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Journal articles on the topic 'T-dependent'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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1

Andersen, Mads Hald. "T-cell dependent immunoselection." OncoImmunology 1, no. 7 (October 2012): 1003. http://dx.doi.org/10.4161/onci.20927.

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2

Khanolkar, Aaruni, Michael J. Fuller, and Allan J. Zajac. "CD4 T Cell-Dependent CD8 T Cell Maturation." Journal of Immunology 172, no. 5 (February 20, 2004): 2834–44. http://dx.doi.org/10.4049/jimmunol.172.5.2834.

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3

Burattini, Laura, Wojciech Zareba, and Roberto Burattini. "Is T-wave alternans T-wave amplitude dependent?" Biomedical Signal Processing and Control 7, no. 4 (July 2012): 358–64. http://dx.doi.org/10.1016/j.bspc.2011.06.009.

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4

BOHM, ADAM, ARNOLD PINTER, and ISTVAN PREDA. "QT Dependent T Wave Sensing." Pacing and Clinical Electrophysiology 21, no. 7 (July 1998): 1490–91. http://dx.doi.org/10.1111/j.1540-8159.1998.tb00226.x.

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5

Maruyama, Toru. "Rate-Dependent Repolarization Dynamics: Correlation between Electrocardiographic T Wave and U Wave." Rate-Dependent Repolarization Dynamics: Correlation between Electrocardiographic T Wave and U Wave 01, no. 01 (April 6, 2018): 1–5. http://dx.doi.org/10.31546/jcccvt.1007.

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6

El Shikh, Mohey Eldin M., Rania M. El Sayed, Andras K. Szakal, and John G. Tew. "T-Independent Antibody Responses to T-Dependent Antigens: A Novel Follicular Dendritic Cell-Dependent Activity." Journal of Immunology 182, no. 6 (March 5, 2009): 3482–91. http://dx.doi.org/10.4049/jimmunol.0802317.

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7

Yuntao Wu, Margaret H. Beddall, and Jon W. Marsh. "Rev-Dependent Indicator T Cell Line." Current HIV Research 5, no. 4 (July 1, 2007): 394–402. http://dx.doi.org/10.2174/157016207781024018.

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8

Jeurissen, Axel, and Xavier Bossuyt. "T Cell-Dependent and -Independent Responses." Journal of Immunology 172, no. 5 (February 20, 2004): 2728. http://dx.doi.org/10.4049/jimmunol.172.5.2728.

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9

Ketland, J. "Conservativeness and translation-dependent T-schemes." Analysis 60, no. 4 (October 1, 2000): 319–28. http://dx.doi.org/10.1093/analys/60.4.319.

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10

Cascalho, M., and JL Platt. "B cell-dependent T cell development." Acta Paediatrica 93 (January 2, 2007): 52–53. http://dx.doi.org/10.1111/j.1651-2227.2004.tb03057.x.

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11

Tsuji, Ryohei F., Marian Szczepanik, Ivana Kawikova, Vipin Paliwal, Regis A. Campos, Atsuko Itakura, Moe Akahira-Azuma, Nicole Baumgarth, Leonore A. Herzenberg, and Philip W. Askenase. "B Cell–dependent T Cell Responses." Journal of Experimental Medicine 196, no. 10 (November 11, 2002): 1277–90. http://dx.doi.org/10.1084/jem.20020649.

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Contact sensitivity (CS) is a classic example of in vivo T cell immunity in which skin sensitization with reactive hapten leads to immunized T cells, which are then recruited locally to mediate antigen-specific inflammation after subsequent skin challenge. We have previously shown that T cell recruitment in CS is triggered by local activation of complement, which generates C5a that triggers C5a receptors most likely on mast cells. Here, we show that B-1 cell–derived antihapten IgM antibodies generated within 1 day (d) of immunization combine with local challenge antigen to activate complement to recruit the T cells. These findings overturn three widely accepted immune response paradigms by showing that (a) specific IgM antibodies are required to initiate CS, which is a classical model of T cell immunity thought exclusively due to T cells, (b) CS priming induces production of specific IgM antibodies within 1 d, although primary antibody responses typically begin by day 4, and (c) B-1 cells produce the 1-d IgM response to CS priming, although these cells generally are thought to be nonresponsive to antigenic stimulation. Coupled with previous evidence, our findings indicate that the elicitation of CS is initiated by rapidly formed IgM antibodies. The IgM and challenge antigen likely form local complexes that activate complement, generating C5a, leading to local vascular activation to recruit the antigen-primed effector T cells that mediate the CS response.
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12

Hron, Jonathan D., Liron Caplan, Andrea J. Gerth, Pamela L. Schwartzberg, and Stanford L. Peng. "SH2D1A Regulates T-dependent Humoral Autoimmunity." Journal of Experimental Medicine 200, no. 2 (July 19, 2004): 261–66. http://dx.doi.org/10.1084/jem.20040526.

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The signaling lymphocytic activation molecule (SLAM)/CD150 family includes a family of chromosome 1–encoded cell surface molecules with costimulatory functions mediated in part by the adaptor protein SH2D1A (SLAM-associated protein, SAP). Deficiency in SH2D1A protects mice from an experimental model of lupus, including the development of hypergammaglobulinemia, autoantibodies including anti–double stranded DNA, and renal disease. This protection did not reflect grossly defective T or B cell function per se because SH2D1A-deficient mice were susceptible to experimental autoimmune encephalomyelitis, a T cell–dependent disease, and they were capable of mounting normal T-independent antigen-specific immunoglobulin responses. Instead, T-dependent antibody responses were impaired in SH2D1A-deficient mice, reflecting defective germinal center formation. These findings demonstrate a specific role for the SLAM–SH2D1A system in the regulation of T-dependent humoral immune responses, implicating members of the CD150–SH2D1A family as targets in the pathogenesis and therapy of antibody-mediated autoimmune and allergic diseases.
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13

Parker, D. C. "T Cell-Dependent B Cell Activation." Annual Review of Immunology 11, no. 1 (April 1993): 331–60. http://dx.doi.org/10.1146/annurev.iy.11.040193.001555.

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14

Quintana, Ariel, D�sir�e Griesemer, Eva C. Schwarz, and Markus Hoth. "Calcium-dependent activation of T-lymphocytes." Pfl�gers Archiv - European Journal of Physiology 450, no. 1 (November 26, 2004): 1–12. http://dx.doi.org/10.1007/s00424-004-1364-4.

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15

Bollinger, T., A. Bollinger, L. Skrum, S. Dimitrov, T. Lange, and W. Solbach. "Sleep-dependent activity of T cells and regulatory T cells." Clinical & Experimental Immunology 155, no. 2 (February 2009): 231–38. http://dx.doi.org/10.1111/j.1365-2249.2008.03822.x.

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16

Basten, Antony, and Barbara Fazekas de St Groth. "Special regulatory T-cell review: T-cell dependent suppression revisited." Immunology 123, no. 1 (January 2008): 33–39. http://dx.doi.org/10.1111/j.1365-2567.2007.02772.x.

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17

Wernimont, Sarah A., Andrew J. Wiemer, David A. Bennin, Susan J. Monkley, Thomas Ludwig, David R. Critchley, and Anna Huttenlocher. "Contact-Dependent T Cell Activation and T Cell Stopping Require Talin1." Journal of Immunology 187, no. 12 (November 9, 2011): 6256–67. http://dx.doi.org/10.4049/jimmunol.1102028.

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18

Salinas, Gabriela Franco, Leen De Rycke, Tineke Cantaert, Philip Remans, Mirjam van der Burg, Barbara Barendregt, Paul P. Tak, and Dominique Baeten. "T.21. TNF Alpha Blockade Impairs T Cell Dependent Antibody Responses." Clinical Immunology 131 (2009): S57. http://dx.doi.org/10.1016/j.clim.2009.03.162.

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19

Shinohara, M. L., M. Jansson, E. S. Hwang, M. B. F. Werneck, L. H. Glimcher, and H. Cantor. "T-bet-dependent expression of osteopontin contributes to T cell polarization." Proceedings of the National Academy of Sciences 102, no. 47 (November 14, 2005): 17101–6. http://dx.doi.org/10.1073/pnas.0508666102.

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20

Kern, J. A., J. C. Reed, R. P. Daniele, and P. C. Nowell. "The role of the accessory cell in mitogen-stimulated human T cell gene expression." Journal of Immunology 137, no. 3 (August 1, 1986): 764–69. http://dx.doi.org/10.4049/jimmunol.137.3.764.

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Abstract The role of the accessory cell in optimizing T cell proliferative responses to mitogens is a well known but poorly understood phenomenon. To further dissect the function of the accessory cell in allowing T cell proliferation, we compared mitogen-induced c-myc, interleukin 2 (IL 2), and IL 2 receptor gene expression in peripheral blood mononuclear cells (PBMC) and in T cells rigorously depleted of accessory cells through differential adherence and anti-Dr (anti-class II major histocompatibility antigen) monoclonal antibody complement-directed cytotoxicity. In cultures stimulated with phytohemagglutinin (PHA), a mitogen that requires accessory cells to induce T cell proliferation, expression of all measured genes was accessory cell dependent, since accumulation of their mRNA in PBMC was greater than that in cultures depleted of accessory cells. These genes varied in their accessory cell dependence, with IL 2 expression most dependent, c-myc expression least dependent, and IL 2 receptor expression intermediate in dependency. Use of 12-O-tetradecanoyl-phorbol-13-acetate (TPA) or ionomycin, mitogens that stimulate T cell proliferation independent of accessory cells, induced equal levels of gene expression in PBMC and in T cells depleted of accessory cells. These results suggest that PHA-stimulated T cells are dependent on an accessory cell signal(s) for optimal expression of the genes for c-myc, IL 2, and IL 2 receptor, and for proliferation. In addition, this signal(s) appears to be delivered early in the course of T cell activation events, since it can be bypassed by mitogens that directly activate protein kinase C (TPA) or induce calcium translocation (ionomycin). In addition, these data provide further evidence that expression of the c-myc protooncogene is insufficient for T cell mitogenesis, since PHA-induced accumulation of c-myc mRNA was only partially accessory cell dependent, whereas proliferation was completely accessory-cell dependent.
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21

ZAKHAROV, B. G. "JET QUENCHING WITH T -DEPENDENT RUNNING COUPLING." ПИСЬМА В ЖУРНАЛ ЭКСПЕРИМЕНТАЛЬНОЙ И ТЕОРЕТИЧЕСКОЙ ФИЗИКИ 112, no. 11-12(12) (2020): 723–24. http://dx.doi.org/10.31857/s1234567820230019.

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22

Martinez, Fanny, Julien Novarino, José Enrique Mejía, Nicolas Fazilleau, and Meryem Aloulou. "Ageing of T-dependent B cell responses." Immunology Letters 233 (May 2021): 97–103. http://dx.doi.org/10.1016/j.imlet.2021.03.012.

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23

Shelah, Saharon. "Dependent $T$ and existence of limit models." Tbilisi Mathematical Journal 7, no. 1 (2014): 99–128. http://dx.doi.org/10.2478/tmj-2014-0010.

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24

Stiegler, Peter, Stefan Schüchner, Valia Lestou, and Erhard Wintersberger. "Polyomavirus large T antigen-dependent DNA amplification." Oncogene 14, no. 8 (February 1997): 987–95. http://dx.doi.org/10.1038/sj.onc.1200904.

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25

Huang, Y., and J. K. Burkhardt. "T-cell-receptor-dependent actin regulatory mechanisms." Journal of Cell Science 120, no. 5 (March 1, 2007): 723–30. http://dx.doi.org/10.1242/jcs.000786.

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26

Bach, Jean-François, and Hôpital Necker. "T cells and insulin-dependent diabetes mellitus." Current Opinion in Endocrinology and Diabetes 2, no. 1 (February 1995): 12–16. http://dx.doi.org/10.1097/00060793-199502000-00003.

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27

Noelle, Randolph J., and E. Charles Snow. "T helper cell‐dependent B cell activation." FASEB Journal 5, no. 13 (October 1991): 2770–76. http://dx.doi.org/10.1096/fasebj.5.13.1833257.

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28

Rock, Michael T., William H. Brooks, and Thomas L. Roszman. "Calcium-dependent Signaling Pathways in T Cells." Journal of Biological Chemistry 272, no. 52 (December 26, 1997): 33377–83. http://dx.doi.org/10.1074/jbc.272.52.33377.

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29

Thiel, Andreas, Marco Frentsch, Joanna Listopad, Regina Stark, Alberto Sada Japp, Nadine Matzmohr, Sarah Meier, Ichiro Taniuchi, and Thomas Blankenstein. "CD40L+ CD8+ T-Cell Dependent Antitumor Immunity." Blood 124, no. 21 (December 6, 2014): 5818. http://dx.doi.org/10.1182/blood.v124.21.5818.5818.

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Abstract CD40 is frequently expressed on malignant cells of different origin. Due to the observed antitumorigenic effects induced after CD40 engagement it represents an attractive target for immunotherapies. We demonstrate here that CD40L expressing tumor-specific CD8+ T-cell population can act as potent physiological CD40 agonist against CD40 expressing tumor cells. We demonstrate that in the course of cancer cell rejection high frequencies of tumor-specific CD40L+ CD8+ T cells are induced. Strikingly, in contrast to wild-type (wt), CD40L deficient CD8+ T cells were unable to prevent tumor formation in lymphopenic as well as in fully immunocompetent hosts. Apparently, in our setting CD40L expressed by CD8+ T cells is essential for cancer cell rejection. CD40L-mediated rejection does not depend on interaction with CD40+ host cells such as antigen-presenting cells but on CD40 expression by cancer cells. Our findings disclose CD40L expression by CD8+ T cells as a new antitumor effector function that should be implemented in future adoptive T-cell therapies against cancer. Disclosures No relevant conflicts of interest to declare.
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30

Wirth, Jens. "On t-dependent hyperbolic systems. Part 2." Journal of Mathematical Analysis and Applications 448, no. 1 (April 2017): 293–318. http://dx.doi.org/10.1016/j.jmaa.2016.11.026.

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31

Panayi, G. S. "T-cell-dependent pathways in rheumatoid arthritis." Current Opinion in Rheumatology 9, no. 3 (May 1997): 236–40. http://dx.doi.org/10.1097/00002281-199705000-00010.

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32

Mills, Kingston H. G. "TLR-dependent T cell activation in autoimmunity." Nature Reviews Immunology 11, no. 12 (November 18, 2011): 807–22. http://dx.doi.org/10.1038/nri3095.

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33

DeCoursey, T. E., K. G. Chandy, S. Gupta, and M. D. Cahalan. "Voltage-dependent ion channels in T-lymphocytes." Journal of Neuroimmunology 10, no. 1 (November 1985): 71–95. http://dx.doi.org/10.1016/0165-5728(85)90035-9.

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34

Casetta, Leonardo. "Nonclassical t-Dependent Energy Integral of q″+aq′+b(t)q+c(t)qn=0." Zeitschrift für Naturforschung A 72, no. 10 (September 26, 2017): 973–76. http://dx.doi.org/10.1515/zna-2017-0153.

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AbstractIn the present note, we address the general nonlinear oscillator of the form q″+aq′+b(t)q+c(t)qn=0, where q as well as the coefficients b(t) and c(t) are complex or real-valued functions of the real variable t; a is a real constant, and n is a real number. By starting with a certain Hamiltonian function, we discuss conditions on the functions b(t) and c(t) for which such differential equation becomes able to admit a nonclassical energy integral – i.e. a t-dependent energy integral. A method to inversely elicit the corresponding conservative solutions of this differential equation is consequently established, and two examples addressing periodic conservative solutions are shown.
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35

Philipp, Stephan, Bettina Strauss, Daniela Hirnet, Ulrich Wissenbach, Laurence Méry, Veit Flockerzi, and Markus Hoth. "TRPC3 Mediates T-cell Receptor-dependent Calcium Entry in Human T-lymphocytes." Journal of Biological Chemistry 278, no. 29 (May 6, 2003): 26629–38. http://dx.doi.org/10.1074/jbc.m304044200.

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36

Cobb, Dustin, Siqi Guo, Ana M. Lara, Patricio Manque, Gregory Buck, and Ronald B. Smeltz. "T-bet-dependent regulation of CD8+T-cell expansion during experimentalTrypanosoma cruziinfection." Immunology 128, no. 4 (December 2009): 589–99. http://dx.doi.org/10.1111/j.1365-2567.2009.03169.x.

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37

Pietrobon, Patricia J. Freda, Nathalie Garcon, Chung H. Lee, and Howard R. Six. "Liposomes That Provide T-Dependent Help to Weak Antigens (T-Independent Antigens)." ImmunoMethods 4, no. 3 (June 1994): 236–43. http://dx.doi.org/10.1006/immu.1994.1026.

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38

Soderberg, Lee S. F., and John B. Barnett. "Inhaled isobutyl nitrite compromises T-dependent, but not T-independent, antibody induction." International Journal of Immunopharmacology 15, no. 7 (October 1993): 821–27. http://dx.doi.org/10.1016/0192-0561(93)90019-u.

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39

Shikh, Mohey Eldin El, Rania El Sayed, Andras K. Szakal, and John G. Tew. "Conversion of T‐dependent (TD) antigens to T‐independent (TI) antigens: A novel follicular dendritic cell (FDC)‐dependent activity." FASEB Journal 22, S2 (April 2008): 379. http://dx.doi.org/10.1096/fasebj.22.2_supplement.379.

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40

Lu, H. K., R. J. Fern, J. J. Nee, and P. Q. Barrett. "Ca(2+)-dependent activation of T-type Ca2+ channels by calmodulin-dependent protein kinase II." American Journal of Physiology-Renal Physiology 267, no. 1 (July 1, 1994): F183—F189. http://dx.doi.org/10.1152/ajprenal.1994.267.1.f183.

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The T-type Ca2+ channel is unique among voltage-dependent Ca2+ channels in its low threshold for opening and its slow kinetics of deactivation. Here, we evaluate the importance of intracellular Ca2+ (Cai2+) in promoting low-threshold gating of T-type channels in adrenal glomerulosa cells. We observe that 390 nM to 1.27 microM Cai2+ enhances T-type current by shifting the voltage dependence of channel activation to more negative potentials. This Ca(2+)-induced shift is mediated by calmodulin-dependent protein kinase II (CaMKII), because it is abolished by inhibitors of CaMKII but not of protein kinase C and is subsequently restored by exogenous calmodulin. This Ca(2+)-induced reduction in gating threshold would render T-type Ca2+ channels uniquely suited to transduce depolarizing stimuli of low amplitude into a Ca2+ signal sufficient to support a physiological response.
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41

Discacciati, Marco, Claudia Garetto, and Costas Loizou. "Inhomogeneous wave equation with t-dependent singular coefficients." Journal of Differential Equations 319 (May 2022): 131–85. http://dx.doi.org/10.1016/j.jde.2022.02.039.

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42

Furlan, Mattia, Eugenia Galeota, Stefano De Pretis, Michele Caselle, and Mattia Pelizzola. "m6A-Dependent RNA Dynamics in T Cell Differentiation." Genes 10, no. 1 (January 8, 2019): 28. http://dx.doi.org/10.3390/genes10010028.

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N6-methyladenosine (m6A) is the most abundant RNA modification. It has been involved in the regulation of RNA metabolism, including degradation and translation, in both physiological and disease conditions. A recent study showed that m6A-mediated degradation of key transcripts also plays a role in the control of T cells homeostasis and IL-7 induced differentiation. We re-analyzed the omics data from that study and, through the integrative analysis of total and nascent RNA-seq data, we were able to comprehensively quantify T cells RNA dynamics and how these are affected by m6A depletion. In addition to the expected impact on RNA degradation, we revealed a broader effect of m6A on RNA dynamics, which included the alteration of RNA synthesis and processing. Altogether, the combined action of m6A on all major steps of the RNA life-cycle closely re-capitulated the observed changes in the abundance of premature and mature RNA species. Ultimately, our re-analysis extended the findings of the initial study, focused on RNA stability, and proposed a yet unappreciated role for m6A in RNA synthesis and processing dynamics.
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43

Sacks, David L. "B cell dependent T lymphocyte responses in leishmaniasis." Memórias do Instituto Oswaldo Cruz 82, suppl 1 (November 1987): 341–48. http://dx.doi.org/10.1590/s0074-02761987000500015.

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44

Sacks, David L. "B cell dependent T lymphocyte responses in leishmaniasis." Memórias do Instituto Oswaldo Cruz 83, suppl 1 (November 1988): 506–13. http://dx.doi.org/10.1590/s0074-02761988000500060.

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45

BELL, CLARA G. H., and ANDREW J. EDWARDS. "Microbial-dependent γδ receptor-bearing T-cell localization?" Biochemical Society Transactions 20, no. 2 (May 1, 1992): 221S. http://dx.doi.org/10.1042/bst020221s.

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46

Hirokawa, Makoto, Muneyasu Lee, Atsushi Kitabayashi, Akihiko Chubachi, Toshihiro Itoh, Ikuo Miura, Masahiro Saitoh, and Akira B. Miura. "Autoreactive T Cell-Dependent Polyclonal Hypergammaglobulinemia in Mantle." Leukemia & Lymphoma 14, no. 5-6 (January 1994): 509–13. http://dx.doi.org/10.3109/10428199409049712.

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47

Salinas, G. F., L. D. Rycke, T. Cantaert, M. van de Burg, B. Barendregt, P. Remans, P. P. Tak, and D. Baeten. "TNF blockade impairs T cell dependent humoural responses." Annals of the Rheumatic Diseases 69, Suppl 2 (March 1, 2010): A13. http://dx.doi.org/10.1136/ard.2010.129585f.

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48

Bruckner, Shane, Souad Rhamouni, Lutz Tautz, Jean-Bernard Denault, Andres Alonso, Barbara Becattini, Guy S. Salvesen, and Tomas Mustelin. "YersiniaPhosphatase Induces Mitochondrially Dependent Apoptosis of T Cells." Journal of Biological Chemistry 280, no. 11 (January 4, 2005): 10388–94. http://dx.doi.org/10.1074/jbc.m408829200.

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49

Gavin, Marc A., Jeffrey P. Rasmussen, Jason D. Fontenot, Valeria Vasta, Vincent C. Manganiello, Joseph A. Beavo, and Alexander Y. Rudensky. "Foxp3-dependent programme of regulatory T-cell differentiation." Nature 445, no. 7129 (January 14, 2007): 771–75. http://dx.doi.org/10.1038/nature05543.

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50

Wang, Monica. "IL-6-dependent regulatory T cells in GN." Nature Reviews Nephrology 15, no. 11 (August 5, 2019): 662. http://dx.doi.org/10.1038/s41581-019-0193-9.

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