Готові списки джерел за темами / Th2-dependent

Добірка наукової літератури з теми "Th2-dependent"

Автор: Grafiati

Опубліковано: 14 березня 2023

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Статті в журналах з теми "Th2-dependent"

Müller, K. M., F. Jaunin, I. Masouyé, J. H. Saurat, and C. Hauser. "Th2 cells mediate IL-4-dependent local tissue inflammation." Journal of Immunology 150, no. 12 (June 15, 1993): 5576–84. http://dx.doi.org/10.4049/jimmunol.150.12.5576.

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Abstract We investigated whether polyclonal murine Th1 and Th2 cells obtained after short term culture in vitro were capable of mediating tissue inflammation in vivo. Th cells were pulsed with mAb to the TCR/CD3 complex and injected into the footpads or ears of naive syngeneic recipient mice. Th1 induced delayed swelling that peaked at 24 to 48 h and lasted > or = 5 days. Th2-induced swelling peaked at 6 h and lasted < or = 48 h. Similar responses were also observed in athymic nude mice. Lesions with both Th1 and Th2 cells contained a predominant neutrophilic infiltrate at 6 h, and mainly mononuclear cells at 48 h. The inflammatory response with Th2 was blocked by cyclosporin A, by mAb to IL-4 or by soluble rIL-4R. The requirement for IL-4 was early and transient. Four alloreactive short term Th2 clones induced swelling in allogeneic recipients. mAb- and IL-4-dependent swelling responses were also observed with two long term Th2 clones. Our results demonstrate that Th2 cells mediate IL-4-dependent tissue inflammation, and strengthen the concept that Th2 cells play an important role in some T cell-dependent immune reactions and, possibly, in allergic disorders such as atopic dermatitis and allergic asthma.

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Foucras, Gilles, Christiane Coureau, Leo Beijleveld, Philippe Druet, Abdelhadi Saoudi та Jean-Charles Guéry. "β2-Microglobulin-Dependent T Cells Are Not Necessary for Alloantigen-Induced Th2 Responses After Neonatal Induction of Lymphoid Chimerism in Mice". Journal of Immunology 161, № 4 (15 серпня 1998): 1751–57. http://dx.doi.org/10.4049/jimmunol.161.4.1751.

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Abstract We have analyzed the requirement for β2-microglobulin (β2m)-dependent T cells in the generation of allogeneic Th2 responses in vivo. A neonatal injection of semiallogeneic cells in BALB/c mice induces a state of chimerism that promotes the differentiation of donor-specific CD4+ T cells toward the Th2 phenotype. Polyclonal T-B cell interactions occur in this model between host Th2 and donor B cells, resulting in the production of IgE Abs. IgE production and Th2-priming are critically dependent upon the early production of IL-4. Our data in the present paper demonstrate that: 1) IgE synthesis and the up-regulation of MHC class II and CD23 molecules on B cells are independent of β2m expression in the host, 2) no difference in the induction of CD4 alloreactive Th2 cells could be observed between β2m−/− and their wild-type control littermates when Th2-priming was measured in adult mice, and 3) the Th2 response and IgE production is induced in the complete absence of β2m-dependent T cells both in the host and in the inoculum. Therefore, using a variety of assays, we could not demonstrate diminished responses in mice with a disrupted β2m gene in this model of Th2-mediated allogeneic interaction, indicating that β2m-dependent NK1.1+ and CD8+ T cells are not required for the generation of alloreactive Th2 responses in vivo.

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Hasegawa, Akihiro, and Toshinori Nakayama. "Impaired GATA3-dependent chromatin remodeling and Th2 cell differentiation leading to attenuated allergic airway inflammation in aging mice (85.1)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S118. http://dx.doi.org/10.4049/jimmunol.178.supp.85.1.

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Abstract Age-related changes in lymphocytes are most prominent in the T cell compartment. In the present study, we used 8–12 month-old aging mice and a well-established in vitro Th1/Th2 cell differentiation culture system to identify molecular defects in Th1/Th2 cell differentiation that can be detected in the relatively early stages of aging. The capability to differentiate into Th2 cells is reduced in aging mouse CD4+ T cells. Decreased activation of the ERK MAPK cascade upon TCR stimulation, but normal [Ca2+]i mobilization and normal IL-4-induced STAT6 activation were observed in aging mouse CD4+ T cells. In addition, reduced expression of GATA3 was detected in developing Th2 cells. Chromatin remodeling of the Th2 cytokine gene locus was found to be impaired. Th2-dependent allergic airway inflammation was milder in aging mice compared with in young adult mice. These results suggest that the levels of Th2 cell differentiation and resulting Th2-dependent immune responses, including allergic airway inflammation, decline during aging through defects in the activation of the ERK MAPK cascade, expression of GATA3 protein and GATA3-dependent chromatin remodeling of the Th2 cytokine gene locus. In the present study, we provide the first evidence indicating that a chromatin-remodeling event in T cells is impaired by aging.

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Tjota, Melissa, Kelly Blaine, Nora Barrett та Anne Sperling. "Signaling through FcRγ receptors on dendritic cells drives IL-33 dependent Th2-type responses (HYP6P.262)". Journal of Immunology 192, № 1_Supplement (1 травня 2014): 118.7. http://dx.doi.org/10.4049/jimmunol.192.supp.118.7.

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Abstract Dendritic cells (DCs) play a critical role in the development of Th2 responses during atopic asthma, but the mechanism by which allergens drive DCs to promote Th2 responses is still unclear. Previously, we demonstrated that allergen-specific IgG immune complexes (ICs) enhance secondary Th2 responses via an IL-33-dependent mechanism by ligating FcγRIII on antigen presenting cells. To identify if this pathway was common to other Th2 stimuli, we used house dust mite (HDM) extract. While HDM-mediated allergic inflammation was not dependent on FcγRIII, it was reliant on the common signaling component FcRγ as FcRγ-/- mice failed to develop Th2 responses in the lung. Notably, ligation of FcRγ associated receptors, FcγRIII and Dectin-2, on DCs treated with ICs or HDM respectively, upregulated IL-33 in an FcRγ and PI3-kinase dependent manner suggesting a common pathway by which Th2 stimuli can direct the development of DCs that induce Th2 differentiation. Reestablishment of Th2 responses in the FcRγ-/- mice with an adoptive transfer of HDM-sensitized FcRγ+/- DCs indicated that the lack of response in the FcRγ-/- mice was due to a deficient response from the DCs. Interestingly, addition of recombinant IL-33 during HDM sensitization was sufficient to restore airway inflammation in FcRγ-/- mice. Overall, these data identify a mechanism whereby Th2 stimuli signal through FcRγ associated receptors on DCs to upregulate IL-33 production and induce Th2-mediated allergic airway inflammation.

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Zhou, Meixia, Wenjun Ouyang, Qian Gong, Samuel G. Katz, J. Michael White, Stuart H. Orkin, and Kenneth M. Murphy. "Friend of GATA-1 Represses GATA-3–dependent Activity in CD4+ T Cells." Journal of Experimental Medicine 194, no. 10 (November 12, 2001): 1461–71. http://dx.doi.org/10.1084/jem.194.10.1461.

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The development of naive CD4+ T cells into a T helper (Th) 2 subset capable of producing interleukin (IL)-4, IL-5, and IL-13 involves a signal transducer and activator of transcription (Stat)6-dependent induction of GATA-3 expression, followed by Stat6-independent GATA-3 autoactivation. The friend of GATA (FOG)-1 protein regulates GATA transcription factor activity in several stages of hematopoietic development including erythrocyte and megakaryocyte differentiation, but whether FOG-1 regulates GATA-3 in T cells is uncertain. We show that FOG-1 can repress GATA-3–dependent activation of the IL-5 promoter in T cells. Also, FOG-1 overexpression during primary activation of naive T cells inhibited Th2 development in CD4+ T cells. FOG-1 fully repressed GATA-3–dependent Th2 development and GATA-3 autoactivation, but not Stat6-dependent induction of GATA-3. FOG-1 overexpression repressed development of Th2 cells from naive T cells, but did not reverse the phenotype of fully committed Th2 cells. Thus, FOG-1 may be one factor capable of regulating the Th2 development.

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Ho, I.-Cheng, David Lo, and Laurie H. Glimcher. "c-maf Promotes T Helper Cell Type 2 (Th2) and Attenuates Th1 Differentiation by Both Interleukin 4–dependent and –independent Mechanisms." Journal of Experimental Medicine 188, no. 10 (November 16, 1998): 1859–66. http://dx.doi.org/10.1084/jem.188.10.1859.

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The c-maf protooncogene is a T helper cell type 2 (Th2)-specific transcription factor that activates the interleukin (IL)-4 promoter in vitro. Although it has been postulated that c-maf directs the Th2-specific expression of the IL-4 gene in vivo, direct evidence that c-maf functions during the differentiation of normal, primary T cells is lacking. We now demonstrate that overexpression of c-maf in vivo skews the Th immune response along a Th2 pathway, as evidenced by increased production of Th2 cytokines and the IL-4–dependent immunoglobulins, IgG1 and IgE. The overproduction of IgGl and IgE in the CD4 promoter/c-maf transgenic mice was IL-4 dependent since this was not observed in c-maf transgenic mice bred onto an IL-4–deficient background. Ectopic expression of c-maf in mature Th1 cells did not confer on them the ability to produce IL-4, but did decrease the production of IFN-γ. The attenuation of Th1 differentiation by c-maf overexpression occurred by a mechanism that was independent of IL-4 and other Th2 cytokines, and could be overcome by IL-12. These studies demonstrate that c-maf promotes Th2 differentiation by IL-4–dependent mechanisms and attenuates Th1 differentiation by Th2 cytokine-independent mechanisms.

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Kaplan, Mark H., Andrea L. Wurster, Stephen T. Smiley, and Michael J. Grusby3. "Stat6-Dependent and -Independent Pathways for IL-4 Production." Journal of Immunology 163, no. 12 (December 15, 1999): 6536–40. http://dx.doi.org/10.4049/jimmunol.163.12.6536.

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Abstract Stat6 has been shown to have a crucial role in the IL-4-dependent differentiation of Th2 cells. In this report, we explore whether in vitro Th2 differentiation driven by altered costimulatory signals or Ag dose is Stat6 dependent. We find that blocking B7-1 signaling in vitro promotes the differentiation of IL-4-secreting Th2 cells in wild-type but not Stat6-deficient T cell cultures. Additionally, stimulation with peptide Ag doses that normally result in the production of Th2 cells in vitro fails to do so in cultures of Stat6-deficient cells. We also demonstrate that Stat6 is required for the in vitro differentiation of CD8+ T cells into IL-4-secreting cytotoxic T cell type 2 cells. However, IL-4 expression is not absolutely dependent on Stat6. We demonstrate that populations of T cells that do not require IL-4 for their development, such as NK T cells, are still competent to secrete IL-4 in the absence of Stat6. These results demonstrate that Stat6 is required for the differentiation program leading to the generation of Th2 and cytotoxic T cell type 2 cells but not for IL-4 expression in cells that do not undergo differentiation in response to IL-4.

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Magalhaes, Joao Gamelas, Jörg H. Fritz, Lionel Le Bourhis, Gernot Sellge, Leonardo H. Travassos, Thirumahal Selvanantham, Stephen E. Girardin, Jennifer L. Gommerman, and Dana J. Philpott. "Nod2-Dependent Th2 Polarization of Antigen-Specific Immunity." Journal of Immunology 181, no. 11 (November 18, 2008): 7925–35. http://dx.doi.org/10.4049/jimmunol.181.11.7925.

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Kim, Daniel C., F. Ida Hsu, Nora A. Barrett, Daniel S. Friend, Roland Grenningloh, I.-Cheng Ho, Amal Al-Garawi, et al. "Cysteinyl Leukotrienes Regulate Th2 Cell-Dependent Pulmonary Inflammation." Journal of Immunology 176, no. 7 (March 17, 2006): 4440–48. http://dx.doi.org/10.4049/jimmunol.176.7.4440.

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Hook, Sarah, Melanie Prout, Mali Camberis, Monika Konig, Andreas Zimmer, Gino Van Heeke, and Graham Le Gros. "Th2-dependent airway eosinophilia is regulated by preproenkephalin." Journal of Neuroimmunology 107, no. 1 (July 2000): 59–65. http://dx.doi.org/10.1016/s0165-5728(00)00243-5.

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Більше джерел

Дисертації з теми "Th2-dependent"

G, Truglio. "Synthesis and biological evaluation of hAMCase inhibitors and anomeric equilibrium of gluco and xylopyranose derivatives in D2O." Doctoral thesis, Università di Siena, 2019. http://hdl.handle.net/11365/1070882.

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Asthma is considered a serious health and socioeconomic issue all over the world, affecting more than 300 million individuals. It is a chronic inflammatory disease characterized by airway inflammation, mucus hypersecretion and airway hyperresponsiveness. One of the causes of this disorder is the result of an abnormal Th2-dependent response to environmental antigens. In particular, Th2 cells produce cytokines, such as interleukin (IL)-4, IL-5, IL-9, and especially IL-13, in the airway wall, associated with the asthma symptoms. Acidic Mammalian Chitinase (AMCase) is a chitinolytic enzyme belonging to glycosyl hydrolases family. AMCase seems to be involved in Th2 inflammatory diseases, such as asthma. It has been demonstrated that during Th2-dependent inflammation IL-13 induces the AMCase expression in the airways epithelial cells and alveolar macrophages, which stimulates the release of chemokines, recruiters of proinflammatory agents. In conclusion, AMCase contributes to the pathogenesis of asthma and represents a potential therapeutic target for the treatment of this disease and other forms of Th2-mediated inflammation. Prof. Botta research group, after a careful study, designed and synthesized an innovative AMCase inhibitor, BM22 (Ki = 13.2 μM), characterized by a macrocyclic structure. The aim of this work was the study of BM22 chemical space in order to improve its activity with the exploration of the macrocyclic portion, the linker length and substitution the amidinourea terminal moiety with a diamino-triazole group. Some of these compounds have been tested against AMCase enzyme and showed a better activity compared to that of BM22. The last chapter of this thesis deals with the study of the anomeric equilibrium of xylo and glucopyranoses in D2O at room temperature. The anomeric effect is an effect that determines the increased preference of the axial position of the C1 substituent in a pyranose ring, rather than the sterically preferred equatorial position. Two models were proposed to explain this effect: Electrostatic model and Hyperconjugation model. The anomeric ratio was established by qNMR, which involved integration of resolved signals in 1H-NMR spectrum. Interesting results have been obtained, as all compounds showed a preference for α-anomer, including, surprisingly, the electron donating methoxy group as well.

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Swaidani, Shadi. "THE ROLE OF ACT1 IN IL-25 DEPENDENT TH2 RESPONSES AND ALLERGIC AIRWAY INFLAMMATION AND AIRWAY HYPERRESPONSIVENESS." Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1270240862.

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Klein, Sebastian [Verfasser]. "Modulation of the TH1/TH2 differentiation by B cells, C5aR1 and CD154 in antigen dose dependent mouse models / Sebastian Klein." Lübeck : Zentrale Hochschulbibliothek Lübeck, 2018. http://d-nb.info/1153039354/34.

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Neumann, Andersen Grethe. "Systemic sclerosis : vascular, pulmonary and immunological aspects." Doctoral thesis, Umeå universitet, Reumatologi, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-1806.

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In systemic sclerosis (SSc), interstitial lung disease (ILD) and engagement of the vascular system lead to increased morbidity and mortality. The aim of this thesis was to elucidate, in a consecutively included cohort of SSc (limited and diffuse) patients (n = 33), the T cell cytokine profile driving the disease in ILD and to explore the role of matrix metalloproteinase 9 (MMP-9) and its inhibitor: tissue inhibitor of metalloproteinase 1 (TIMP-1) in the extracellular matrix (ECM) degrading process leading to fibrous scarring and honey combing. Moreover, to characterize the role of nitric oxide (NO) in vascular engagement. Peripheral arterial changes cause Raynaud’s phenomenon and digital ulcers. Nitric oxide (NO) a main inducer of vasodilation is produced by endothelial nitric oxide synthase (eNOS) in response to changes in blood flow or by inflammatory cytokine inducible (i) NOS. In the vascular smooth muscle cell (VSMC) NO activates guanylate cyclase to produce cGMP, causing relaxation. We showed elevated plasma nitrate, a degradation product of NO, and increased urinary excretion of nitrate and cGMP. Plasma nitrate correlated with elevated levels of endothelial adhesion molecules: endothelial (E) selectin and vascular adhesion molecule 1, indicating that the activated endothelium is the site of NO synthesis by iNOS. Endothelial staining for E-selectin and the finding of iNOS and eNOS in SSc skin biopsies supported this notion. In SSc increased vascular stiffness may limit the NO vasodilatory effects. We found normal endothelium-dependent (i.e. flow mediated (FMD%)) and endothelium-independent (i.e. nitroglycerin-induced (NTG%)) vasodilation in the brachial artery. Radial arterial wall stiffness measured as maximum increase in pulse pressure (dP/dtmax) was increased. FMD% and especially NTG% correlated negatively and dP/dtmax positively to measures of endothelial inflammation: plasma- nitrate and adhesion molecule levels. Thus inflammatory vascular wall changes may interfere with dilation as may the presence of nitrate tolerance. We found elevated alveolar MMP-9 in both its pro- and active form in ILD. The levels correlated to decline in lung capacity, pointing at a causal relation. We suggest that neutrophils secrete MMP-9, which may degrade collagen IV, (the main constituent of basal membranes), collagen V, gelatins, proteoglycans and elastin. MMP-9 activity is partly regulated by the binding of pro- and active form to TIMP-1. Alveolar TIMP-1, which even stimulates fibroblast ECM synthesis, was increased independent of ILD. The inflammatory process in ILD is orchestrated by activated T helper (h) lymphocytes. We found a mixed Th1/Th2 reaction in SSc alveolar T cells expressing messenger for interferon gamma (Th1), IL-6 and IL-10 (both Th2). No particular cytokine mRNA profile distinguished alveolar T cells in ILD. Neutrophils invaded the bronchial epithelium, which seemed otherwise inert as levels of inflammatory cytokine sensitive transcription factors and their nuclear translocation tended to be low. The neutrophil recruitment pathway is uncertain as chemoattractants and endothelial adhesion molecules were normally expressed. In conclusion, MMP-9 probably causes degradation of lung tissue in ILD and may represent a future therapeutic target. Alveolar T cells show a mixed Th1/Th2 cytokine profile independent of ILD. Neutrophils invade the bronchial epithelium. Activated endothelium produces increased amounts of NO and adhesion molecules and the level of activation influences brachial arterial FMD% and NTG% and radial arterial compliance. Nitrate tolerance may be present.

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Частини книг з теми "Th2-dependent"

Lee, A. "Elimination of Helicobacter pylori is dependent on a Th2 response." In Helicobacter pylori, 187–91. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-3927-4_19.

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Croitoru, K. "Elimination of Helicobacter pylori is not dependent on a Th2 cytokine response." In Helicobacter pylori, 193–95. Dordrecht: Springer Netherlands, 2000. http://dx.doi.org/10.1007/978-94-011-3927-4_20.

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Тези доповідей конференцій з теми "Th2-dependent"

Lin, Rui, David A. Zidar, and Julia K. L. Walker. "Beta-arrestin-2-dependent Signaling Promotes Th2 Cell CCR4-mediated Chemotaxis." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4049.

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Nakada, Emily M., Jichuan Shan, Margaret Kinyanjui, and Elizabeth Fixman. "Alum-dependent Regulation Of Th2/Th17 Responses In Experimental Allergic Airways Disease." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4052.

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Conejero Hall, Laura, Sofía Chayeb Khouili, Sarai Martínez Cano, Helena Izquierdo Fernández, Paola Brandi, and David Sancho Madrid. "Batf3-dependent dendritic cells control house dust mite-driven Th2 and Th17 response through IL-12 production." In ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa3631.

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Goodwin, Meagan, Amanda Daly, and Daniel J. Weiss. "Systemic Administration Of Mesenchymal Stromal Cells Inhibits Th2-Mediated Allergic Airways Inflammation In Mice Through An IFNg-Dependent Mechanism." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a1251.

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Takyar, Seyedtaghi (Shervin), Hema H. Vasavada, Bing Ma, Chun G. Lee, and Jack A. Elias. "MicroRNA (miR)-1 Inhibits Adaptive Th2 Inflammation In The Lung Via A VEGF/Myeloproliferative Leukemia Virus Oncogene (MPL)-Dependent Mechanism." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a1002.

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