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176 results on '"Zenewicz, Lauren A."'

6. Cx3cr1 controls kidney resident macrophage heterogeneity

Author

Yashchenko, Alex, primary, Bland, Sarah J., additional, Song, Cheng J., additional, Ahmed, Ummey Khalecha Bintha, additional, Sharp, Rachel, additional, Darby, Isabella G., additional, Cordova, Audrey M., additional, Smith, Morgan E., additional, Lever, Jeremie M., additional, Li, Zhang, additional, Aloria, Ernald J., additional, Khan, Shuja, additional, Maryam, Bibi, additional, Liu, Shanrun, additional, Crowley, Michael R., additional, Jones, Kenneth L., additional, Zenewicz, Lauren A., additional, George, James F., additional, Mrug, Michal, additional, Crossman, David K., additional, Hopp, Katharina, additional, Stavrakis, Stavros, additional, Humphrey, Mary B., additional, Ginhoux, Florent, additional, and Zimmerman, Kurt A., additional

Published
2023
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17. IL-22BP is regulated by the inflammasome and modulates tumorigenesis in the intestine

Author

Huber, Samuel, Gagliani, Nicola, Zenewicz, Lauren A., Huber, Francis J., Bosurgi, Lidia, Hu, Bo, Hedl, Matija, Zhang, Wei, OConnor, Jr., William, Murphy, Andrew J., Valenzuela, David M., Yancopoulos, George D., Booth, Carmen J., Cho, Judy H., Ouyang, Wenjun, Abraham, Clara, and Flavell, Richard A.

Subjects
Metastasis -- Research, Colorectal cancer -- Physiological aspects -- Development and progression, Interleukins -- Physiological aspects -- Health aspects, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Chronic mucosal inflammation and tissue damage predisposes patients to the development of colorectal cancer (1). This association could be explained by the hypothesis that the same factors and pathways important [...]

Published
2012

24. Sugar-Coated Regulation of T Cells

Author

Eynon, Elizabeth E., Zenewicz, Lauren A., and Flavell, Richard A.

Subjects
Microbial polysaccharides, T cells, Biological sciences
Abstract

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.cell.2005.06.035 Byline: Elizabeth E. Eynon (1)(2), Lauren A. Zenewicz (1), Richard A. Flavell (1)(2) Abstract: The human gut is host to hundreds of different species of commensal bacteria that live in peaceful partnership with the host immune system. These commensal bacteria are far from neutral bystanders as they are intimately involved in the development of the immune system. Reporting in this issue of Cell, Kasper and colleagues (Mazmanian et al., 2005) reveal that a bacterial polysaccharide, PSA, produced by the commensal bacterium Bacteroides fragilis directs development of the immune system of the mouse host. Author Affiliation: (1) Section of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520 (2) Howard Hughes Medical Institute, New Haven, Connecticut 06520

Published
2005

32. Defective Intestinal Mucin-Type O-Glycosylation Causes Spontaneous Colitis-Associated Cancer in Mice

Author

Bergstrom, Kirk, primary, Liu, Xiaowei, additional, Zhao, Yiming, additional, Gao, Nan, additional, Wu, Qian, additional, Song, Kai, additional, Cui, Yi, additional, Li, Yun, additional, McDaniel, J. Michael, additional, McGee, Samuel, additional, Chen, Weichang, additional, Huycke, Mark M., additional, Houchen, Courtney W., additional, Zenewicz, Lauren A., additional, West, Christopher M., additional, Chen, Hong, additional, Braun, Jonathan, additional, Fu, Jianxin, additional, and Xia, Lijun, additional

Published
2016
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34. Memory/effector (CD45RB lo ) CD4 T cells are controlled directly by IL-10 and cause IL-22–dependent intestinal pathology

Author

O'Connor, William, Nakae, Susumu, Gagliani, Nicola, Wan, Yisong Y., Kamanaka, Masahito, Rathinam, Chozhavendan, Zenewicz, Lauren A., Hao, Liming, Huber, Samuel, Iwakura, Yoichiro, and Flavell, Richard A.

Subjects
chemical and pharmacologic phenomena, hemic and immune systems
Abstract

Interleukin-10 acts directly on CD45RBlo but not CD45RBhi cells to control colitis upon transfer into Rag1-deficient recipients.The role of direct IL-10 signaling in different T cell subsets is not well understood. To address this, we generated transgenic mice expressing a dominant-negative IL-10 receptor specifically in T cells (CD4dnIL-10Rα). We found that Foxp3-depleted CD45RBlo (regulatory T cell [Treg cell]–depleted CD45RBlo) but not CD45RBhi CD4+ T cells are controlled directly by IL-10 upon transfer into Rag1 knockout (KO) mice. Furthermore, the colitis induced by transfer of Treg cell–depleted CD45RBlo CD4+ T cells into Rag1 KO mice was characterized by reduced Th1 and increased Th17 cytokine messenger RNA levels in the colon as compared with the colitis induced by transfer of CD45RBhi T cells. In contrast to the CD45RBhi transfer colitis model, in which IL-22 is protective, we found that T cell–derived IL-22 was pathogenic upon transfer of Treg cell–depleted CD45RBlo T cells into Rag1 KO mice. Our results highlight characteristic differences between colitis induced by naive (CD45RBhi) and memory/effector (Treg cell–depleted CD45RBlo) cells and different ways that IL-22 impacts inflammatory bowel disease.

Published
2011
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35. Correction: Corrigendum: NLRP10 is a NOD-like receptor essential to initiate adaptive immunity by dendritic cells

Author

Eisenbarth, Stephanie C., primary, Williams, Adam, additional, Colegio, Oscar R., additional, Meng, Hailong, additional, Strowig, Till, additional, Rongvaux, Anthony, additional, Henao-Mejia, Jorge, additional, Thaiss, Christoph A., additional, Joly, Sophie, additional, Gonzalez, David G., additional, Xu, Lan, additional, Zenewicz, Lauren A., additional, Haberman, Ann M., additional, Elinav, Eran, additional, Kleinstein, Steven H., additional, Sutterwala, Fayyaz S., additional, and Flavell, Richard A., additional

Published
2015
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36. Bacterial flagellin stimulates TLR5-dependent defense against vancomycin-resistant Enterococcus infection

Author

Kinnebrew, Melissa A., Ubeda, Carles, Zenewicz, Lauren A., Smith, Nichole, Flavell, Richard A., and Pamer, Eric G.

Subjects
Male, Interleukins, Gene Expression, Proteins, Cell Count, Pancreatitis-Associated Proteins, Vancomycin Resistance, biochemical phenomena, metabolism, and nutrition, Immunohistochemistry, Article, Immunity, Innate, Anti-Bacterial Agents, Mice, Inbred C57BL, Disease Models, Animal, Mice, Toll-Like Receptor 5, Intestine, Small, Animals, Cytokines, Female, Enterococcus, Gram-Positive Bacterial Infections, Flagellin
Abstract

Treatment of vancomycin-resistant Enterococcus (VRE) infections is limited by the paucity of effective antibiotics. Administration of broad-spectrum antibiotics promotes VRE colonization by down-regulating homeostatic innate immune defenses. Intestinal epithelial cells and Paneth cells express antimicrobial factors on direct or indirect stimulation of the Toll-like receptor (TLR)-myeloid differentiation factor 88-mediated pathway by microbe-derived molecules. Here, we demonstrate that the TLR5 agonist flagellin restores antibiotic-impaired innate immune defenses and restricts colonization with VRE. Flagellin stimulates the expression of RegIIIgamma, a secreted C-type lectin that kills gram-positive bacteria, including VRE. Systemic administration of flagellin induces RegIIIgamma expression in intestinal epithelial cells and Paneth cells along the entire length of the small intestine. Induction of RegIIIgamma requires TLR5 expression in hematopoietic cells and is dependent on interleukin 22 expression. Systemic administration of flagellin to antibiotic-treated mice dramatically reduces VRE colonization. By enhancing mucosal resistance to multidrug-resistant organisms, flagellin administration may provide a clinically useful approach to prevent infections in patients treated with broad-spectrum antibiotics.

Published
2010

37. Anti- and Pro-inflammatory Roles of TGF-β, IL-10, and IL-22 In Immunity and Autoimmunity

Author

Sanjabi, Shomyseh, Zenewicz, Lauren A., Kamanaka, Masahito, and Flavell, Richard A.

Subjects
Inflammation, Transforming Growth Factor beta, Interleukins, Anti-Inflammatory Agents, Animals, Humans, Cell Differentiation, Inflammation Mediators, Article, Autoimmune Diseases, Interleukin-10
Abstract

Cytokines play a major role in maintaining lymphocyte homeostasis under both steady-state and inflammatory conditions. Unregulated lymphocytes in steady-state conditions can lead to autoimmunity, whereas during inflammation they can cause excessive tissue damage. Regulatory cytokines function in combination with other environmental signals to properly modulate the function and the extent of lymphocyte activation. Many recent studies have highlighted the importance of regulatory cytokines in controlling the differentiation and function of lymphocytes under steady-state and inflammatory conditions, as well as minimizing tissue damage.

Published
2009

38. Hypoxic modulation of hepatocyte responses to the cytokine interleukin-22.

Author

Budda, Scott A, Bhattarai, Krishna, Alexander, Justine L, and Zenewicz, Lauren A

Subjects
INTERLEUKIN-22, INFLAMMATION, EPITHELIAL cells, LIPOCALIN-1, MITOGEN-activated protein kinases, DISEASES, GENETICS
Abstract

The cytokine interleukin-22 (IL-22) is a potent regulator of tissue responses during inflammation. Depending on the context of inflammation, IL-22 can have protective or inflammatory effects on epithelial cells. This dual nature of IL-22 leads us to hypothesize that its activity must be exquisitely regulated to prevent host tissue damage. Environmental factors may act as a cellular cue as to how cells respond to IL-22. Inflammatory environments are characterized by low oxygen and thus we examined whether cells respond differently to IL-22 hypoxia compared with normoxia. In this study, we show that hepatocyte responses to IL-22 stimulation are reduced in hypoxic environments. IL-22 stimulation of hepatocytes incubated in low oxygen led to reduced levels of activated signal transducer and activator of transcription 3 and further downstream effects such as reduced induction of the anti-microbial protein, lipocalin-2. This modulation appears to be independent of the hypoxia-inducible factor-1α signaling pathway. Thus, hypoxia that accompanies chronic inflammation may be a mechanism to regulate the bioactivity of the dual-natured IL-22 cytokine. [ABSTRACT FROM AUTHOR]

Published
2017
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40. IL-22 Signaling Contributes to West Nile Encephalitis Pathogenesis

Author

Wang, Penghua, primary, Bai, Fengwei, additional, Zenewicz, Lauren A., additional, Dai, Jianfeng, additional, Gate, David, additional, Cheng, Gong, additional, Yang, Long, additional, Qian, Feng, additional, Yuan, Xiaoling, additional, Montgomery, Ruth R., additional, Flavell, Richard A., additional, Town, Terrence, additional, and Fikrig, Erol, additional

Published
2012
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41. Modulation of the immune response by Gram -positive bacterial pathogens

Author

Zenewicz, Lauren A and Zenewicz, Lauren A

Abstract

Pathogens have evolved mechanisms to counteract different arms of the immune system. By downmodulating components of the immune response, a pathogen can interfere with the ability of the immune system to respond appropriately to each infection. In these studies, we examine how two different Gram-positive pathogens, Listeria monocytogenes and Bacillus anthracis, modulate the immune response. L. monocytogenes is a facultative intracellular pathogen that is an ideal pathogen for modeling the immune response since its pathogenesis has been well described at a molecular, cellular and organism level. L. monocytogenes invades macrophages, can escape into the cytoplasm and spread intercellularly. Due to the intracellular nature of infection, CD4 and CD8 T cells are important for control of infection and are essential for mediating protective immunity. On the other hand, the immune response during pulmonary B. anthracis infection has not been well examined. Inhalational anthrax is a rapidly progressing disease in which spores germinate within alveolar macrophages and then disseminate to the lymph nodes, causing an uncontrollable infection. Homologous virulence factors, such as phosphoslipases (PLCs) and hemolysins, may play similar roles in the pathogenesis of these two bacterial species. In these studies, we examine: (1) how antigen compartmentalization by L. monocytogenes can affect the ability of memory CD8 T cells to provide protective immunity, (2) the role of two virulence factors, listeriolysin O and phosphatidylcholine-preferring-PLC, in inducing FasL on T cells during L. monocytogenes infection, (3) the role of neutrophils during pulmonary B. anthracis infection, (4) the generation of an antigen-specific T cell response during pulmonary B. anthracis infection, and (5) the downmodulation of the immune response by B. anthracis phosphatidylinositol-specific-PLC during infection. These studies reveal how bacterial pathogens have evolved alongside their hosts to modulate

Published
2004

42. Memory/effector (CD45RBlo) CD4 T cells are controlled directly by IL-10 and cause IL-22–dependent intestinal pathology

Author

Kamanaka, Masahito, primary, Huber, Samuel, additional, Zenewicz, Lauren A., additional, Gagliani, Nicola, additional, Rathinam, Chozhavendan, additional, O'Connor, William, additional, Wan, Yisong Y., additional, Nakae, Susumu, additional, Iwakura, Yoichiro, additional, Hao, Liming, additional, and Flavell, Richard A., additional

Published
2011
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