Gotowe bibliografie tematyczne / T-helper

Gotowa bibliografia na temat „T-helper”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 11 marca 2023

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Artykuły w czasopismach na temat "T-helper"

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F. Abdel Hamid, Mahmoud, Safaa M. Morsy, Mostafa Abou El Ela, Rehab A. Hegazy, Marwa M. Fawzy, Laila A. Rashed, Ahmed M. Omar, Eman R. Abdel Fattah i Doaa M. Hany. "T helper-17 cells and T regulatory cells in vitiligo". International Journal of Academic Research 5, nr 6 (10.12.2013): 273–78. http://dx.doi.org/10.7813/2075-4124.2013/5-6/a.34.

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Noelle, R. "T helper cells". Current Opinion in Immunology 4, nr 3 (czerwiec 1992): 333–37. http://dx.doi.org/10.1016/0952-7915(92)90085-s.

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Ernerudh, J., A. Forsberg, E. Straka, E. Johansson, R. B. Mehta, J. Svensson, L. Matthiesen i in. "T helper cells and T helper cell plasticity in pregnancy". Journal of Reproductive Immunology 90, nr 2 (sierpień 2011): 131. http://dx.doi.org/10.1016/j.jri.2011.06.003.

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Khurana, Surbhi, Purva Mathur, Nidhi Bhardwaj, Minu Kumari, Sushma Sagar, Subodh Kumar, Amit Gupta, Richa Aggarwal, Kapil Dev Soni i Rajesh Malhotra. "Dynamics of T helper 9, T helper 22, and regulatory T helper cells in minor & major trauma". Journal of Allergy and Clinical Immunology 143, nr 2 (luty 2019): AB109. http://dx.doi.org/10.1016/j.jaci.2018.12.331.

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Dabbagh, Karim, i David B. Lewis. "Toll-like receptors and T-helper-1/T-helper-2 responses". Current Opinion in Infectious Diseases 16, nr 3 (czerwiec 2003): 199–204. http://dx.doi.org/10.1097/00001432-200306000-00003.

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Schwarz, Markus J., Sonnig Chiang, Norbert Müller i Manfred Ackenheil. "T-helper-1 and T-helper-2 Responses in Psychiatric Disorders". Brain, Behavior, and Immunity 15, nr 4 (grudzień 2001): 340–70. http://dx.doi.org/10.1006/brbi.2001.0647.

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Mjösberg, Jenny, Göran Berg, Maria C. Jenmalm i 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, nr 4 (1.04.2010): 698–705. http://dx.doi.org/10.1095/biolreprod.109.081208.

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Hirahara, Kiyoshi, Ami Aoki i Toshinori Nakayama. "Pathogenic helper T cells". Allergology International 70, nr 2 (kwiecień 2021): 169–73. http://dx.doi.org/10.1016/j.alit.2021.02.001.

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HERMANS G, BLOCKMANS D, BOCKAERT J i BOBBAERS H. "Idiopathische T-helper lymfocytopenie". Tijdschrift voor Geneeskunde 54, nr 6 (1.01.1998): 408–12. http://dx.doi.org/10.2143/tvg.54.6.5000073.

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Saravia, Jordy, Nicole M. Chapman i Hongbo Chi. "Helper T cell differentiation". Cellular & Molecular Immunology 16, nr 7 (12.03.2019): 634–43. http://dx.doi.org/10.1038/s41423-019-0220-6.

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Rozprawy doktorskie na temat "T-helper"

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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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Trüb, Marta. "Follicular T helper cell populations". Thesis, University of Edinburgh, 2016. http://hdl.handle.net/1842/20466.

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Humoral immunity provides protection against subsequent infections. Antigen-specific, high-affinity, class-switched antibodies are produced by B cells through rounds of proliferation, B cell receptor rearrangement and selection in the germinal centres (GC). T cells play an essential and indispensable role in this process and in the recent years the term T follicular helper cells (TFH) was coined to describe this cell subset. The aim of my thesis is to investigate whether there is more than one type of T cells within the TFH population and whether it has important functional consequences. Firstly, I use sheep red blood cell immunisation (SRBC) and Salmonella enterica infection to show phenotypical differences between TFH expressing high and low level of surface molecule PD-1. In order to investigate the relationship between different TFH populations gene profiling was carried out on the microarray platform. Detailed transcriptome analysis revealed the discrete nature of isolated TFH cell subsets and provided an overview of their genetic landscape. Secondly, I have investigated the dependence of TFH subsets on cognate interactions with B cell in SRBC model by generating BM chimeras. I have demonstrated that generation of PD-1HI TFH, but not of PD-1LO TFH, depends on antigen presentation by B cells. Furthermore, I have shown that provision of wild-type but not MHC II knock-out B cells rescues PD-1HI formation in BM chimeras after SRBC immunisation. Finally, I have explored plasticity within TFH subsets and showed that none of the populations is in a terminally differentiated state, as they can convert into one another. Thirdly, experiments with S. enterica model revealed that the absence of PD- 1HI TFH is independent of the splenic architecture disruption present within the first week of the response. Surprisingly, co-immunisation studies showed that PD-1HI population is not only present but even enhanced in the group which received both SRBC and S. enterica when compared to single immunisations. The work presented in the thesis documents that there is a significant and previously unappreciated heterogeneity within TFH subset. This knowledge is important for designing optimal vaccine strategies and treating autoimmune diseases, as in both processes the antibody production plays a crucial role and its manipulation (either enhancing or blocking antibody production, respectively) can significantly improve clinical interventions.
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Sullivan, Andrew. "The role of T-helper 17 and T-helper 22 lymphocytes in beta-lactam hypersensitivity". Thesis, University of Liverpool, 2016. http://livrepository.liverpool.ac.uk/3004574/.

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Beta-lactam antibiotics are used to treat recurrent opportunistic infections that occur in patients with cystic fibrosis. However, the incidence of reported hypersensitivity in these patients is greatly higher than the healthy population. Due to the delayed nature of beta-lactam hypersensitivity, a T-cell mediated immune response is implicated. Type IV drug hypersensitivity is a major clinical concern, with a cutaneous aetiology driven through antigen specific T cells. Pro- and anti-inflammatory cytokines can be detected in reactions to β-lactam drugs in responsive T cells from hypersensitive patients. Classical Th1/Th2 phenotypes are currently used to classify the reactions, though these do not accurately characterise the function of the immune cells. In addition, this classification does not reference the newer Th subsets such as Th9, Th17 and Th22. To characterise the nature of the T-cell response observed in piperacillin hypersensitive patients with cystic fibrosis, T-cell clones from both blood and inflamed skin of hypersensitive patients were generated, then characterised in terms of phenotype and function. Additional investigations into PBMC responses were conducted. Naive T cells from healthy donors were also primed to piperacillin, as well as attempted regulation of the cytokine response through modulation of a selected nuclear receptor involved in the progression of a Th22 mediated response. Drug-specific clones were generated from both blood (n=570, 84% CD4) and skin (n=96, 83% CD4) samples obtained from patients hypersensitive to piperacillin. All clones secreted high levels of IFN-γ and IL-13. Interleukin-22, perforin and granzyme B were secreted in over 50% of clones, with none from either blood or skin showing any detectable level of IL-17A. Naive T cells primed to piperacillin via autologous dendritic cells showed proliferative responses (p=0.001, SI > 2). Clones generated from primed T-cells showed similar patterns of cytokine secretion when compared alongside clones generated from hypersensitive patients. Significant differences in chemokine receptor expressions were observed between blood-derived piperacillin-specific clones, skin-derived piperacillin-specific clones and skin-derived non piperacillin-specific clones. CLA, CXCR6 and CCR1 expression was higher on piperacillin-specific skin derived clones when compared to non-piperacillin specific skin derived clones (p=0.01). CCR2, CCR4, CXCR1 and E-cadherin were higher on skin specific clones when compared to blood specific clones (p=0.01). Piperacillin specific clones isolated from blood and skin of hypersensitive patients, as well as healthy donor PBMC migrated in the presence of chemokines specific to their respective cell surface receptors, with migration to CCR4 and CCR10 most prevalent. In addition, modulation of the aryl hydrocarbon receptor showed that an abrogation of the cytokine response was observed in cells treated with an AhR inhibitor. This abrogation was only observed in the secretion of interleukin-22, a key cytokine in a Th22 response. Currently, T-cell mediated hypersensitivity involving drug binding to the HLA molecule has only been shown for HLA class I molecules; no data has provided evidence for HLA class II interactions with drugs being able to activate CD4+ T-cells. To investigate whether HLA class II molecules binding to drugs could activate T-cells, an investigation into the COX-2 specific NSAID lumiracoxib was performed. Lumiracoxib was withdrawn from use after incidences of liver toxicity were reported in 2008. Utilising a naive T-cell dendritic cell co-culture assay, attempts were made to generate drug-specific responses from lymphocytes to either lumiracoxib or its major/minor metabolites. No positive responses were generated, with all assays performed showing no activation of drug-specific T-cells following re-challenge with the drugs. In conclusion, the data generated over the course of this thesis has shown that there is a subset of piperacillin-specific T-cells in hypersensitive patients with cystic fibrosis that secrete IL-22, IFN-γ, perforin and granzyme B in response to antigen challenge. No cells secreted IL17, suggesting a strong Th22 phenotype rather than Th17. In addition, The AhR signalling pathway is also heavily implicated in the development of hypersensitivity, giving further evidence for the role of both IL-22 and Th22 lymphocytes in beta-lactam hypersensitivity.
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Fernández, Barriga Ximena Beatriz. "Efecto inmunomodulador de las células madre mesenquimales sobre linfocitos T helper 1 y T helper 17". Tesis, Universidad de Chile, 2012. http://repositorio.uchile.cl/handle/2250/132032.

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Memoria para optar el título de Bioquímico
Las Células Madre Mesenquimales (MSCs) se han convertido en un interesante campo de estudio. Inicialmente fueron estudiadas por su capacidad de diferenciarse a células de diversos tejidos mesodermales, sin embargo, con el paso de los años se determinó que las MSCs tenían una amplia capacidad de escapar del reconocimiento de células del sistema inmune. Más tarde se descubrió que las MSCs no solo tienen la capacidad de escapar del reconocimiento, sino que también son capaces de inhibir la activación y proliferación de células del sistema inmune. Diversas enfermedades autoinmunes y proinflamatorias están mediadas por linfocitos T, principales células efectores del sistema inmune adaptativo, por tanto, dadas las características inmunosupresoras de las MSCs, han sido propuestas como nueva estrategia terapéutica para el tratamiento de estas enfermedades. Con este objetivo, varios autores han enfocado sus estudios para determinar el mecanismo por el cual las MSCs ejercen este efecto inhibitorio. Algunos autores postulan que el contacto celular, entre MSCs y linfocitos, es indispensable para producir este efecto, sin embargo otros postulan que las MSCs secretan una amplia variedad de factores solubles inmunosupresores que son suficientes para producir el efecto inmunosupresor. Dentro de las estirpes linfocitarias sobre las cuales las MSCs podrían ejercer su efecto inmunosupresor encontramos a los linfocitos T helper (TH), las cuales son células efectoras que se clasifican principalmente en: linfocitos TH1 que participan en la respuesta contra bacterias intracelulares, linfocitos TH2 que participan en la respuesta contra parásitos, linfocitos TH17 que participan en la respuesta contra bacterias extracelulares y hongos y, finalmente, los linfocitos T reguladores (Treg) cuya función es mantener la homeostasis del sistema inmune y promover la tolerancia inmunológica frente a antígenos propios. Durante más de una década fue ampliamente descrita la capacidad inmunosupresora de las MSCs sobre linfocitos T, sin embargo en los últimos años se ha descrito que bajo ciertas condiciones las MSCs producen un efecto estimulador sobre algunas de estas estirpes linfocitarias. El objetivo de este estudio fue determinar si las MSCs suprimen la proliferación y diferenciación de linfocitos TH1 y TH17. Estos linfocitos fueron estudiados ya que se ha descrito que diversas enfermedades autoinmunes se caracterizan por un aumento o desbalance de estas estirpes. Para esto, investigamos si es que el efecto inmunomodulador de las MSCs era dependiente del estado de activación y diferenciación de linfocitos, del ratio MSCs:CD4+, del contacto celular o de factores solubles. Dado que ha sido ampliamente descrito que las MSCs son capaces de secretar basalmente IL-6, la cual corresponde a una citoquina que cumple diversas funciones sobre el sistema inmune, entre ellas promover la secreción de citoquinas y factores de crecimiento necesarias para la respuestas de linfocitos T y que además son capaces de promover la estirpe, altamente proinflamatoria, TH17, y que esta secreción aumenta cuando las MSCs se encuentran frente a estímulos proinflamatorios como IFN-γ o TNF-α, postulamos que la IL-6 secretada por las MSCs es el principal factor soluble involucrado en la inmunomodulación ejercida por las MSCs. Las MSCs fueron obtenidas a partir de médula ósea de ratones C57BL/6 y caracterizadas por el patrón de expresión de antígenos de superficie y por su capacidad de multidiferenciación. Los linfocitos T CD4+ fueron obtenidos a partir de bazo de ratones C57BL/6, purificados mediante kit comercial y cultivados en presencia de citoquinas que favorecen la diferenciación hacia la estirpe TH1 o TH17. Las MSCs fueron agregadas a los cultivos de linfocitos TH1 o TH17 a distintos tiempos de cultivo celular en presencia o ausencia de contacto celular, contacto MSCs-linfocito. La diferenciación de los linfocitos fue medida por medio de la detección de citoquinas intracelulares características de ambas estirpes, IFN-γ e IL-17 para linfocitos TH1 y TH17 respectivamente, por medio de citometría de flujo. Demostramos que las MSCs son capaces de inhibir a linfocitos TH1 independiente del estado de activación y del ratio MSCs:CD4+. Determinamos que el efecto inmunosupresor está presente incluso en condiciones donde no existe contacto celular y que este efecto es independiente de la IL-6 secretadas por las MSCs. A diferencia de lo que ocurre con linfocitos TH1, las MSCs sólo son capaces de inhibir a linfocitos TH17 cuando estas son agregadas a tiempo temprano al cultivo celular y este efecto es dependiente del contacto celular, mientras que cuando las MSCs son agregadas al cultivo a tiempos tardíos, al día 4 de cultivo celular, promueven la diferenciación de linfocitos TH17. Concluimos que el efecto inmunomodulador que ejercen las MSCs sobre linfocitos TH1 y TH17 es por medio de mecanismos diferenciales. El efecto inmunosupresor sobre linfocitos TH1 es independiente de IL-6, sin embargo, no ha sido posible determinar el efecto real que ejerce la IL-6 secretada por las MSCs sobre linfocitos TH17 ya que la diferenciación de linfocitos TH17 requiere de IL-6 en el medio de cultivo. Sin embargo, determinamos que las MSCs en baja concentración no solo pierden su capacidad inhibitoria cuando se encuentran con linfocitos TH17 diferenciados sino que son capaces de promover su diferenciación. Observamos también que la IL-6 proveniente de MSCs podría, bajo ciertas, de revertir este efecto
Mesenchymal Stem Cells (MSCs) have become an interesting field of study. Initially MSCs where studied for their capacity to differentiate into various cell types from different tissues from the mesoderm, however, over the years was determined that MSCs have a large capacity to escape from the recognition by cells from the immune system. Later it was discovered that MSCs not only have the capacity to escape recognition, but are also able to inhibit the activation and proliferation of immune cells. Several autoimmune and proinflammatory diseases are mediated by T cells, major effectors cells of the adaptive immune system, therefore, given the immunosuppressive properties of MSCs they have been proposed as a new therapeutic strategy for treating these diseases. To this end, several authors have focused their studies to determine the mechanisms by which MSCs exert this inhibitory effect. Some authors postulate that cell contact between MSCs and lymphocytes is essential to produce this effect, while others postulate that MSCs secrete a wide variety of immunosuppressive soluble factors that are sufficient to produce the immunosuppressive effect on T lymphocytes. MSCs can exert their immunosuppressive effect on lymphocytes called T helper (TH), which are an effectors cell line mainly classified into: TH1 cells that participate in the response against intracellular bacteria, TH2 cells that participate in the response against parasites, TH17 cells that participate in the response against extracellular bacteria and fungi. Finally there are T regulatory (Treg) cells which main function is to maintain immune system homeostasis and to promote immunologic tolerance against self antigens. For over a decade, it was widely described the immunosuppressive capacity of MSCs on T lymphocytes, however in recent years it has been described that under certain conditions MSCs may produce a stimulatory effect on some of these lymphocytes strains. The aim of this study was to determine whether MSCs are able to suppress TH1 and TH17 proliferation and differentiation. These cells were studied because it has been previously described that many autoimmune disease are characterized by and increase or imbalance of this two strains. For this purpose, we investigated whether de immunomodulatory effect of MSCs was dependent on lymphocytes activation and differentiation state, MSCs: CD4+ ratio, cell contact or soluble factors. It has also been highly described that MSCs are able to secrete basal amounts of IL-6, cytokine which has a variety of function on the immune system, among them, to promote cytokine and growth factor secretion necessary for T cell response, and to promote differentiation of the highly proinflammatory TH17 cells. These IL-6 basal secretion is augmented when MSCs are in presence of proinflammatory stimulus like IFN-γ or TNF-α, thus we postulate that MSCs secreted IL-6 main soluble factor involved in MSCs immunomodulation. MSCs were obtained from mice bone marrow and characterized by their surface antigen expression pattern and their capability of multilineage differentiation. CD4+ T cells were obtained from mice splenocytes, purified by a commercial Kit and cultivated with cytokines that promote the differentiation to TH1 or TH17 cells. MSCs were added to TH1 or TH17 cultures at early or late time points and in the presence or absence of cell to cell contact, MSCs-T cell contact, mediated by a transwell system. The differentiation of TH1 or TH17 cell was measured by the detection of intracellular cytokines characteristics for each population, IFN-γ and IL-17 for TH1 and TH17 cells respectably, by flow cytometry. We demonstrated that MSCs are capable to suppress TH1 cells differentiation despite on their state of activation or MSCs:CD4+ ratio. We determined that the immune suppressor effect of MSCs is present even in the absence of cell to cell contact and that this effect is independent of MSCs secreted IL-6. In contrast with TH1 cells, MSCs are only capable to suppress TH17 cells when added at early time points of cell culture and that this effect requires cell to cell contact, while promoting TH17 differentiation when added at later time points, at day 4 of cell culture. We concluded that the immune modulator effect of MSCs on TH1 and TH17 cells is mediated by differential mechanism. The immune suppressor effect on TH1 cells is independent from IL-6, though it was not possible to determined de real effect of MSCs secreted IL-6 over TH17 cells, since the TH17 differentiation media requires IL-6. However, we determined that low concentration of MSCs in the coculture, fail to inhibit TH17 differentiation more over they promote an augmentation of TH17 cells. We also observed that under certain culture conditions MSCs secreted IL-6 may revert this effect
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Bergmann, Claudia C. "T helper regulation a theoretical approach /". [S.l.] : [s.n.], 2000. http://deposit.ddb.de/cgi-bin/dokserv?idn=96215511X.

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Jansson, Andreas Biotechnology &amp Biomolecular Sciences Faculty of Science UNSW. "Modelling T helper cell activation and development". Awarded by:University of New South Wales. School of Biotechnology and Biomolecular Sciences, 2006. http://handle.unsw.edu.au/1959.4/30602.

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T helper (Th) cell activation and development is one of the most critical events in regulating the adaptive immune response. Understanding its regulation could be of great therapeutical value as many severe diseases are associated with failure in controlling T cell activation and development. However, the regulation of T cell activation appears to be one of the most complex set of cellular and molecular interactions known in the immune system. There is therefore an urgent need for tools to unravel this complexity, and to make use of the quantitative experimental data. To address this issue, mathematical and computational models, based on rigorous biophysical and kinetic data, were developed to study the specific role of some of the major costimulatory molecules involved in Th cell activation, and others developed to investigate proposed theories about mechanisms involved in Th cell differentiation. The simulations of costimulation reveal new implications for the function of the costimulatory molecules CD28 and CTLA-4, and their ligands B7-1 and B7-2, and show how binding affinity, stoichiometric properties, expression levels, and, in particular, competition effects, all profoundly influence complex formation at the immunological synapse. The results support the concept that B7-2 and B7-1 are the dominant ligands of CD28 and CTLA-4, respectively, and indicate that the inability of B7-2 to recruit CTLA-4 to the synapse cannot be, as has been previously proposed, due to the different binding properties of B7-1 and B7-2. Simulations of Th cell development reveal that both instructive and selective processes are likely to be involved in Th cell differentiation. In addition, further simulations indicate that Th2 cells are more likely to become dominant by inhibiting Th1 cells (negative selection), rather than selecting their own growth (positive selection). This thesis also includes an experimental work in which the immunomodulatory role of the bacterial signalling molecule N-3-(oxododecanoyl)-L-homoserine lactone (OdDHL) was analysed. This study strongly suggests that OdDHL suppresses Th cell activation and development, and that it is likely targeting the intracellular signalling events involved in the early stages of Th cell activation.
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Alfonso, Christopher. "The function of helper T cell epitopes". Thesis, University of Newcastle Upon Tyne, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.319190.

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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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Wang, Qixin. "Genetic analysis of differentiation of T-helper lymphocytes". Thesis, University of Southern California, 2013. http://pqdtopen.proquest.com/#viewpdf?dispub=1546784.

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In the human immune system, T-helper cells are able to differentiate into two lymphocyte subsets: Th1 and Th2. The intracellular signaling pathways of differentiation form a dynamic regulation network by secreting distinctive types of cytokines, while differentiation is regulated by two major gene loci: T-bet and GATA-3. We developed a system dynamics model to simulate the differentiation and re-differentiation process of T-helper cells, based on gene expression levels of T-bet and GATA-3 during differentiation of these cells. We arrived at three ultimate states of the model and came to the conclusion that cell differentiation potential exists as long as the system dynamics is at an unstable equilibrium point; the T-helper cells will no longer have the potential of differentiation when the model reaches a stable equilibrium point. In addition, the time lag caused by expression of transcription factors can lead to oscillations in the secretion of cytokines during differentiation.

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Książki na temat "T-helper"

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Annunziato, Francesco, Laura Maggi i Alessio Mazzoni, red. T-Helper Cells. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1311-5.

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Waisman, Ari, i Burkhard Becher, red. T-Helper Cells. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1212-4.

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Graca, Luis, red. T-Follicular Helper Cells. New York, NY: Springer US, 2022. http://dx.doi.org/10.1007/978-1-0716-1736-6.

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Espéli, Marion, i Michelle Linterman, red. T follicular Helper Cells. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2498-1.

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Waisman, Ari, i Burkhard Becher. T-helper cells: Methods and protocols. New York: Humana Press, 2014.

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Sun, Bing, red. T Helper Cell Differentiation and Their Function. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-9487-9.

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Espéli, Marion, i Michelle Linterman. T follicular helper cells: Methods and protocols. New York, NY: Humana Press, 2015.

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Wierenga, Edsko Albert. Functional subsets of T helper cells: Implications for allergic disease. [Amsterdam: University of Amsterdam, 1992.

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Horowitz, Jay Bruce. Autocrine growth regulation of a cloned murine T helper cell line. [New Haven: s.n.], 1987.

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Reto, Crameri, red. Allergy and asthma in modern society: A scientific approach : dedicated to Kurt Blaser. Basel: Karger, 2006.

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Części książek na temat "T-helper"

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Kamath, Arati B. "Helper T Lymphocytes". W Encyclopedia of Immunotoxicology, 359–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-54596-2_649.

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Gooch, Jan W. "Helper T Cell". W Encyclopedic Dictionary of Polymers, 897. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13889.

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Mehlhorn, Heinz. "T-Helper Cells (Th)". W Encyclopedia of Parasitology, 2675–76. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_4397.

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Mehlhorn, Heinz. "T-Helper Cells (Th)". W Encyclopedia of Parasitology, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27769-6_4397-1.

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Ahlers, Jeffrey, Mario Clerici, Anne Hosmalin, Gene M. Shearer i Jay A. Berzofsky. "T Helper Cell Responses". W Techniques in HIV Research, 211–22. London: Palgrave Macmillan UK, 1990. http://dx.doi.org/10.1007/978-1-349-11888-5_12.

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Woody, James N., Jonathan R. Lamb, Edward D. Zanders i Marc Feldman. "Antigen-Specific T Cell Helper Factors". W Human T Cell Clones, 361–68. Totowa, NJ: Humana Press, 1985. http://dx.doi.org/10.1007/978-1-4612-4998-6_33.

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Kumar, Vinay, Sahil Gupta, Rachel Rosenzweig i Shyam S. Bansal. "Helper T-Lymphocytes in Cardiovascular Diseases". W Immune Cells, Inflammation, and Cardiovascular Diseases, 25–46. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/b22824-3.

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Gorczyca, Wojciech. "Nodal T-Cell Lymphomas with T Follicular Helper Phenotype". W Atlas of Differential Diagnosis in Neoplastic Hematopathology, 414–26. Wyd. 4. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.1201/9781003120445-23.

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

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van Lunzen, Jan, i Madelene Lindqvist. "T Follicular Helper Cells in HIV Infection". W Encyclopedia of AIDS, 1–8. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-9610-6_181-1.

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Streszczenia konferencji na temat "T-helper"

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Wang, Jung-Hao, Chih-Hung Wang, Chun-Che Lin i Gwo-Bin Lee. "Integrated microfluidic chip for measuring T helper cells". W 2010 IEEE 23rd International Conference on Micro Electro Mechanical Systems (MEMS). IEEE, 2010. http://dx.doi.org/10.1109/memsys.2010.5442366.

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Meghraoui-Kheddar, Aïda, Mehdi Sellami, Sandra Audonnet, Moncef Guenounou i Richard Le Naour. "Elastin peptides modulate T helper response during murine emphysema". W Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa5054.

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Barcelos, Filipe, Catarina Martins, Ricardo Monteiro, Carlos Geraldes, Ana Luísa Papoila, Joana Cardigos, Nathalie Madeira i in. "THU0207 HELPER AND CYTOTOXIC FOLLICULAR T-CELLS IN SJÖGREN’S SYNDROME". W Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.5352.

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Boieri, Margherita, Anna Malishkevich, Lauren Steidl, Kenneth Ngo, Sowmya Iyer, Mary Awad, Johannes Kreuzer, Wilhelm Haas, Miguel Rivera i Shadmehr Demehri. "Abstract 4948: T helper 2 cells block breast cancer promotion". W 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 i Shadmehr Demehri. "Abstract 4948: T helper 2 cells block breast cancer promotion". W 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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Bayes, Hannah K., i Thomas Evans. "Novel T Helper Cell Subsets In Immunity To Pseudomonas Aeruginosa Infections". W 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.a6111.

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van Uden, Denise, Menno Van Nimwegen, Thomas Koudstaal, Peter Heukels, Jennifer Van Hulst, Karin Boomars, Rudi Hendriks i Mirjam Kool. "Alterations in circulating helper T-cells in idiopathic pulmonary arterial hypertension". W ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa5051.

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Magen, Assaf, Pauline Hamon, Nathalie Fiaschi, Raquel Deering, Sacha Gnjatic, Myron Schwartz, Thomas Marron, Gavin Thurston, Alice Kamphorst i Miriam Merad. "541 mregDC/T helper niches enable local reactivation of CD8 T cells upon PD-1 blockade". W SITC 37th Annual Meeting (SITC 2022) Abstracts. BMJ Publishing Group Ltd, 2022. http://dx.doi.org/10.1136/jitc-2022-sitc2022.0541.

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LEE, YUE-HIEN, MANUELA BENARY, RIA BAUMGRASS i HANSPETER HERZEL. "PREDICTION OF REGULATORY TRANSCRIPTION FACTORS IN T HELPER CELL DIFFERENTIATION AND MAINTENANCE". W Proceedings of the 9th Annual International Workshop on Bioinformatics and Systems Biology (IBSB 2009). IMPERIAL COLLEGE PRESS, 2010. http://dx.doi.org/10.1142/9781848165786_0008.

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Rehman, Tayyab, Fokhrul Hossain i David A. Welsh. "T Helper 17 Cells Are Increased In The Lungs Of Older Mice". W 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.a4159.

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Raporty organizacyjne na temat "T-helper"

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Gridley, Daila S. Mechanisms of Low Dose Radiation-induced T helper Cell Function. Office of Scientific and Technical Information (OSTI), październik 2008. http://dx.doi.org/10.2172/940241.

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Bice, D. E., i M. R. Schuyler. Dysfunction of pulmonary immuity in atopic asthma: Possible role of T helper cells. Office of Scientific and Technical Information (OSTI), grudzień 1995. http://dx.doi.org/10.2172/381395.

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Mitchell, Malcolm S. Development of Superagonist Mimics to Epitopes Defined by Cytotoxic and Helper T Cells. Fort Belvoir, VA: Defense Technical Information Center, sierpień 2002. http://dx.doi.org/10.21236/ada413745.

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