Relevant bibliographies by topics / Follicular T cells

Academic literature on the topic 'Follicular T cells'

Author: Grafiati
Published: 7 July 2024
Last updated: 7 July 2024

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Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Journal articles on the topic "Follicular T cells":

1

Zhu, Yangyang, Le Zou, and Yun-Cai Liu. "T follicular helper cells, T follicular regulatory cells and autoimmunity." International Immunology 28, no. 4 (December 29, 2015): 173–79. http://dx.doi.org/10.1093/intimm/dxv079.

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Vinuesa, Carola G., Michelle A. Linterman, Di Yu, and Ian C. M. MacLennan. "Follicular Helper T Cells." Annual Review of Immunology 34, no. 1 (May 20, 2016): 335–68. http://dx.doi.org/10.1146/annurev-immunol-041015-055605.

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Sage, Peter T., and Arlene H. Sharpe. "T follicular regulatory cells." Immunological Reviews 271, no. 1 (April 18, 2016): 246–59. http://dx.doi.org/10.1111/imr.12411.

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4

Deng, Jun, Yunbo Wei, Válter R. Fonseca, Luis Graca, and Di Yu. "T follicular helper cells and T follicular regulatory cells in rheumatic diseases." Nature Reviews Rheumatology 15, no. 8 (July 9, 2019): 475–90. http://dx.doi.org/10.1038/s41584-019-0254-2.

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Balasubramani, Anand. "Priming T follicular helper cells." Science 358, no. 6368 (December 7, 2017): 1266.21–1268. http://dx.doi.org/10.1126/science.358.6368.1266-u.

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Wu, Xin, Yun Wang, Rui Huang, Qujing Gai, Haofei Liu, Meimei Shi, Xiang Zhang, et al. "SOSTDC1-producing follicular helper T cells promote regulatory follicular T cell differentiation." Science 369, no. 6506 (August 20, 2020): 984–88. http://dx.doi.org/10.1126/science.aba6652.

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Germinal center (GC) responses potentiate the generation of follicular regulatory T (TFR) cells. However, the molecular cues driving TFR cell formation remain unknown. Here, we show that sclerostin domain-containing protein 1 (SOSTDC1), secreted by a subpopulation of follicular helper T (TFH) cells and T–B cell border–enriched fibroblastic reticular cells, is developmentally required for TFR cell generation. Fate tracking and transcriptome assessment in reporter mice establishes SOSTDC1-expressing TFH cells as a distinct T cell population that develops after SOSTDC1– TFH cells and loses the ability to help B cells for antibody production. Notably, Sostdc1 ablation in TFH cells results in substantially reduced TFR cell numbers and consequently elevated GC responses. Mechanistically, SOSTDC1 blocks the WNT–β-catenin axis and facilitates TFR cell differentiation.
7

Suh, Woong-Kyung. "Life of T Follicular Helper Cells." Molecules and Cells 38, no. 3 (December 24, 2014): 195–201. http://dx.doi.org/10.14348/molcells.2015.2331.

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Walters, Giles Desmond, and Carola G. Vinuesa. "T Follicular Helper Cells in Transplantation." Transplantation 100, no. 8 (August 2016): 1650–55. http://dx.doi.org/10.1097/tp.0000000000001217.

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Metes, Diana M. "T follicular Helper Cells in Transplantation." Transplantation 100, no. 8 (August 2016): 1603–4. http://dx.doi.org/10.1097/tp.0000000000001218.

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Teitell, Michael A. "T cells in mouse follicular lymphoma." Blood 103, no. 6 (March 15, 2004): 1981–82. http://dx.doi.org/10.1182/blood-2004-01-0012.

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Journal articles Dissertations / Theses

Dissertations / Theses on the topic "Follicular T cells":

1

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.
2

Sayin, Ismail. "Characterization of human T follicular regulatory cells." Case Western Reserve University School of Graduate Studies / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=case1560336991188191.

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3

Misiak, Jan. "The interactions of stromal cells and follicular helper T cells resulting in a B-cell supporting, IL4-producing phenotype in the context of follicular lymphoma." Thesis, Rennes 1, 2016. http://www.theses.fr/2016REN1B030.

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Un microenvironnement riche en IL-4 a été mis en évidence dans le lymphome folliculaire (FL). Cette IL-4 impliquée dans la croissance tumorale a été démontrée comme principalement secrétée par les lymphocytes T follicular helper (Tfh). Dans cette étude, nous étudions l’interaction bidirectionnelle entre les cellules fibroblastiques réticulaires (FRC) dont le réseau est augmenté dans le FL et les lymphocytes Tfh par analyse des profils d’expression génique, et co-culture in vitro des lymphocytes Tfh primaires avec des cellules fibroblastiques humaines de type FRC-like. Nous démontrons que les cellules FRC-like augmentent in vitro la croissance des sous-populations de Tfh. De plus, nous avons mis en évidence une augmentation spécifique de la sécrétion d’IL-4 par les précurseurs Tfh (pre-Tfh) co-cultivés avec les cellules FRC-like, augmentation d’IL-4 impliquant les voies Notch et ICAM1/LFA1. Cette observation est particulièrement intéressante dans le contexte du FL car les lymphocytes pre-Tfh de FL comparés à des lymphocytes pre-Tfh d’amygdales non tumorales sont caractérisés par un profil d’expression génique enrichi en gènes des voies Notch et des intégrines en plus d’une surexpression d’IL-4. En conclusion, notre description de l’interaction entre les cellules stromales et les sous-populations Tfh démontrent une modification du profil cytokinique des Tfh au stade précurseur qui pourrait expliquer le profil cytokinique retrouvé dans le microenvironnement du FL, et apporter de nouveaux éléments pour la mise en évidence de nouvelles cibles thérapeutiques
The enrichment of the microenvironment with tumor-promoting interleukin 4 (IL4) has been implicated in the pathogenesis of follicular lymphoma (FL) and was found to be conferred mainly by T follicular helper (Tfh) cells. In this study, we investigated the bidirectional crosstalk of fibroblastic reticular cells that are expanded in FL and Tfh cells with the analysis of gene expression profiles of the respective, and an in-vitro co-culture model of human induced FRC-like cells. We demonstrated that FRC-like cells enhance the growth of Tfh cell subsets in vitro. Crucially, we uncovered a specific upregulation of IL-4 secretion by precursor Tfh (pre-Tfh) cells co-cultured with FRC-like cells. Additionally, we demonstrated that Notch and ICAM1/LFA1 are two pathways involved in IL-4 secretion following FRClike cell / Tfh cell crosstalk. This observation was particularly interesting in FL context, because FL pre-Tfh cells display an enriched Notch and integrin gene expression profile as well as an overexpression of IL-4, compared to their tonsil counterpart. Altogether, we described new interactions between stromal cells and Tfh subsets and uncovered a specific cytokine profile modification at pre-Tfh stage after contact with FRC-like cells that could explain the high levels of IL-4 in FL and provide a novel target for therapy
4

Vanderleyden, Ine. "Follicular regulatory T cell migration and differentiation." Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/288422.

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The germinal centre (GC) response is critical for generating highly effective humoral immune responses and immunological memory that forms the basis of successful immunisation. Control of the output of the GC response requires Follicular regulatory T (Tfr) cells, a subset of Foxp3+ Treg cells located within germinal centres. Tfr cells were first characterised in detail in 2011 and because of this relatively little is known about the exact role of Tfr cells within the GC, and the mechanism/s through which they exert their suppressive function. At the outset of this work, the major barrier to understanding Tfr cell biology was the lack of appropriate tools to study Tfr cells specifically, without affecting Tfh cells or other Treg cell subsets. This thesis set out to develop a strain of mice that specifically lacks Tfr cells. A unique feature of Tfr cells is their CXCR5-dependent localisation within the GC. Therefore, genetic strategies that exclude Treg cells from entering the GC are a rational approach to generating a mouse model that lacks Tfr cells. To this end, I generated a strain of mice that lacks CXCR5 on Foxp3+ Treg cells. These animals show a ~50% reduction in GC localised Tfr cells, and a GC response that is comparable to control animals. These data indicated that redundant mechanisms are involved in Treg cell homing to the GC. I identified CXCR4 as a chemokine receptor that is also highly expressed on Tfr cells, and hypothesised that it may also be involved in Tfr cell localisation to the GC. Surprisingly, simultaneous deletion of both CXCR4 and CXCR5 in Treg cells resulted in a less marked reduction in Tfr cells compared to deletion of CXCR5 alone, suggesting that CXCR4 might be involved in negative regulation of Treg homing to the GC. These data identify both CXCR4 and CXCR5 as key regulators of Tfr cell biology. Bcl6 drives Tfr cell differentiation, but how this transcriptional repressor facilitates commitment to the Tfr cell subset is unknown. I hypothesised that Bcl6 drives Tfr cell differentiation by repressing Tbx21, the transcriptional regulator involved in the differentiation of Th1-like Treg cells. I tested this hypothesis in Bcl6fl/fl CD4cre/+ animals and unexpectedly found that loss of Bcl6 regulates Treg cell differentiation in the absence of immunisation or infection. I have demonstrated that thymic loss of Bcl6 results in an increase in activated effector Treg cells, which occurs very early in life. These data point to a novel role for Bcl6 in preventing early thymic Treg activation, indicating that Bcl6 has a global role in Treg development and differentiation that is not simply limited to Tfr cells.
5

Wang, Changna. "Follicular Dendritic Cells, Resting CD4+ T Cells and Human Immunodeficiency Virus Expression." BYU ScholarsArchive, 2011. https://scholarsarchive.byu.edu/etd/2906.

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Many events associated with Human Immunodeficiency Virus (HIV) infection/replication occur in and around the germinal centers (GCs) of secondary lymphoid tissues where follicular dendritic cells (FDCs) reside, suggesting that this microenvironment may contribute unique signaling that is important to viral progression. My research focused on characterizing signaling, both positive and negative, contributed by FDCs that affects HIV infection and replication. Specifically, I determined if FDC signals could induce the expression of latent HIV in T cells and if so, to characterize the signaling pathways involved. Moreover, I also examined the ability of FDCs to produce inhibitory signals that might block active virus expression. I approached these problems using FDCs from tonsils and coculturing these with primary CD4+ T cells or latently-infected Jurket cells with a GFP reporter. Results indicated that FDCs dramatically augmented HIV production of these cells. FDC signaling was costimulatory in nature and was mediated by soluble TNFα. However, when ex vivo latently infected T cells were treated with PMA/ionomycin or IL2/IL7, little virus expression was observed until FDCs were added, which greatly increased virus production. The transcription factor NFAT is important for the reactivation of latent HIV. Inhibition studies as well as ELISA suggested that JAK/STAT signaling pathway was involved in virus reactivation. Because FDCs produce prostaglandins (PGs) E2 and I2, I determined the effect of PGE2 and PGI2 analogs on HIV infected T cells. Results indicated that both the PGE2 and PGI2 analogs inhibited proliferation and activation-induced cell death of HIV infected T cells in a dose- and time-dependent manner. Additionally, it was shown that indomethacin and CAY10404, cyclooxygenase and cyclooxygenase-2 inhibitors, partially restored HIV production in the presence of FDCs, suggesting that FDC-produced PGE2 and PGI2 may inhibit virus replication. Thus, FDCs produce PGs that can block virus gene expression in T cells, which may be ideal for viral persistence. Therefore, FDC signaling appears to both promote and inhibit HIV production. A better understanding of FDC signaling and regulation in GCs may suggest new treatment strategies that would be beneficial to infected subjects.
6

Pandey, Shubham. "Identification of Interleukin 4 - CXCL12 supportive loop in follicular lymphoma." Thesis, Rennes 1, 2016. http://www.theses.fr/2016REN1B031/document.

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Le lymphome folliculaire (FL) est le lymphome B indolent le plus fréquent. Outre des altérations géniques récurrentes, le micro-environnement tumoral, et notamment les cellules stromales lymphoides,joue un rôle majeur dans le développement de ce cancer. Cependant, la caractérisation in-situ des cellules stromales lymphoïdes chez l'homme tout comme les facteurs menant à la polarisation du stroma en un stroma protumoral ont été peu étudiés. Dans cette thèse, nous avons montré, que les cellules stromales présentes dans les ganglions et la moelle osseuse envahis des patients atteints de FL surexpriment fortement la chimiokine CXCL12. Nous avons ensuite tenté de comprendre les mécanismes responsables de cette induction. Alors que les cellules B tumorales induisent une surexpression de la chimiokine CCL2 dans les cellules stromales de façon dépendante de leur synthèse de TNF, elles ne contribuent pas à l'induction de CXCL12. A l'inverse, le principal compartiment TCD4 impliqué dans la croissance tumorale du FL, les cellules T follicular helper (TFH), augmentent l'expression de CXCL12 dans les cellules stromales. Le taux d'IL-4, la principale cytokine produite par les TFH de FL, est d'ailleurs corrélé à celui de CXCL12 au sein de ma niche tumorale du FL. De plus, à l’aide d'un modèle de différenciation en stroma lymphoide, nous avons démontré que l’IL4 induit l’expression de CXCL12 par les cellules stromale in vitro. Cette production est augmentée quand les cellules stromales sont déjà engagées vers la voie de différentiation lymphoide par un traitement TNF/LT qui favorise l'activation de STAT6 par l'IL-4. Nous avons validé ces résultats dans un modèle de formation d'organe lymphoide ectopique chez la souris. Enfin, CXCL12 induit la migration et l'adhésion au stroma des B de FL via l'activation de cascades de signalisations qui peuvent être abrogées par l'utilisation d'un inhibiteur de Btk utilisé en clinique, l'Ibrutinib. Ces résultats sont en faveur de l'intérêt de considérer la boucle IL-4/CXCL12 pour développer de nouvelles stratégies thérapeutiques dans cette pathologie constamment fatale
Follicular lymphoma (FL) is the most frequent indolent B-cell lymphoma. Beside recurrent genetic alterations, tumor microenvironment, including lymphoid stromal cells, has been shown to play a key role in FL development. However, in situ characterization of lymphoid stromal cells is still lacking in humans and there are very few studies focusing on the factors that could lead to stroma polarization in normal and pathological context. In this thesis, we showed first that in FL, lymph node (LN) and bone marrow (BM) infiltrating stromal cells highly express the chemokine CXCL12. We next focused on the mechanisms underlying this upregulation. Interestingly, whereas malignant FL B cells induced overexpression of CCL2 in stromal cells in a TNF-dependent manner, they did not contribute to CXCL12 induction. Conversely, FL-infiltrating follicular helper T cells (FL-TFH), the key FL-supportive T-cell subset could trigger CXCL12 expression in stromal cells. IL-4 is the main FL-TFH-derived cytokine and showed a positive correlation with CXCL12 expression inside FL cell niches. Moreover, based on our in vitro lymphoid stroma differentiation model, we demonstrated that IL-4 promoted CXCL12 expression in stromal cells, together with a phenotype close to that identified in situ within FL cell niche. Such IL4 dependent CXCL12 regulation is more pronounced in stromal cells already committed towards lymphoid stromal cells by a prestimulation by TNF/LT in association with an increased STAT6 activation. These data were validated in a model of ectopic lymphoid organ formation in mice. Finally, CXCL12 induced FL B-cell migration, and adhesion to stromal cells through the activation of a signaling pathway that could be abrogated by the Btk inhibitor Ibrutinib. These data argue for considering IL-4/CXCL12 axis as a potential therapeutic target to disrupt FL protective cell niche in this still fatal malignancy
7

Kawamoto, Shimpei. "Preferential Generation of Follicular B Helper T Cells from Foxp3+ T Cells in Gut Peyer's Patches." Kyoto University, 2011. http://hdl.handle.net/2433/142110.

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8

Thomas, Jessica. "T follicular helper cells in health and inflammatory bowel disease." Thesis, King's College London (University of London), 2013. https://kclpure.kcl.ac.uk/portal/en/theses/t-follicular-helper-cells-in-health-and-inflammatory-bowel-disease(1c45e306-6a7b-4d84-b02f-e4e1c500dbea).html.

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The intestinal IgA response has features that are different to those of the systemic humoral response, which is dominated by IgG. Although the IgA response, like the IgG response, includes an antigen specific component, it is also associated with polyspecificity and autoimmunity. The profile of intestinal immunoglobulins changes in inflammatory bowel disease (IBD) where there is a disproportionate increase in IgG production and in ulcerative colitis (UC), this includes the production of autoantibodies. In this thesis, two immunoregulatory T cell subsets that could influence the intestinal B cell response have been studied; T follicular helper cells (TFH) and regulatory T cells (Treg). Results in chapter 3 show that there is a higher density of TFH in gut associated lymphoid tissue (GALT) compared to peripheral lymphoid tissue due to a higher density of CD57- TFH- The expression of cytokines and CD40L was almost comparable between CD57+ and CD57- TFH- However, culturing experiments suggest that CD57-TFH may develop into CD57+ TFH and there is a constant turnover of TFH in the gut. Experiments in chapter 4 attempted to seek evidence for a developmental relationship between TFH and Treg by analysis of T cell receptor sequences. No evidence of plasticity between these subsets was observed. Experiments in chapter 5 set out to characterise TFH in IBD. In the appendix of UC patients, nearly all TFH were CD57+ and at a high density within germinal centres (GC). This thesis concludes that TFH are more phenotypically diverse and denser in GALT compared to peripheral lymphoid tissue. This may reduce the threshold for GC B cell survival in the gut permitting the propagation of plasma cells that secrete polyspecific and autoreactive IgA. TFH are denser still in the small GC in UC appendix. This may be relevant to the production of autoantibodies and disease pathogenesis.
9

Townsend, William Mathew. "A study of CD4+ follicular helper T cells in the follicular lymphoma microenvironment and normal germinal centres." Thesis, King's College London (University of London), 2017. https://kclpure.kcl.ac.uk/portal/en/theses/a-study-of-cd4-follicular-helper-t-cells-in-the-follicular-lymphoma-microenvironment-and-normal-germinal-centres(744b7c2f-f848-4c41-8fd1-687dc2201f6b).html.

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Follicular lymphoma is a common B cell malignancy which usually follows an indolent course but it is a heterogeneous disease and there are no biomarkers that can accurately predict outcome or prognosis at the time of diagnosis. There is now clear evidence that the microenvironment plays an important role in the pathogenesis of this disease and the composition of the microenvironment has been linked to prognosis with variable results. The biological basis for the influence of the microenvironment and the contribution of individual cell types remain unclear. In this research we focus on CD4+ T cell subsets, in particular T follicular helper cells and characterise their number, phenotype and distribution in follicular lymphoma with comparisons to normal germinal centres in reactive lymph nodes. We also investigate if T follicular helper cells have a role in promoting B cell proliferation, and induction of AID, whether B and T cells form immunological synapses in follicular lymphoma, and if there is evidence of antigen specificity in the T-cell receptor repertoire.
10

Rasheed, Mohammed Ata Ur. "Gene signatures and functional analysis of follicular B helper T cells." [S.l.] : [s.n.], 2006. http://www.diss.fu-berlin.de/2006/538/index.html.

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Books on the topic "Follicular T cells":

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

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Graca, Luis. T-Follicular Helper Cells: Methods and Protocols. Springer, 2022.

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Espéli, Marion, and Michelle Linterman. T Follicular Helper Cells: Methods and Protocols. Springer New York, 2016.

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Graca, Luis. T-Follicular Helper Cells: Methods and Protocols. Springer, 2021.

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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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Carton, James. Haematopathology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198759584.003.0015.

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This chapter discusses haematopathology, including iron deficiency anaemia, anaemia of chronic disease, megaloblastic anaemias, hereditary spherocytosis, glucose-6-phosphate dehydrogenase deficiency, thalassaemias, sickle-cell disorders, idiopathic thrombocytopenic purpura (ITP), thrombotic thrombocytopenic purpura (TTP), von Willebrand disease, haemophilia, thrombophilia, acute B-lymphoblastic leukaemia, acute myeloid leukaemias, chronic lymphocytic leukaemia (CLL), chronic myelogenous leukaemia, polycythaemia vera (PV), essential thrombocythaemia (ET), primary myelofibrosis (PMF), myelodysplastic syndromes (MDS), follicular lymphoma, diffuse large B-cell lymphoma, Burkitt’s lymphoma (BL), extranodal marginal zone lymphoma of mucosa-associated lymphoid tissue (MALT lymphoma), mantle cell lymphoma, classical Hodgkin’s lymphoma (cHL), lymphoplasmacytic lymphoma (LPL), plasma cell myeloma, primary amyloidosis, and mature T-cell non-Hodgkin’s lymphomas.

Book chapters on the topic "Follicular T cells":

1

Yu, Sulan, Meiling Wu, Yun Feng, Jiangang Shen, Liwei Lu, and Xiang Lin. "Detection of T Follicular Helper Cells and T Follicular Regulatory Cells in Experimental Sjögren’s Syndrome." In Methods in Molecular Biology, 211–24. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1736-6_18.

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van Lunzen, Jan, and Madelene Lindqvist. "T Follicular Helper Cells in HIV Infection." In 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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Courey-Ghaouzi, Alan, and Mauro Gaya. "Identification of Non-classical Follicular T Cells." In Methods in Molecular Biology, 77–84. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1736-6_7.

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Jandl, Christoph, Claudia Loetsch, and Cecile King. "Cytokine Expression by T Follicular Helper Cells." In Methods in Molecular Biology, 95–103. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7095-7_8.

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van Lunzen, Jan, and Madelene Lindqvist. "T Follicular Helper Cells in HIV Infection." In Encyclopedia of AIDS, 1957–63. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7101-5_181.

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Schmitt, Nathalie, and Hideki Ueno. "Human T Follicular Helper Cells: Development and Subsets." In Crossroads Between Innate and Adaptive Immunity IV, 87–94. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-6217-0_10.

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Georgiev, Hristo, Georgia Papadogianni, and Günter Bernhardt. "Identification of Follicular T Cells in the Gut." In Methods in Molecular Biology, 85–95. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1736-6_8.

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Vanderleyden, Ine, and Michelle A. Linterman. "Identifying Follicular Regulatory T Cells by Confocal Microscopy." In Methods in Molecular Biology, 87–93. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7095-7_7.

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Ding, Yanna, John D. Mountz, and Hui-Chen Hsu. "Identification of Follicular T Helper Cells in Tissue Sections." In Methods in Molecular Biology, 13–25. New York, NY: Springer New York, 2015. http://dx.doi.org/10.1007/978-1-4939-2498-1_2.

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Aloulou, Meryem, and Nicolas Fazilleau. "The Use of Peptide-MHCII Tetramers to Identify Antigen-Specific T Follicular Helper and T Follicular Regulatory Cells." In Methods in Molecular Biology, 141–47. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1736-6_12.

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Conference papers on the topic "Follicular T cells":

1

Barcelos, Filipe, Catarina Martins, Ricardo Monteiro, Carlos Geraldes, Ana Luísa Papoila, Joana Cardigos, Nathalie Madeira, et al. "THU0207 HELPER AND CYTOTOXIC FOLLICULAR T-CELLS IN SJÖGREN’S SYNDROME." In 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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2

Seth, Abhinav, Edward I. Herman, Jason S. Weinstein, Jin-Young Choi, and Joseph E. Craft. "AI-15 Decreased intracellular calcium flux in follicular helper T cells after T cell receptor stimulation." In Abstracts of the Third Biannual Scientific Meeting of the North and South American Lupus Community, Armonk, New York, USA, September 29 – October 1, 2016. Lupus Foundation of America, 2016. http://dx.doi.org/10.1136/lupus-2016-000179.15.

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3

Pontarini, E., W. Murray-Brown, C. Croia, E. Astorri, D. Lucchesi, N. Lepse, N. Sutcliffe, A. Tappuni, C. Pitzalis, and M. Bombardieri. "OP0300 Enrichment of T follicular-helper cells (TFH) and exclusion of t follicular-regulatory cells (TFR) from ectoPIC germinal centers in salivary glands of sjogren's syndrome patients." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.6121.

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4

Noël, Grégory, Mireille Langouo, Soizic Garaud, Anaïs Boisson, Hugues Duvillier, Gert Van den Eynden, Denis Larsimont, and Karen Willard-Gallo. "Abstract A40: The balance between activated follicular helper T cells and follicular regulatory T cells within tertiary lymphoid structures guides antitumor immune responses in human breast cancer." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; November 27-30, 2018; Miami Beach, FL. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/2326-6074.tumimm18-a40.

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5

Curtiss, M. L., B. Mousseau, B. Leon, A. Ballesteros-Tato, C. Steele, T. Randall, and F. Lund. "Chi3l1 (BRP-39) Is Required for IgE Antibody and T Follicular Helper Cells." In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a1342.

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6

Mansfield, James, Lilli Nelson, Chris van der Loos, and Richard Byers. "Abstract 468: Phenotyping TILs in situ: Automated enumeration of intra- and extra-follicular Foxp3+ regulatory T cells in follicular lymphoma." In Proceedings: AACR 104th Annual Meeting 2013; Apr 6-10, 2013; Washington, DC. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1538-7445.am2013-468.

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7

Desbois, Anne-Claire, Anna Maciejewski-Duval, Paul Régnier, Valentin Quiniou, Cloé Comarmond, Hélène Vallet, Patrick Bruneval, et al. "SAT0222 COOPERATION OF T FOLLICULAR HELPER CELLS AND B CELLS IN TERTIARY LYMPHOID STRUCTURES IN TAKAYASU ARTERITIS." In 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.4852.

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8

Asai, Yuichiro, Hirofumi Chiba, Syun Kondoh, Hirotaka Nishikiori, Mamoru Takahashi, Koji Kuronuma, Mitsuo Otsuka, et al. "Deterioration of regulatory B cells and activation of follicular helper T cells in idiopathic interstitial pneumonias patients." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa911.

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9

Ehrlich, S., K. Wild, M. Smits, K. Zoldan, M. Hofmann, R. Thimme, and T. Boettler. "Type I Interferons promote maintenance and function of follicular T helper cells in vitro." In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677255.

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10

Overacre-Delgoffe, Abigail E., Hannah J. Bumgarner, Anthony R. Cillo, Ansen H. P. Burr, Justin T. Tometich, Amrita Bhattacharjee, Tullia C. Bruno, Dario A. A. Vignali, and Timothy W. Hand. "Abstract PR08: Context is everything: Microbiota-specific T follicular helper cells in colorectal cancer." In Abstracts: AACR Virtual Special Conference: Tumor Immunology and Immunotherapy; October 5-6, 2021. American Association for Cancer Research, 2022. http://dx.doi.org/10.1158/2326-6074.tumimm21-pr08.

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