Relevant bibliographies by topics / T helper 2

Academic literature on the topic 'T helper 2'

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Published: 4 June 2021
Last updated: 28 January 2023

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Journal articles on the topic "T helper 2"

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Dabbagh, Karim, and David B. Lewis. "Toll-like receptors and T-helper-1/T-helper-2 responses." Current Opinion in Infectious Diseases 16, no. 3 (June 2003): 199–204. http://dx.doi.org/10.1097/00001432-200306000-00003.

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Schwarz, Markus J., Sonnig Chiang, Norbert Müller, and Manfred Ackenheil. "T-helper-1 and T-helper-2 Responses in Psychiatric Disorders." Brain, Behavior, and Immunity 15, no. 4 (December 2001): 340–70. http://dx.doi.org/10.1006/brbi.2001.0647.

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Azuma, Naoko, Minoru Ando, Ken Tsuchiya, Takashi Akiba, and Hiroshi Nihei. "T helper 1 and T helper 2 balance in chronic hemodialysis patients." Nihon Toseki Igakkai Zasshi 35, no. 13 (2002): 1549–55. http://dx.doi.org/10.4009/jsdt.35.1549.

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Suzuki, Shunji, and Nozomi Ouchi. "T Helper 1/T Helper 2 Cell Immunity in Preeclamptic Twin Pregnancy." Journal of Nippon Medical School 74, no. 6 (2007): 434–36. http://dx.doi.org/10.1272/jnms.74.434.

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Mjösberg, Jenny, Göran Berg, Maria C. Jenmalm, and Jan Ernerudh. "FOXP3+ Regulatory T Cells and T Helper 1, T Helper 2, and T Helper 17 Cells in Human Early Pregnancy Decidua1." Biology of Reproduction 82, no. 4 (April 1, 2010): 698–705. http://dx.doi.org/10.1095/biolreprod.109.081208.

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Smart, Joanne M., and Andrew S. Kemp. "Ontogeny of T-helper 1 and T-helper 2 cytokine production in childhood." Pediatric Allergy and Immunology 12, no. 4 (August 2001): 181–87. http://dx.doi.org/10.1034/j.1399-3038.2001.012004181.x.

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Iavicoli, Ivo, Luca Fontana, Alessandro Marinaccio, Antonio Bergamaschi, and Edward J. Calabrese. "Iridium alters immune balance between t helper 1 and t helper 2 responses." Human & Experimental Toxicology 29, no. 3 (January 22, 2010): 213–19. http://dx.doi.org/10.1177/0960327109360215.

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The recent introduction of iridium (Ir) into the catalytic converter has resulted in an increase of Ir levels into the environment, especially ambient air and soil. These observations suggested the need to evaluate potential toxicity due to Ir exposure. Since Ir compounds have been previously shown to cause immune sensitization in humans, the effects of Ir via drinking water for 90 days was assessed in adult female Wistar rats with respect to selected immune parameters. The Ir exposure induced dose-dependent decrease (p < .01) in T helper 1 (Th1) cytokines and increase (p < .001) in a T helper 2 (Th2) cytokine. The findings show that the Ir exposure affects an immune imbalance with a skewing toward a Th2 bias, a risk factor for asthma.
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Osna, N., N. Vilgert, E. Hagina, G. Silonova, V. Kuse, L. Viksna, A. Sochnev, V. Gidraitis, A. Zvirbule, and M. Mauricas. "T helper 1/T helper 2 balance in pathogenesis of chronic hepatitis C." Immunology Letters 56 (May 1997): 146. http://dx.doi.org/10.1016/s0165-2478(97)85585-x.

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Osna, N. "T helper 1/T helper 2 balance in pathogenesis of chronic hepatitis C." Immunology Letters 56, no. 1-3 (May 1997): 146. http://dx.doi.org/10.1016/s0165-2478(97)87423-8.

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O’Garra, Anne, and Naoko Arai. "The molecular basis of T helper 1 and T helper 2 cell differentiation." Trends in Cell Biology 10, no. 12 (December 2000): 542–50. http://dx.doi.org/10.1016/s0962-8924(00)01856-0.

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Dissertations / Theses on the topic "T helper 2"

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Hewitt, Susannah Louise. "T helper 1/T helper 2 commitment and nuclear localisation." Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.415427.

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Passini, Nadia. "Molecular mechanisms of T helper 1 and T helper 2 cell development : differential signaling in response to Interleukin-12." Thesis, Open University, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.299005.

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Kelly, Helena T. "The role of T helper 1 and T helper 2 lymphocyte subsets in the pathogenesis of experimental autoimmune uveoretinitis." Thesis, University of Aberdeen, 1995. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU543992.

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CD4+ T cells can be subdivided on the basis of their lymphokine repertoire produced on activation resulting in TH1 like and TH2 like populations. The purpose of this study was to measure the intraocular expression of cytokines as a means of defining the CD4+ lymphocyte subsets present during the development of uveoretinitis. Lewis rats were immunised with retinal antigen and pertussis toxin resulting in early signs of disease activity evident by day 9 with increasing severity evident by day 12. Extensive clinical and histological damage was observed by day 14 with a reduction in severity through to end stage disease at day 24. In this study, the failure to establish pure populations of retinal antigen specific T lymphocyte cell lines and the observation of the lack of sensitivity of Northern hybridization to signals expressed at low levels resulted in the more sensitive technique of RT-PCR being utilized. Both IL2 and IFN mRNA expression was detected at all stages of disease with highest levels being present early in uveitis. In contrast IL4 mRNA levels increased with disease progression. This study suggests a pathogenic role for TH1 like cells and a protective role for TH2 like cells in this autoimmune disease. In order to provide an insight into alternative treatment strategies of the disease, immunomodulation of EAU was carried out using the immunosuppressive drugs CsA, FK506 and rapamycin and the resultant cytokine mRNA profiles examined. The results indicated that CsA and FK506 downregulated the TH1 response having suppressive effects on the levels of IL2 and IFN mRNA respectively. In contrast rapamycin was found to modulate the TH2 response enhancing IL4 levels. From this data, a drug based strategy employing rapamycin appears to be the most favourable approach.
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Kropf, Pascale. "Characterisation of T Helper 2 responses in non-healing Leishmania major infections." Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.395473.

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Özgönen, Özlem Şahin Ünal. "Malign ve tüberküloz plörezi ayırıcı tanısında T helper 1 ve T helper 2 sitokinlerden IFN-y,IL-12,IL-18 ve IL-10'un tanısal değeri /." Isparta: SDÜ Tıp Fakültesi, 2006. http://tez.sdu.edu.tr/Tezler/TT00277.pdf.

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MacKenzie, Jason Roderick, and Jason Mackenzie@ipaustralia gov au. "The Role of Eosinophils in the Regulation of CD4+ T helper 2 Regulated Inflammation." The Australian National University. The John Curtin School of Medical Research, 2004. http://thesis.anu.edu.au./public/adt-ANU20051007.121844.

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The eosinophil is a leukocyte whose intracellular mediators are considered to play a central role in the pathogenesis of allergic diseases, including allergic asthma, allergic rhinitis and atopic dermatitis, and which is also involved in immunological responses to parasites. Eosinophil differentiation and maturation from bone marrow progenitors is regulated by interleukin-5 (IL-5), which may be secreted by T helper 2 (Th2) T lymphocytes, and is consistently upregulated in allergic conditions. Eotaxin is a potent chemoattractant for circulating and tissue eosinophils, and the production of this chemokine promotes eosinophil infiltration and accumulation within sites of allergic inflammation.¶ Eosinophils obtained from inflammatory tissues and secretions display an altered phenotype in comparison to peripheral blood eosinophils, with increased surface expression of major histocompatibility complex (MHC) proteins and adhesion molecules (Hansel et al., 1991), and migration across the microvascular endothelium may also increase their capacity to generate an oxidative burst (Walker et al., 1993; Yamamoto et al., 2000). Eosinophils are phagocytic cells, and have been shown to present simple (no requirement for intracellular processing) and complex antigens to MHC-restricted, antigen-specific T lymphocytes (Del Pozo et al., 1992; Weller et al., 1993). Furthermore, eosinophils express the costimulatory molecules required for effective antigen presentation (Tamura et al., 1996), and ligation of costimulatory molecules on the eosinophil cell surface can induce the release of eosinophil derived cytokines (Woerly et al., 1999; Woerly et al., 2002). Therefore the eosinophil may also regulate immune responses.¶ To date, no studies have demonstrated the ability of eosinophils to modulate activated T lymphocyte function via presentation of relevant antigen in the context of MHC class II (MHC-II), concomitant with Th2 cytokine release. In the experiments described in this thesis, murine eosinophils have been observed to rapidly migrate to sites of antigen deposition within the airways mucosa of naïve mice, suggesting a potential role for this granulocyte in the primary response to inhaled antigen. However, human allergic diseases are often diagnosed after the establishment of allergic responses, and symptom development. Therefore, a murine model of allergic airways disease (AAD) was used to investigate the ability for eosinophils to participate as antigen presenting cells (APCs), and thereby modulate activated T lymphocyte function both in vitro and in vivo. Detailed histological analysis of the pulmonary draining lymph nodes following antigen challenge in sensitised mice revealed a rapid infiltration of eosinophils into this tissue, which preceded the accumulation of eosinophils in bronchoalveolar lavage fluid (BALF). This suggested that eosinophils were preferentially translocating to the draining lymph nodes following antigen challenge, and that the subsequent accumulation of these cells in the BALF was a consequence of continued antigen delivery to the lower airways.¶ Eosinophil trafficking to lymphoid tissue via the afferent lymphatics was substantiated using electron microscopy of lymph node sections and the intravenous (i.v.) transfer of fluorescently labeled eosinophils, which did not traffic to lymph nodes via the blood. During the resolution of AAD, eosinophils were noted for their persistence in the pulmonary draining lymph nodes. These observations suggested a continued modulation of T cell function by lymph node dwelling eosinophils during AAD resolution, particularly in light of recent observations for draining lymph node T cell proliferation following instillation of antigen-pulsed eosinophils into the allergic mouse lung (Shi et al., 2000).¶ To further investigate the antigen presenting capacity, eosinophils were obtained from the BALF of mice with AAD, and their surface expression of MHC class II (MHC-II) proteins and costimulatory molecules confirmed using flow cytometric analysis. The ability to acquire and process complex antigen both in vitro and in vivo was also confirmed using naturally quenching fluorescenated ovalbumin (OVA), which is degraded into fluorescent peptides by the action of intracellular proteases. Thus, eosinophil expression of the surface molecules necessary for effective antigen presentation was confirmed, as was their ability to process complex antigen. Further investigations revealed that eosinophils can present complex OVA antigen to CD4+ T lymphocytes obtained from the allergic mouse, and to in vitro derived OVA-specific Th2 cells. In the presence of exogenous antigen, eosinophils co-cultured with T lymphocytes were able to induce Th2 cytokine production, and demonstrated an ability for eosinophils to modulate T lymphocyte function in vitro.¶ The ability for eosinophils to act as antigen presenting cells in vivo was also investigated. Eosinophils obtained from the antigen-saturated lungs of OVA sensitised and challenged mice were transferred to the peritoneal cavities of naïve host mice. When subsequently challenged with aerosolised OVA, eosinophil recipients developed a pulmonary eosinophilia similar to that of OVA sensitised and challenged mice. To validate this finding, the experimental procedure was altered to accommodate the use of non-allergy derived eosinophils, which were pulsed with OVA in vitro, prior to transfer into naïve recipients. When subsequently challenged with aerosolised OVA, eosinophil recipients developed a peripheral blood and pulmonary eosinophilia, and stimulation with OVA induced IL-5 and IL-13 cytokine production from pulmonary draining lymph node cells. Notably, the AAD induced by transfer of antigen pulsed eosinophils did not induce detectable OVA-specific IgG1, which may be attributed to the lack of soluble antigen required for B cell antibody production.¶ During the course of these investigations, an OVA T cell receptor (TCR) transgenic mouse (OT-II) was procured with a view to defining the interaction between eosinophils and activated T lymphocytes (Barnden et al., 1998). Despite having specificity for the OVA323-339 peptide, an immunodominant epitope that skews naïve T cell responses towards Th2 cytokine release (Janssen et al., 2000), T lymphocytes from the OT-II mouse preferentially secreted IFN-γ in response to stimulation with either OVA peptide or OVA. These mice were further characterised in a mouse model of AAD, and found to be refractory to disease induction and progression, which may be attributed to significant IFN-γ secretion by transgenic CD4+ T lymphocytes during antigen sensitisation. Indeed, these cells were noted for their ability to attenuate pulmonary eosinophilia when transferred to OVA sensitised and challenged wild type mice, although serum OVA-specific IgG1, peripheral blood eosinophilia levels and airways response to methacholine challenge remained intact.¶ Knowledge of the biased Th1 phenotype in naïve OT-II provided a unique opportunity to investigate the fate of T lymphocytes bearing high affinity OVA-specific TCRs following neonatal antigen exposure to soluble OVA. In a previous study, subcutaneous (s.c.) administration of soluble OVA to wild type neonatal mice was suspected to have deleted OVA-specific T cells from the T cell repertoire (Hogan et al., 1998a). Using flow cytometry and TCR specific antibody, the delivery of s.c. OVA to OT-II neonates did not alter transgenic T cell populations in adult mice. Instead, it was surprising to find a skewing towards the Th2 phenotype and loss of IFN-γ secretion following OVA sensitisation and challenge in adult mice. A mechanism for this reprogramming of the transgenic T cell from the Th1 to a Th2 phenotype following OT-II neonatal exposure to soluble OVA is proposed, and further experimentation may validate this hypothesis.¶ In conclusion, eosinophils residing in the allergic lung have the capacity to interact with activated T cells, both within this tissue and the draining lymph nodes. Despite their relative inefficiency as antigen presenting cells (Mawhorter et al., 1994), eosinophils may participate en masse in the serial triggering of activated TCRs, and provide appropriate costimulatory signals that modulate T lymphocyte function. Through the elaboration of Th2 cytokines and stimulation of T cell proliferation, antigen presenting eosinophils may transiently prolong or exacerbate the symptoms of allergic diseases. Alternatively, eosinophils presenting relevant antigens may inhibit T cell activity via degranulation, and such activity has recently been observed in a parasite model (Shinkai et al., 2002). Finally, experiments in the OT-II mouse have provided valuable information to suggest that therapies designed to modulate eosinophil numbers in allergic tissues through the secretion of opposing cytokines such as IFN-γ, may be of limited benefit. The results shown here suggest that airways dysfunction remains intact despite significantly reduced pulmonary eosinophilia
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MacKenzie, Jason Roderick. "The role of eosinophils in the regulation of CD4+ T helper 2 regulated inflammation /." View thesis entry in Australian Digital Theses Program, 2004. http://thesis.anu.edu.au/public/adt-ANU20051007.121844/index.html.

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Powell, Michael D. "Insights Into the Regulatory Requirements for T Follicular Helper Cell Development." Diss., Virginia Tech, 2019. http://hdl.handle.net/10919/89085.

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During the course of an immune response, CD4+ T helper cells differentiate into a number of subsets including: T helper 1 (TH1), TH2, TH17, and T follicular helper (TFH) populations. The functional diversity of CD4+ T effector cells results in a coordinated, pathogen-specific immune response. For example, the production of IFNγ by TH1 cells is vital for the clearance of intracellular pathogens, while TFH cell engagement with cognate B cells is required for germinal center (GC) formation and the generation of pathogen- and vaccine- induced antibody production. The development of CD4+ subsets is contingent on extracellular signals, in the form of cytokines, and downstream transcriptional networks responsible for promoting the unique gene expression profile for each subset while simultaneously suppressing alternative cell fates. However, the exact composition of, and stage-specific requirements for, these environmental cytokines and transcription factor networks in the governance of TFH cell differentiation remain incompletely understood. The work in this dissertation seeks to understand how cell-extrinsic cytokine signals and cell-intrinsic transcription factor activities are integrated to properly regulate TFH cell development. Here, we demonstrate that in response to decreased IL-2 and constant IL-12 signaling, T helper 1 (TH1) cells upregulate a TFH-like phenotype, including expression of the TFH lineage defining transcription factor Bcl-6. Intriguingly, our work established that signals from IL-12 were required for both the differentiation and function of this TFH-like population. Mechanistically, IL-12 signals are propagated through both STAT3 and STAT4, leading to the upregulation of the TFH associated genes Bcl6, Il21, and Icos, correlating with increased B cell helper activity. Conversely, exposure of these TFH-like cells to IL-7 results in the STAT5-dependent repression of Bcl-6 and subsequent inhibition of the TFH phenotype. Finally, we describe a novel regulatory mechanism wherein STAT3 and the Ikaros zinc finger transcription factors Ikaros and Aiolos cooperate to regulate Bcl-6 expression in these TFH-like cells. Collectively, the work in this dissertation significantly advances our understanding of the regulatory mechanisms that govern TFH cell differentiation, setting the basis for the rational design of novel immunotherapeutic strategies and increasingly effective vaccines.
Ph. D.
Specialized cells called T helper cells serve as a critical interface between the innate (first line of defense) and adaptive (specialized and long-term) immune systems. During the course of an infection, T helper cells are responsible for orchestrating the immune-mediated elimination of invading viruses, bacteria, and parasites. This wide breadth of functionality is achieved through the formation of distinct T helper subsets including T helper 1 (TH1), TH2, TH17, and T follicular helper (TFH) populations. Individual subsets have distinct developmental requirements and have unique functions within the immune system. For example, TFH cells are required for the production of effective antibodies that recognize invading pathogens, leading to their subsequent elimination. This naturally occurring process is the basis for a number of modern medical therapies including vaccination. Conversely, aberrant generation of antibodies that recognize host tissues can result in the onset of various autoimmune diseases including lupus, multiple sclerosis, and crohn’s disease. Due to the importance of TFH cells to human health, there is intense interest in understanding how these cells are formed. It is recognized that the generation of these therapeutically important immune cells is mediated by numerous cell-extrinsic andintrinsic influences, including proteins in their cellular environment called cytokines, and important proteins inside of the cell called transcription factors. However, as this is a complicated and multi-step process, many questions remain regarding the identity of these cytokines and transcription factors. The work in this dissertation seeks to understand how cellextrinsic cytokine signals and cell-intrinsic transcription factor activities are integrated to properly regulate TFH cell development. Collectively, this body of work significantly advances our understanding of the regulatory mechanisms that govern TFH cell differentiation, setting the basis for the rational design of novel immunotherapeutic strategies and increasingly effective vaccines.
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Mayer, Johannes Urban. "Induction of T helper 2 cell responses against Schistosoma mansoni eggs in the murine intestine." Thesis, University of Glasgow, 2017. http://theses.gla.ac.uk/7972/.

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T helper 2 (Th2) cell responses typify the immune response to parasitic organisms, which frequently invade the intestine. Dendritic cells (DCs) are considered vital for the induction of Th2 responses as they present parasite- derived antigens to naive T cells in draining lymph nodes. However, the identities of the DC populations responsible for priming Th2 cells in the intestine are still unclear. We developed an experimental immunization protocol to deliver Schistosoma mansoni eggs into the intestine. During live infection by the parasite, these eggs cause intestinal damage, granuloma formation, tissue fibrosis and strong type 2 immune responses. Many aspects of type 2 immunity are controlled by the transcription factor IRF4 and we observed that intestinal Th2 responses against Schistosoma mansoni eggs did not develop in the draining lymph nodes in the absence of IRF4+ DCs. IRF4f/f CD11c-cre positive mice had fewer CD11b-expessing migrating DCs, and fewer parasite antigen-carrying DCs were present in the mesenteric lymph nodes (MLNs) draining the small intestine and colon. However, transfer of antigen-loaded IRF4-deficient DCs directly into the MLN revealed that these cells could induce antigen-specific Th2 responses, suggesting that IRF4 controlled the migration of CD11b-expessing DCs rather than their Th2 inducing capacity. Furthermore, immature DCs from the intestinal lamina propria, and semi-mature DCs from lymph were sufficient to prime antigen-specific Th2 responses against egg antigens when transferred into naive recipient mice. This induction was dependent on MHCII expression but not on the production of IL-4 by the transferred DCs, indicating that conventional intestinal DCs are fully capable of inducing Th2 responses against S. mansoni egg antigens upon transfer. Further analysis of migratory small intestinal and colonic lymph DCs revealed that distinct subsets of CD11b-expressing DCs were sufficient for the induction of Th2 responses in the small intestine and colon. CD11b+CD103+ DCs transported parasite antigen from the small intestine, whereas CD11b+CD103- DCs performed this role in the colon. Of note, these same small intestinal and colonic DC subsets were also the populations that were most efficient at priming antigen-specific Th2 responses in vivo. Thus, we have not only identified that IRF4-dependent CD11b-expressing DCs are specialized to drive Th2 responses in the intestine but have also revealed that different DC subsets promote Th2 responses in the small intestine and colon. These findings not only advance our knowledge of intestinal Th2 responses against parasite antigens but also reveal a hitherto unappreciated functional heterogeneity among intestinal DCs, which could also be relevant for other tissue- specific intestinal conditions like Crohn’s disease, ulcerative colitis and celiac disease.
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Dumont, Larry Joe. "Human cytomegalovirus reactivation following seasonal allergen exposure and switch to T-helper cell type 2 profile /." Connect to full text at ProQuest Digital Dissertations. IP filtered, 2005.

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Thesis (Ph.D. in Clinical Sciences) -- University of Colorado at Denver and Health Sciences Center, 2005.
Typescript. Includes bibliographical references (leaves 140-156). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;
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Books on the topic "T helper 2"

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Fousteri, Georgia, Shahram Salek-Ardakani, and Maria Pia Cicalese, eds. Follicular Helper T Cells in Immunity and Autoimmunity. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88963-847-5.

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Books, Dialog Abroad. T�gliche Franz�sische Konversationen, Die Ihnen Helfen, Franz�sisch Zu Lernen - Woche 1 & 2: Semestre d'Oliver en France. Independently Published, 2019.

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Book chapters on the topic "T helper 2"

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Coffman, Robert L., Rodrigo Correa-Oliviera, and Simonetta Mocci. "Reversal of Polarized T Helper 1 and T Helper 2 Cell Populations in Murine Leishmaniasis." In Novartis Foundation Symposia, 20–41. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470514849.ch3.

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King, Christopher L., and Thomas B. Nutman. "Biological Role of Helper T-Cell Subsets in Helminth Infections (Part 2 of 2)." In Regulation and Functional Significance of T-Cell Subsets, 151–65. Basel: KARGER, 1992. http://dx.doi.org/10.1159/000319120.

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Fedyk, Eric R., Deborah M. Brown, and Richard P. Phipps. "PGE2 Regulation of B Lymphocytes and T Helper 1 and T Helper 2 Cells: Induction of Inflammatory versus Allergic Responses." In Advances in Experimental Medicine and Biology, 237–42. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-1813-0_35.

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Parronchi, P., S. Sampognaro, E. Maggi, and S. Romagnani. "Role of Type 2 T Helper Cells (TH2) in Allergic Disorders." In Advances in Experimental Medicine and Biology, 359–63. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4615-5855-2_51.

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Romagnani, Sergio. "Role for CD30 Antigen in Human T Helper 2-Type Responses." In Novartis Foundation Symposia, 55–67. Chichester, UK: John Wiley & Sons, Ltd., 2007. http://dx.doi.org/10.1002/9780470514849.ch5.

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Usuki, Kensuke, Akiko Furuya, Yuji Hirai, Seiko Iki, and Akio Urabe. "Helper T Cell Subsets and Th1/2 Balance in Aplastic Anemia." In Paroxysmal Nocturnal Hemoglobinuria and Related Disorders, 259–62. Tokyo: Springer Japan, 2003. http://dx.doi.org/10.1007/978-4-431-67867-0_28.

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King, Christopher L., and Thomas B. Nutman. "Biological Role of Helper T-Cell Subsets in Helminth Infections (Part 1 of 2)." In Regulation and Functional Significance of T-Cell Subsets, 136–51. Basel: KARGER, 1992. http://dx.doi.org/10.1159/000319119.

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Chen, Zhian, Kaili Liang, Jun Deng, and Di Yu. "Therapeutic Modulation of T Follicular Helper Cells by Low-Dose IL-2 Treatment." In Methods in Molecular Biology, 255–65. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1736-6_21.

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Keane-Myers, Andrea, Vincenzo Casolaro, and Santa Jeremy Ono. "Molecular Basis and Role of Differential Cytokine Production in T Helper Cell Subsets in Immunologic Disease." In Lacrimal Gland, Tear Film, and Dry Eye Syndromes 2, 479–84. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5359-5_66.

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Romagnani, S. "Human Types I and 2 T Helper Subsets: Functional Properties, Role in Disease and Regulation of Development." In Symposium in Immunology III, 35–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78438-5_5.

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Conference papers on the topic "T helper 2"

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Boieri, Margherita, Anna Malishkevich, Lauren Steidl, Kenneth Ngo, Sowmya Iyer, Mary Awad, Johannes Kreuzer, Wilhelm Haas, Miguel Rivera, and Shadmehr Demehri. "Abstract 4948: T helper 2 cells block breast cancer promotion." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4948.

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Boieri, Margherita, Anna Malishkevich, Lauren Steidl, Kenneth Ngo, Sowmya Iyer, Mary Awad, Johannes Kreuzer, Wilhelm Haas, Miguel Rivera, and Shadmehr Demehri. "Abstract 4948: T helper 2 cells block breast cancer promotion." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-4948.

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Loza, Matthew, Irina Strambu, Michel Laviolette, David Singh, J. Mark FitzGerald, Stephen Lam, Steven Steven Kelsen, et al. "Clinical biomarkers identify T-helper 2 status defined by mucosal CCL26 in the ADEPT-asthma study." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.oa1771.

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Kaul, Nathalie-Christin, Soumya Mohapatra, Isabell Adam, Stefan Krienke, Christine Tucher, Christiane Opitz, Hanns-Martin Lorenz, and Lars Tykocinski. "04.11 Hypoxia and rheumatoid phenotype prevent synovial fibroblasts from suppressing t helper cell proliferation through ido1-mediated tryptophan metabolism." In 37th European Workshop for Rheumatology Research 2–4 March 2017 Athens, Greece. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2016-211051.11.

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Rogier, Rebecca, Heather Evans-Marin, Birgitte Walgreen, Monique M. Helsen, Liduine A. van den Bersselaar, Peter M. van der Kraan, Fons A.J. van de Loo, et al. "07.04 Partial elimination of intestinal microbiota dampens t helper 17 cell differentiation and established collagen-induced arthritis in mice." In 37th European Workshop for Rheumatology Research 2–4 March 2017 Athens, Greece. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2016-211054.4.

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Sakurai, S., K. Furuhashi, R. Horiguchi, H. Yasui, H. Hozumi, Y. Suzuki, M. Karayama, et al. "Conventional Type 2 Lung Dendritic Cells in Asthma Mouse Model Significantly Induce Follicular Helper T Cells Than Conventional Type 1." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7408.

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Coughlan, Catherine A., Sanjay H. Chotirmall, Julie Renwick, Tidi M. Hassan, Teck B. Low, Gudmundur Bergsson, Kathleen Bennett, et al. "Itraconazole Up-Regulates The Vitamin D Receptor And Reduces T-Helper 2 Responses In Aspergillus Fumigatus Colonised Individuals With Cystic Fibrosis." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2807.

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Ricard, L., V. Jachiet, F. Malard, Y. Ye, N. Stocker, S. Rivière, P. Senet, et al. "P039/O03 Circulating follicular helper T cells are increased in systemic sclerosis and promote plasmablast differentiation through the IL-21 pathway which can be inhibited by ruxolitinib." In 39th European Workshop for Rheumatology Research, 28 February–2 March 2019, Lyon, France. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2019.31.

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Gu-Trantien, Chunyan, and Karen Willard-Gallo. "Abstract B87: CXCL13-producing follicular helper CD4+ T cells infiltrating human breast cancer signal an organized immune response and predict a favorable clinical outcome." In Abstracts: AACR Special Conference on Tumor Immunology: Multidisciplinary Science Driving Basic and Clinical Advances; December 2-5, 2012; Miami, FL. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.tumimm2012-b87.

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Gewirtz, A., W. Y. Xu, B. Rucinski, and S. Niewiarowski. "SELECTIVE INHIBITION OF HUMAN MEGAKARYOCYTOPOIESIS IN VITRO BY HIGHLY PURIFIED PLATELET FACTOR 4." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644621.

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Abstract:
Platelet (plt) factor 4 (PF4) is an alpha granule protein which can modulate T lymphocyte function. T cells may help regulate megakaryocytopoiesis. Therefore, we hypothesized that T cell-PF4 interactions might play a role in autoregulating marrow megakaryocyte (MEG) production. To test this idea, we studied MEG colony formation in plasma clot cultures containing human serum derived solely from pit poor normal AB plasma, enriched hematopoietic progenitor cells (HPC), autologous T cells, and exogenous PF4. Highly purified PF4 (single band on SDS gel) was prepared from outdated human pits by a combination of heparin-agarose, Sephacryl G-200, and Sephadex G-50 column chromatography. HPC were prepared by depleting normal light density marrow mononuclear cells of adherent monocytes, and T cells. T cells were further fractionated into helper (Leu 3+) and suppressor (Leu 2+) subtypes by solid phase immunoabsorption ("panning"). MEG colonies were enumerated by indirect immunofluorescence with an anti-human platelet glycoprotein antiserum. HPC(5×105/ml) were co-cultured with Leu 3+, or Leu 2+ T cells at target;T cell ratios of 2:1 (n=3; n=4 respectively) and l:l(n=4; n=4 respectively) in the presence of 2.5 μg/ml PF4. Under these growth conditions, MEG colony formation was unchanged (p>0.5) when compared to colonies formed by HPC in the absence of PF4. When the above experiments were repeated (n=2-3/condition) at a higher PF4 concentration [25 μg/ml], MEG colony formation was markedly (>60%) inhibited. To determine if PF4 directly inhibited MEG or erythroid progenitor cell growth (CFU-Meg; CFU-E) in vitro, HPC were cloned in PF4 (25μg/ml) without added T cells. Mean ± SEM of MEG and CFU-E derived colonies formed without vs. with PF4 was as follows:These results suggest that: 1) PF4 may be a non-T cell dependent, lineage specific inhibitor of CFU-MEG, and 2) PF4 may play a role in autoregulating human megakaryocytopoiesis.
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