 (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 (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 (2000): G829—G833. http://dx.doi.org/10.1152/ajpgi.2000.278.6.g829.

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Abstract (sommario):
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 diseas
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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 (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 (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 (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, et al. "IL-10 subfamily members: IL-19, IL-20, IL-22, IL-24 and IL-26." Immunology Letters 88, no. 3 (2003): 171–74. http://dx.doi.org/10.1016/s0165-2478(03)00087-7.

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9

Murray, Henry W., Christina M. Lu, Smita Mauze, et al. "Interleukin-10 (IL-10) in Experimental Visceral Leishmaniasis and IL-10 Receptor Blockade as Immunotherapy." Infection and Immunity 70, no. 11 (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
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10

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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11

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

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12

Doddy, Febryan*1 Parluhutan Siagian2 &. Ricke Loesnihari1. "INTERLEUKIN LEVEL 10 AS A BIOMARKER IN IMPROVING TREATMENT OF PULMONARY TUBERCULOSIS BEFORE TREATMENT AND AFTER 2 MONTHS OF ANTI TUBERCULOSIS TREATMENT." INTERNATIONAL JOURNAL OF RESEARCH SCIENCE & MANAGEMENT 7, no. 5 (2020): 48–52. https://doi.org/10.5281/zenodo.3865414.

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<strong>Background</strong> Tuberculosis (TB) is an important community health problem in the world. Indonesia ranks third in the world after China and India. The cause of TB is Mycobacterium tuberculosis. The disease is the result of chronic interactions between intracellular microorganisms and the immune system response. Interleukin 10 (IL-10) is ananti-inflammatory cytokine. These cytokines are produced by macrophages and T cells during tuberculosis infection. The success of TB control is highly dependent on the diagnosis and appropriate treatment and evaluating its treatment. Many TB suffe
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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 (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 m
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14

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

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15

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 (2017): 35–38. http://dx.doi.org/10.20969/vskm.2017.10(3).35-38.

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16

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

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17

Zhang, Guicheng, Maria Nelia Manaca, Michelle McNamara-Smith, 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 (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 monon
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18

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 (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
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19

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 (2012): 39–40. http://dx.doi.org/10.1016/j.molimm.2012.03.004.

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20

Sari, Shinta Dewi Permata, Erlin Listiyaningsih, Wening Tri Mawanti, and Dewi Martalena. "Anti-Inflammatory Cytokine (IL-10) Profiles and Ratio of IL-6/IL-10 in Covid-19 Patients." Muhammadiyah Medical Journal 5, no. 1 (2024): 1. http://dx.doi.org/10.24853/mmj.5.1.1-8.

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Background: The number of COVID-19 cases in Indonesia has continually increased since the first cases appeared in March 2020. This disease is due to SARS-CoV-2 virus infection in the respiratory system that induces an immune response. The innate and adaptive immune response triggered the secretion of an excessive pro-inflammatory cytokine-caused cytokine storm that became one of the mechanisms of acute respiratory distress (ARDS). The anti-inflammatory cytokines (IL-10, IL-13, and IL-4) were secreted as the immune response in the ARDS condition. Purposes: This study aims to determine the ratio
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21

Ramkumar, Hema L., De Fen Shen, Jingsheng Tuo, et al. "IL-10 -1082 SNP and IL-10 in primary CNS and vitreoretinal lymphomas." Graefe's Archive for Clinical and Experimental Ophthalmology 250, no. 10 (2012): 1541–48. http://dx.doi.org/10.1007/s00417-012-2037-1.

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22

Baranova, N. I., B. A. Molotilov, L. A. Ashchina та 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, № 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
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23

M’Bondoukwé, Noé Patrick, Reinne Moutongo, Komi Gbédandé, 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 (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 su
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24

Oral, Haluk B, Sergei V Kotenko, Mustafa Yılmaz, et al. "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 (2006): 380–88. http://dx.doi.org/10.1002/eji.200425523.

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25

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 (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 L
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26

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 (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
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27

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 (1998): 4255–64. http://dx.doi.org/10.1182/blood.v91.11.4255.411a03_4255_4264.

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Abstract (sommario):
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
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28

Körholz, Dieter, Ursula Banning, Halvard Bönig, et al. "The Role of Interleukin-10 (IL-10) in IL-15–Mediated T-Cell Responses." Blood 90, no. 11 (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-
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29

Körholz, Dieter, Ursula Banning, Halvard Bönig, et al. "The Role of Interleukin-10 (IL-10) in IL-15–Mediated T-Cell Responses." Blood 90, no. 11 (1997): 4513–21. http://dx.doi.org/10.1182/blood.v90.11.4513.4513_4513_4521.

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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 recepto
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30

de Waal Malefyt, R., J. Abrams, B. Bennett, C. G. Figdor, and J. E. de Vries. "Interleukin 10(IL-10) inhibits cytokine synthesis by human monocytes: an autoregulatory role of IL-10 produced by monocytes." Journal of Experimental Medicine 174, no. 5 (1991): 1209–20. http://dx.doi.org/10.1084/jem.174.5.1209.

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In the present study we demonstrate that human monocytes activated by lipopolysaccharides (LPS) were able to produce high levels of interleukin 10 (IL-10), previously designated cytokine synthesis inhibitory factor (CSIF), in a dose dependent fashion. IL-10 was detectable 7 h after activation of the monocytes and maximal levels of IL-10 production were observed after 24-48 h. These kinetics indicated that the production of IL-10 by human monocytes was relatively late as compared to the production of IL-1 alpha, IL-1 beta, IL-6, IL-8, tumor necrosis factor alpha (TNF alpha), and granulocyte col
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31

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 (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, I
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32

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 (1999): 1929–39. http://dx.doi.org/10.1016/s0002-9440(10)65512-5.

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33

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 (1995): 129. http://dx.doi.org/10.1097/00002371-199508000-00014.

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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 (1995): 201–6. http://dx.doi.org/10.1007/bf00262298.

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35

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 (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 sa
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36

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 (2007): S241. http://dx.doi.org/10.1016/j.jaci.2006.12.311.

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37

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

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38

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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39

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

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40

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

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41

Yin, Zhinan, Gul Bahtiyar, Na Zhang, et al. "IL-10 Regulates Murine Lupus." Journal of Immunology 169, no. 4 (2002): 2148–55. http://dx.doi.org/10.4049/jimmunol.169.4.2148.

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42

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

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43

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

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

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Otsumi, Takemi, Kenichiro Yata, Haruko Sakaguchi, et al. "IL-10 in Myeloma Cells." Leukemia & Lymphoma 43, no. 5 (2002): 969–74. http://dx.doi.org/10.1080/10428190290021579.

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46

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

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47

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

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Abstract (sommario):
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&amp;lt;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,
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48

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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49

Myers, Daniel D., Angela E. Hawley, Diana M. Farris, et al. "Cellular IL-10 is more effective than viral IL-10 in decreasing venous thrombosis." Journal of Surgical Research 112, no. 2 (2003): 168–74. http://dx.doi.org/10.1016/s0022-4804(03)00144-6.

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50

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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