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Journal articles on the topic 'Follicular T cells'

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Author: Grafiati

Published: 7 July 2024

Last updated: 7 July 2024

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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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2

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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3

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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5

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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6

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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8

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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9

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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10

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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11

Sargent, Jennifer. "Follicular helper T cells in T1DM." Nature Reviews Endocrinology 11, no. 2 (December 9, 2014): 65. http://dx.doi.org/10.1038/nrendo.2014.216.

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12

Crotty, Shane. "Follicular Helper CD4 T Cells (TFH)." Annual Review of Immunology 29, no. 1 (April 23, 2011): 621–63. http://dx.doi.org/10.1146/annurev-immunol-031210-101400.

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13

Park, Hong-Jai, Do-Hyun Kim, and Je-Min Choi. "Germinal Center Formation Controlled by Balancing Between Follicular Helper T Cells and Follicular Regulatory T Cells." Hanyang Medical Reviews 33, no. 1 (2013): 10. http://dx.doi.org/10.7599/hmr.2013.33.1.10.

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14

Yeh, Chen-Hao, Masayuki Kuraoka, Heather Lynch, Gregory D. Sempowski, and Garnett H. Kelsoe. "TCR Repertoire Analysis of Mouse T Follicular Helper Cells and T Follicular Regulatory Cells Following Immunization." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 133.37. http://dx.doi.org/10.4049/jimmunol.196.supp.133.37.

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Abstract Generation of high-affinity and class-switched antibody requires the germinal center (GC) reaction after infection or immunization. Within the B-cell follicles of secondary lymphoid organs, the GC represents a sophisticated collaboration between antigen-specific B cells, follicular dendritic cells, T follicular helper (TFH) cells and T follicular regulatory (TFREG) cells. Despite intensive interest in the development and effector function of TFH and TFREG cells, little is known regarding the selection of T-cell receptor (TCR) repertoire during polyclonal GC reactions. In order to evaluate native, polyclonal TCR responses elicited by a complex antigen, we developed a sorting strategy to isolate TFH/TFREG cell populations that were activated and expanded after s.c. immunization with NP15-OVA. TCRβ VDJ rearrangements were recovered from highly purified TCRβ+CD4+CXCR5hiPD-1+Bcl-6+FoxP3− TFH cells and TCRβ+CD4+ CXCR5hiPD-1+Bcl-6+FoxP3+ TFREG cells, amplified by PCR, and sequenced. Analysis of the antigen-specific TCR repertoire of TFH/TFREG cells provides important insights into the factors influencing T-cell recruitment and clonal expansion following infection or vaccination, especially when linked to contemporary analysis of the GC B-cell repertoire. These findings may inform rational and selective control strategy of the GC reaction. Vaccine development can accordingly focus on modulating TFH/TFREG responses to facilitate optimal adaptive immune responses.

15

Berrih-Aknin, Sonia. "Imbalance between T follicular helper and T follicular regulatory cells in myasthenia gravis." Journal of Xiangya Medicine 2 (2017): 22. http://dx.doi.org/10.21037/jxym.2017.02.06.

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16

Chen, Maogen, Xiaohong Lin, Cheukfai Li, Nancy Olsen, Xiaoshun He, and Song Guo Zheng. "Advances in T follicular helper and T follicular regulatory cells in transplantation immunity." Transplantation Reviews 32, no. 4 (October 2018): 187–93. http://dx.doi.org/10.1016/j.trre.2018.07.002.

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17

Li, Shengbin, Joy M. Folkvord, Eva G. Rakasz, Hadia M. Abdelaal, Reece K. Wagstaff, Katalin J. Kovacs, Hyeon O. Kim, et al. "Simian Immunodeficiency Virus-Producing Cells in Follicles Are Partially Suppressed by CD8+CellsIn Vivo." Journal of Virology 90, no. 24 (October 5, 2016): 11168–80. http://dx.doi.org/10.1128/jvi.01332-16.

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ABSTRACTHuman immunodeficiency virus (HIV)- and simian immunodeficiency virus (SIV)-specific CD8+T cells are typically largely excluded from lymphoid B cell follicles, where HIV- and SIV-producing cells are most highly concentrated, indicating that B cell follicles are somewhat of an immunoprivileged site. To gain insights into virus-specific follicular CD8+T cells, we determined the location and phenotype of follicular SIV-specific CD8+T cellsin situ, the local relationship of these cells to Foxp3+cells, and the effects of CD8 depletion on levels of follicular SIV-producing cells in chronically SIV-infected rhesus macaques. We found that follicular SIV-specific CD8+T cells were able to migrate throughout follicular areas, including germinal centers. Many expressed PD-1, indicating that they may have been exhausted. A small subset was in direct contact with and likely inhibited by Foxp3+cells, and a few were themselves Foxp3+. In addition, subsets of follicular SIV-specific CD8+T cells expressed low to medium levels of perforin, and subsets were activated and proliferating. Importantly, after CD8 depletion, the number of SIV-producing cells increased in B cell follicles and extrafollicular areas, suggesting that follicular and extrafollicular CD8+T cells have a suppressive effect on SIV replication. Taken together, these results suggest that during chronic SIV infection, despite high levels of exhaustion and likely inhibition by Foxp3+cells, a subset of follicular SIV-specific CD8+T cells are functional and suppress viral replicationin vivo. These findings support HIV cure strategies that augment functional follicular virus-specific CD8+T cells to enhance viral control.IMPORTANCEHIV- and SIV-specific CD8+T cells are typically largely excluded from lymphoid B cell follicles, where virus-producing cells are most highly concentrated, suggesting that B cell follicles are somewhat of an immunoprivileged site where virus-specific CD8+T cells are not able to clear all follicular HIV- and SIV-producing cells. To gain insights into follicular CD8+T cell function, we characterized follicular virus-specific CD8+T cellsin situby using an SIV-infected rhesus macaque model of HIV. We found that subsets of follicular SIV-specific CD8+T cells are able to migrate throughout the follicle, are likely inhibited by Foxp3+cells, and are likely exhausted but that, nonetheless, subsets are likely functional, as they express markers consistent with effector function and show signs of suppressing viral replicationin vivo. These findings support HIV cure strategies that increase the frequency of functional follicular virus-specific CD8+T cells.

18

Wallin, Elizabeth F., Elaine C. Jolly, Ondřej Suchánek, J. Andrew Bradley, Marion Espéli, David R. W. Jayne, Michelle A. Linterman, and Kenneth G. C. Smith. "Human T-follicular helper and T-follicular regulatory cell maintenance is independent of germinal centers." Blood 124, no. 17 (October 23, 2014): 2666–74. http://dx.doi.org/10.1182/blood-2014-07-585976.

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19

de Matos Kasahara, Taissa, Cleonice Alves de Melo Bento, and Sudhir Gupta. "Alterations In Circulating Follicular Helper T Cells (cTFH) and Follicular Regulatory T Cells (cTFR) In CVID Patients." Journal of Allergy and Clinical Immunology 143, no. 2 (February 2019): AB118. http://dx.doi.org/10.1016/j.jaci.2018.12.358.

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20

Qian, Jiang, Qinhua Yu, Guoqing Chen, Mingxia Wang, Zhao Zhao, Yueyue Zhang, and Liannv Qiu. "Altered ratio of circulating follicular regulatory T cells and follicular helper T cells during primary EBV infection." Clinical and Experimental Medicine 20, no. 3 (March 23, 2020): 373–80. http://dx.doi.org/10.1007/s10238-020-00621-8.

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21

Chen, Qiang, and Alexander L. Dent. "Nonbinary Roles for T Follicular Helper Cells and T Follicular Regulatory Cells in the Germinal Center Response." Journal of Immunology 211, no. 1 (July 1, 2023): 15–22. http://dx.doi.org/10.4049/jimmunol.2200953.

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Abstract Development of high-affinity Abs in the germinal center (GC) is dependent on a specialized subset of T cells called “T follicular helper” (TFH) cells that help select Ag-specific B cells. A second T cell subset, T follicular regulatory (TFR) cells, can act as repressors of the GC and Ab response but can also provide a helper function for GC B cells in some contexts. Recent studies showed that, apart from their traditional helper role, TFH cells can also act as repressors of the Ab response, particularly for IgE responses. We review how both TFH and TFR cells express helper and repressor factors that coordinately regulate the Ab response and how the line between these two subsets is less clear than initially thought. Thus, TFH and TFR cells are interconnected and have “nonbinary” functions. However, many questions remain about how these critical cells control the Ab response.

22

Kerfoot, Steven, Gur Yaari, Jaymin Patel, Kody Johnson, David Gonzalez, Steven Kleinstein, and Ann Haberman. "Inter-follicular germinal center B cell and T follicular helper cell development precedes follicular Tfh maintenance (63.23)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 63.23. http://dx.doi.org/10.4049/jimmunol.186.supp.63.23.

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Abstract We identify the interfollicular (IF) zone of the lymph node as the site where germinal center B cell and T follicular helper (Tfh) cell differentiation initiates. For the first two days post-immunization, antigen-specific T and B cells remained confined within the IF zone, where they participated in long-lived interactions and upregulated Bcl-6, which controls the differentiation of both cell types. During this time, T cells also acquired the Tfh markers CXCR5, PD-1 and GL7. While T cell immigration into the follicle interior occurred three days post immunization, responding B cells remained largely restricted to the IF zone and the area adjacent to the sub capsular sinus at this timepoint. B cell entry into the follicle interior, and formation of nascent germinal centers, did not occur until a day later. Notably, in the absence of cognate B cells, PD-1hi Tfh cells still formed and migrated to the follicle. However, without such B cells, PD-1, ICOS and GL7 expression was not maintained on T cells that nevertheless persisted within the follicle. Thus, cognate B cells are not required for Tfh cell differentiation in the IF zone, but are instead required for the long-term maintenance of the activated Tfh phenotype.

23

Yang, Zhi-Zhang, Xinyi Tang, Hyo Jin Kim, Prithviraj Mukherjee, Vaishali Bhardwaj, Patrizia Mondello, and Stephen Ansell. "Characterization and clinical significance of T follicular helper cells in follicular lymphoma." Journal of Immunology 210, no. 1_Supplement (May 1, 2023): 88.04. http://dx.doi.org/10.4049/jimmunol.210.supp.88.04.

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Abstract T follicular helper (T FH) cells are a subset of CD4 +T cells that reside within the follicles of secondary lymphoid organs and play an essential role in the germinal center (GC) reaction. To examine the role T FHcells in follicular lymphoma (FL), we first characterized T FHcells using single cell analysis with the high-throughput technologies of mass cytometry (CyTOF) and the Indexing of Transcriptomes and Epitopes by Sequencing (CITE-seq). Clustering analysis revealed that T FHcells form subsets with unique phenotypes, and the expression of many common markers including CXCR5, ICOS, IL-21, TOX2, CD57, GZMK, XCL1, XCL2, CXCL13 and CD40L varies on T FHsubsets. We found that T FHcells are phenotypically more heterogenous in FL than benign tonsil tissues by both proteomic (n=82) and transcriptomic (n=8) profiling. Each FL patient showed different dominant T FHsubsets, in contrast to tonsil donors which were highly homogenous. Some T FHsubsets were only present in FL and absent in tonsil tissues, suggesting the existence of FL-specific T FHcells. Cytokines (IL-2, IL12, IL-17 and IL-21) and activated B cells upregulated T FHmarkers including PD-1, CXCR5 and IL-21 to induce the development of T FHsubsets such as IL-21 +or IL-21 +IFN-g +T FHcells, which was inhibited by rapamycin, an immunosuppressor. We observed that the T FHcell frequency significantly correlated with the number of lymphoma B cells. Futhermore, while T FHcells as a whole showed no correlation with prognosis, T FHsubsets such as CD57 +T FHcells were significantly associated with an inferior patient outcome. Taken together, our results indicate that T FHcells are highly heterogenous with different tumor-specific T FHsubsets present in FL and associated with patient outcomes in FL.

24

Hetta, Helal F., Azza Elkady, Ramadan Yahia, Ahmed Kh Meshall, Mahmoud M. Saad, Mohamed A. Mekky, and Israa M. S. Al-Kadmy. "T follicular helper and T follicular regulatory cells in colorectal cancer: A complex interplay." Journal of Immunological Methods 480 (May 2020): 112753. http://dx.doi.org/10.1016/j.jim.2020.112753.

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25

Akama-Garren, Elliot H., Theo van den Broek, Lea Simoni, Carlos Castrillon, Cees van der Poel, and Michael C. Carroll. "Follicular T cells are clonally and transcriptionally distinct in B cell-driven autoimmune disease." Journal of Immunology 206, no. 1_Supplement (May 1, 2021): 61.15. http://dx.doi.org/10.4049/jimmunol.206.supp.61.15.

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Abstract Pathogenic autoantibodies contribute to tissue damage and clinical decline in autoimmune disease. Follicular T cells are central regulators of germinal centers, although their role in epitope spreading towards autoantigens remains unclear. We performed single cell RNA and T cell receptor (TCR) sequencing of follicular T cells in autoantibody-mediated disease, allowing for analyses of paired transcriptomes and unbiased TCRab repertoires at single cell resolution. A minority of clonotypes were preferentially shared amongst autoimmune follicular T cells, and clonotypic expansion was associated with differential gene signatures in autoimmune disease. Antigen prediction using algorithmic and machine learning approaches revealed convergence towards shared specificities between non-autoimmune and autoimmune follicular T cells. However, differential autoimmune transcriptional signatures were preserved even amongst follicular T cells with shared predicted specificities. These results demonstrate that follicular T cells are phenotypically distinct in B cell-driven autoimmune disease, providing potential therapeutic targets to modulate autoreactive epitope spreading. Supported by grants from NIH (R01AI130307, R01AR074105, T32GM007753).

26

Ochando, Jordi, and Mounia S. Braza. "T follicular helper cells: a potential therapeutic target in follicular lymphoma." Oncotarget 8, no. 67 (November 30, 2017): 112116–31. http://dx.doi.org/10.18632/oncotarget.22788.

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27

Salvatore, Bradley, Rachel Resop, Brent Gordon, Marta Epeldegui, Otoniel Martinez-Maza, Begoña Comin-Anduix, Alex Lam, Ting-Ting Wu, and Christel Uittenbogaart. "Characterization of T Follicular Helper Cells and T Follicular Regulatory Cells in HIV-Infected and Sero-Negative Individuals." Cells 12, no. 2 (January 12, 2023): 296. http://dx.doi.org/10.3390/cells12020296.

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Humoral immune response is important in fighting pathogens by the production of specific antibodies by B cells. In germinal centers, T follicular helper (TFH) cells provide important help to B-cell antibody production but also contribute to HIV persistence. T follicular regulatory (TFR) cells, which inhibit the function of TFH cells, express similar surface markers. Since FOXP3 is the only marker that distinguishes TFR from TFH cells it is unknown whether the increase in TFH cells observed in HIV infection and HIV persistence may be partly due to an increase in TFR cells. Using multicolor flow cytometry to detect TFH and TFR cells in cryopreserved peripheral blood mononuclear cells from HIV-infected and non-infected participants in the UCLA Multicenter AIDS Cohort Study (MACS), we identified CD3+CXCR5+CD4+CD8−BCL6+ peripheral blood TFH (pTFH) cells and CD3+CXCR5+CD4+CD8−FOXP3+ peripheral blood TFR (pTFR) cells. Unlike TFR cells in germinal centers, pTFR cells do not express B cell lymphoma 6 (BCL6), a TFH cell master transcriptional regulator. Our major findings are that the frequency of pTFH cells, but not pTFR cells was higher in HIV-infected participants of the MACS and that pTFH cells expressed less CCR5 in HIV-infected MACS participants. Constitutive expression of CCR5 in TFR cells supports their potential to contribute to HIV persistence.

28

Rolf, Julia, Kirsten Fairfax, and Martin Turner. "Signaling Pathways in T Follicular Helper Cells." Journal of Immunology 184, no. 12 (June 3, 2010): 6563–68. http://dx.doi.org/10.4049/jimmunol.1000202.

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29

Crotty, Shane. "Revealing T follicular helper cells with BCL6." Nature Reviews Immunology 21, no. 10 (September 27, 2021): 616–17. http://dx.doi.org/10.1038/s41577-021-00591-2.

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30

Ichimiya, Shingo, Ryuta Kamekura, Koji Kawata, Motonari Kamei, and Tetsuo Himi. "Functional RNAs control T follicular helper cells." Journal of Human Genetics 62, no. 1 (August 4, 2016): 81–86. http://dx.doi.org/10.1038/jhg.2016.88.

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31

Spolski, R., and W. J. Leonard. "IL-21 and T follicular helper cells." International Immunology 22, no. 1 (November 23, 2009): 7–12. http://dx.doi.org/10.1093/intimm/dxp112.

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32

Papp, Gábor, Krisztina Szabó, Zoltán Szekanecz, and Margit Zeher. "Follicular helper T cells in autoimmune diseases." Rheumatology 53, no. 7 (January 8, 2014): 1159–60. http://dx.doi.org/10.1093/rheumatology/ket434.

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33

Yang, Xi. "Follicular helper T cells in immune homeostasis." Cellular & Molecular Immunology 9, no. 5 (September 2012): 367–68. http://dx.doi.org/10.1038/cmi.2012.27.

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34

Cubas, Rafael, and Matthieu Perreau. "The dysfunction of T follicular helper cells." Current Opinion in HIV and AIDS 9, no. 5 (September 2014): 485–91. http://dx.doi.org/10.1097/coh.0000000000000095.

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35

Ueno, Hideki. "T follicular helper cells in human autoimmunity." Current Opinion in Immunology 43 (December 2016): 24–31. http://dx.doi.org/10.1016/j.coi.2016.08.003.

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36

Fazilleau, Nicolas, Linda Mark, Louise J. McHeyzer-Williams, and Michael G. McHeyzer-Williams. "Follicular Helper T Cells: Lineage and Location." Immunity 30, no. 3 (March 2009): 324–35. http://dx.doi.org/10.1016/j.immuni.2009.03.003.

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37

Vinuesa, Carola G., and Matthew C. Cook. "Blood Relatives of Follicular Helper T Cells." Immunity 34, no. 1 (January 2011): 10–12. http://dx.doi.org/10.1016/j.immuni.2011.01.006.

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38

Vinuesa, Carola G., Sidonia Fagarasan, and Chen Dong. "New Territory for T Follicular Helper Cells." Immunity 39, no. 3 (September 2013): 417–20. http://dx.doi.org/10.1016/j.immuni.2013.09.001.

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39

Hawkes, Jason E., and Ryan M. O’Connell. "MicroRNAs, T follicular helper cells and inflammaging." Oncotarget 6, no. 32 (October 7, 2015): 32295–96. http://dx.doi.org/10.18632/oncotarget.6025.

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40

Jiménez‐Saiz, Rodrigo, Kelly Bruton, and Manel Jordana. "Follicular T cells: From stability to failure." Allergy 75, no. 4 (February 5, 2020): 1006–7. http://dx.doi.org/10.1111/all.14167.

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41

Qi, Hai. "T follicular helper cells in space-time." Nature Reviews Immunology 16, no. 10 (August 30, 2016): 612–25. http://dx.doi.org/10.1038/nri.2016.94.

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42

Wei, Xindi, and Xiaoyin Niu. "T follicular helper cells in autoimmune diseases." Journal of Autoimmunity 134 (January 2023): 102976. http://dx.doi.org/10.1016/j.jaut.2022.102976.

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43

Yu, Meixing, Vanesssa Cavero, Qiao Lu, and Hong Li. "Follicular helper T cells in rheumatoid arthritis." Clinical Rheumatology 34, no. 9 (July 31, 2015): 1489–93. http://dx.doi.org/10.1007/s10067-015-3028-5.

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44

Oja, Anna E., Giso Brasser, Edith Slot, René A. W. van Lier, María F. Pascutti, and Martijn A. Nolte. "GITR shapes humoral immunity by controlling the balance between follicular T helper cells and regulatory T follicular cells." Immunology Letters 222 (June 2020): 73–79. http://dx.doi.org/10.1016/j.imlet.2020.03.008.

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45

Wu, Hao, Yuxin Chen, Hong Liu, Lin-Lin Xu, Paula Teuscher, Shixia Wang, Shan Lu, and Alexander L. Dent. "Follicular regulatory T cells repress cytokine production by follicular helper T cells and optimize IgG responses in mice." European Journal of Immunology 46, no. 5 (March 11, 2016): 1152–61. http://dx.doi.org/10.1002/eji.201546094.

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46

Ballesteros‐Tato, André, and Troy D. Randall. "Priming of T follicular helper cells by dendritic cells." Immunology & Cell Biology 92, no. 1 (October 22, 2013): 22–27. http://dx.doi.org/10.1038/icb.2013.62.

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47

Hasnain, Mujtaba Ali, Samrah Mujtaba, Iqra Javed, Misbah ., Muhammad Shahzad Gul, and Abdul Ghaffar. "Determine the Effect of Immunosuppressant on follicular regulatory T-cells in kidney transplant patients." Pakistan Journal of Medical and Health Sciences 15, no. 10 (October 30, 2021): 2689–91. http://dx.doi.org/10.53350/pjmhs2115102689.

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Abstract:

Background: Over the last few years, there are two major problems identified during organ transplantation such as surgical restrictions and transplant rejections. Few of these obstacles have been partially removed such as the use of immunosuppressant improved it consistently while decreasing graft rejection up to 12.2%. Methods: This study was conducted from 2019-2021. In all patients renal function was examined through glomerular filtration rate. Induction therapy was given to all the transplant recipients. Induction therapy with basiliximab 20mg intravenously on 0 and 4 days. After transplantation tacrolimus and MMF was given with varied concentration dose. Acute rejections were found in patients who had no biopsy or biopsy-proven rejection. In the end, clinical pathologists had analyzed all biopsies again and recipients who were experienced the vascular Banff grade 2 and tubule interstitial rejection. Results: Immunosuppressant tacrolimus treated patients were 71(67.61%) and mycophenolate mofetil used in 34(32.38%). Total 39(37.14%) rejections were received and 66(62.85%) acceptance was recorded. Two types of rejection were highlighted namely cell-mediated rejection 25(23.80%) and 14(13.33%) chronic antibody-mediated rejection. The effect of tacrolimus on follicular helper T cells and follicular regulatory T cells shows the clear difference between the kidney transplant and healthy control cells. Reduction in numbers of follicular regulatory T cells was measured in patients. Conclusion: eventually we find tacrolimus significantly affects the number of follicular regulatory T-cells and follicular helper T cells. Alemtuzumab substantially lowers the follicular regulatory T-cells. Mycophenolate mofetil showed non-significant on T-cells. Keywords: kidney transplant, follicular regulatory T-cells, follicular helper T-cells.

48

Shen, Erxia, Qin Wang, Hardis Rabe, Wenquan Liu, Harvey Cantor, and Jianmei W. Leavenworth. "Chromatin remodeling by the NuRD complex regulates development of follicular helper and regulatory T cells." Proceedings of the National Academy of Sciences 115, no. 26 (June 11, 2018): 6780–85. http://dx.doi.org/10.1073/pnas.1805239115.

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Abstract:

Lineage commitment and differentiation into CD4+T cell subsets reflect an interplay between chromatin regulators and transcription factors (TF). Follicular T cell development is regulated by the Bcl6 TF, which helps determine the phenotype and follicular localization of both CD4+follicular helper T cells (TFH) and follicular regulatory T cells (TFR). Here we show that Bcl6-dependent control of follicular T cells is mediated by a complex formed between Bcl6 and the Mi-2β-nucleosome-remodeling deacetylase complex (Mi-2β-NuRD). Formation of this complex reflects the contribution of the intracellular isoform of osteopontin (OPN-i), which acts as a scaffold to stabilize binding between Bcl6 and the NuRD complex that together regulate the genetic program of both TFHand TFRcells. Defective assembly of the Bcl6–NuRD complex distorts follicular T cell differentiation, resulting in impaired TFRdevelopment and skewing of the TFHlineage toward a TH1-like program that includes expression of Blimp1, Tbet, granzyme B, and IFNγ. These findings define a core Bcl6-directed transcriptional complex that enables CD4+follicular T cells to regulate the germinal center response.

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Vaeth, Martin, Gerd Müller, Dennis Stauss, Lena Dietz, Stefan Klein-Hessling, Edgar Serfling, Martin Lipp, Ingolf Berberich, and Friederike Berberich-Siebelt. "Follicular regulatory T cells control humoral autoimmunity via NFAT2-regulated CXCR5 expression." Journal of Experimental Medicine 211, no. 3 (March 3, 2014): 545–61. http://dx.doi.org/10.1084/jem.20130604.

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Abstract:

Maturation of high-affinity B lymphocytes is precisely controlled during the germinal center reaction. This is dependent on CD4+CXCR5+ follicular helper T cells (TFH) and inhibited by CD4+CXCR5+Foxp3+ follicular regulatory T cells (TFR). Because NFAT2 was found to be highly expressed and activated in follicular T cells, we addressed its function herein. Unexpectedly, ablation of NFAT2 in T cells caused an augmented GC reaction upon immunization. Consistently, however, TFR cells were clearly reduced in the follicular T cell population due to impaired homing to B cell follicles. This was TFR-intrinsic because only in these cells NFAT2 was essential to up-regulate CXCR5. The physiological relevance for humoral (auto-)immunity was corroborated by exacerbated lupuslike disease in the presence of NFAT2-deficient TFR cells.

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Xie, Markus Ming, Hong Liu, and Alexander Dent. "Follicular Regulatory T cells Positively Regulate Follicular Helper T Cells, Germinal Center B Cells and IgE Response in Peanut Allergic Mice." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 107.2. http://dx.doi.org/10.4049/jimmunol.200.supp.107.2.

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Abstract:

Abstract Food allergy remains a major health problem in developed countries such as United States. However, the immunological mechanisms that control peanut allergy are largely unknown. In an oral sensitization food allergy model using peanut protein and cholera toxin (PCT), we found mice (Bcl6FC: FOXP3cre Bcl6 fl/fl) deficient in follicular T regulatory (Tfr) cells had lower follicular helper T (Tfh) cells and germinal center B (GCB) cells after two challenges. The decrease in Tfh/GCB cells was seen in both mesenteric Lymph Node and spleen responses. In this two-challenge model, peanut specific IgE, IgG1 and IgA antibody (Ab) responses were sharply decreased in Bcl6FC mice compared with wild type (WT) ones. However, after eight PCT challenges, Tfh and GCB cells were similar in Bcl6FC mice compared with WT, and peanut specific IgE was elevated in the absence of Tfr cells. We also show that Tfh/GCB cells are required for IgE production in this food allergy model. In mice with Blimp1-deficiency in T regulatory (Treg) cells (Blimp1FC: FOXP3cre Blimp1 fl/fl), Tfr, Tfh and GCB cells were significantly higher compared with WT or Bcl6FC mice while Treg derived IL-10 was much lower. Peanut specific Ab responses trended lower in Blimp1FC mice after two PCT challenges. Our data presented here is the novel evidence showing a positive regulation of Tfh/GCB cells and IgE response by Tfr cells, and suggest that a key regulatory pathway of Tfh/GCB cells and IgE response involves IL-10 production by Tfr cells. Supported by The AAI Careers in Immunology Fellowship Program.