Relevant bibliographies by topics / IL-10 deficiency

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Academic literature on the topic 'IL-10 deficiency'

Author: Grafiati
Published: 1 April 2023

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Journal articles on the topic "IL-10 deficiency"

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) were compared with an age-matched group with normal pregnancy (NP, n = 14) and gestational hypertension (GH, n = 6). Using immunohistochemistry of parrafin-fixed tissues, trophoblast cells were identified by cytokeratin 7 and cytokeratin 18 staining. The cytokine binding of villous trophoblast cells was scored depending on the extent of circumferential cytoplasm staining (<25%; intermediate or >75%). The cytokine positive decidual cells were scored as a percentage of total extravillous trophoblast cells. There was a reduction in villous IL-10 immunostaining compared with normal term placenta (PE, 10.2 ± 1.1, mean ± SEM; NP, 14.07 ± 1.16 Mann-Whitney U test; p = 0.02). In these patients, there was an increase in TNF-α immunostaining. Sparse endovascular extravillous trophoblast cells demonstrated nuclear IL-10 staining in 30% of patients with preeclampsia. Serum IL-10 was diminished in women with preeclampsia compared with normal pregnancy. In conclusion, villous trophoblast demonstrated diminished immunostaining of IL-10 in preeclampsia. This abnormality may be associated with heightened maternal antifetal immunity and therefore inadequate placental development in preeclampsia.
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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 cardioprotection after myocardial I/R. Wild-type, iNOS −/−, IL-10 −/−, and IL-10/iNOS −/− mice were subjected to in vivo myocardial ischemia (30 min) and reperfusion (24 h). Deficiency of iNOS alone did not significantly alter the extent of myocardial necrosis compared with wild-type mice. We found that deficiency of IL-10 resulted in a significantly ( P < 0.05) larger infarct size than that in wild-type hearts. Interestingly, deficiency of both IL-10 and iNOS yielded significantly ( P < 0.01) larger myocardial infarct sizes compared with wild-type animals. Histological examination of myocardial tissue samples revealed augmented neutrophil infiltration into the I/R myocardium of IL-10 −/− and IL-10/iNOS −/− mice compared with hearts of wild-type mice. These results demonstrate that 1) deficiency of endogenous IL-10 exacerbates myocardial injury after I/R; 2) the cardioprotective effects of IL-10 are not dependent on the presence or absence of iNOS; and 3) deficiency of IL-10 enhances the infiltration of neutrophils into the myocardium after I/R.
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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 from IL-10 −/− mice after LPS injection. In contrast, this dose of LPS did not alter relaxation to ACh in vessels from wild-type (IL-10 +/+) mice. Relaxation to nitroprusside and papaverine was similar in arteries from both IL-10 −/− and IL-10 +/+ mice after vehicle or LPS injection. Because inflammation is associated with increased levels of reactive oxygen species, we also tested the hypothesis that superoxide contributes to the impairment of endothelial function by LPS in the absence of IL-10. Results using confocal microscopy and hydroethidine indicated that levels of superoxide are elevated in carotid arteries from IL-10 −/− mice compared with IL-10 +/+ mice after LPS injection. The impaired relaxation of arteries from IL-10 −/− mice after LPS injection was restored to normal by polyethylene glycol-suspended superoxide dismutase (50 U/ml) or allopurinol (1 mM), an inhibitor of xanthine oxidase. These data provide direct evidence that IL-10 protects endothelial function after an acute inflammatory stimulus by limiting local increases in superoxide. The source of superoxide in this model may be xanthine oxidase.
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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, but produced less LPS binding protein (LBP). The deficiency in LBP production may explain the failure of IL-10-/- DCs to respond normally to LPS. Moreover, lack of IL-10 modulated the proportions of CD11c+CD8+ and CD11c+B220+ DCs, which play an important role in local inflammatory responses and tolerance. IL-10 deficiency also blocked expression of galectin-1, CD205 and CD103, which are necessary for central and peripheral tolerance. While they did not respond to LPS, IL-10-/- DCs produced increased levels of IL-6 and CCL4 after TNF-α treatment. Together, our results demonstrate that IL-10 deficiency affects the immune functions of DCs, which may contribute to the increased severity of autoimmune diseases seen in IL-10-/- mice.
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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 that ongoing systemic inflammation was a confounding factor. In a pathogen-free environment, IL-10 deficiency slightly increased infarct volume and neurologic deficits. Induction of proinflammatory molecules in the IL-10 KO brain was similar to that in the WT 6 hours after ischemia, but was higher at day 4, while differences decreased at day 7. Deficiency of IL-10 promoted the presence of more mature phagocytic cells in the ischemic tissue, and enhanced the expression of M2 markers and the T-cell inhibitory molecule CTLA-4. These findings agree with a role of IL-10 in attenuating local inflammatory reactions, but do not support an essential function of IL-10 in lesion resolution. Upregulation of alternative immunosuppressive molecules after brain ischemia can compensate, at least in part, the absence of IL-10.
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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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