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Signal Transduction

Regulation of the Small GTPase Rap1 and Extracellular Signal-Regulated Kinases by the Costimulatory Molecule CTLA-4

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Pages 4117-4128 | Received 13 Dec 2004, Accepted 16 Feb 2005, Published online: 27 Mar 2023

REFERENCES

  • Amsen, D., A. Kruisbeek, J. L. Bos, and K. Reedquist. 2000. Activation of the Ras-related GTPase Rap1 by thymocyte TCR engagement and during selection. Eur. J. Immunol. 30:2832–2841.
  • Bachmann, M. F., A. Gallimore, E. Jones, B. Ecabert, H. Acha-Orbea, and M. Kopf. 2001. Normal pathogen-specific immune responses mounted by CTLA-4-deficient T cells: a paradigm reconsidered. Eur. J. Immunol. 31:450–458.
  • Bivona, T. G., H. H. Wiener, I. M. Ahearn, J. Silletti, V. K. Chiu, and M. R. Philips. 2004. Rap1 up-regulation and activation on plasma membrane regulates T cell adhesion. J. Cell Biol. 164:461–470.
  • Boussiotis, V. A., G. J. Freeman, A. Berezovskaya, D. L. Barber, and L. M. Nadler. 1997. Maintenance of human T cell anergy: blocking of IL-2 gene transcription by activated Rap1. Science 278:124–128.
  • Brinkmann, T., O. Daumke, U. Herbrand, D. Kuhlmann, P. Stege, M. R. Ahmadian, and A. Wittinghofer. 2002. Rap-specific GTPase activating protein follows an alternative mechanism. J. Biol. Chem. 277:12525–12531.
  • Calvo, C. R., D. Amsen, and A. M. Kruisbeek. 1997. Cytotoxic T lymphocyte antigen 4 (CTLA-4) interferes with extracellular signal-regulated kinase (ERK) and Jun NH2-terminal kinase (JNK) activation, but does not affect phosphorylation of T cell receptor ζ and ZAP70. J. Exp. Med. 186:1645–1653.
  • Cantrell, D. A. 2003. GTPases and T cell activation. Immunol. Rev. 192:122–130.
  • Carey, K. D., T. J. Dillon, J. M. Schmitt, A. M. Baird, A. D. Holdorf, D. B. Straus, A. S. Shaw, and P. J. Stork. 2000. CD28 and the tyrosine kinase lck stimulate mitogen-activated protein kinase activity in T cells via inhibition of the small G protein Rap1. Mol. Cell. Biol. 20:8409–8419.
  • Carreno, B. M., F. Bennett, T. A. Chau, V. Ling, D. Luxenberg, J. Jussif, M. L. Baroja, and J. Madrenas. 2000. CTLA-4 (CD152) can inhibit T cell activation by two different mechanisms depending on its level of cell surface expression. J. Immunol. 165:1352–1356.
  • Chambers, C. A. 2001. The expanding world of co-stimulation: the two-signal model revisited. Trends Immunol. 22:217–223.
  • Chambers, C. A., D. Cado, T. Truong, and J. P. Allison. 1997. Thymocyte development is normal in CTLA-4-deficient mice. Proc. Natl. Acad. Sci. USA 94:9296–9301.
  • Chambers, C. A., M. S. Kuhns, J. G. Egen, and J. P. Allison. 2001. CTLA-4-mediated inhibition in regulation of T cell responses: mechanisms and manipulation in tumor immunotherapy. Annu. Rev. Immunol. 19:565–594.
  • da Rocha Dias, S., and C. E. Rudd. 2001. CTLA-4 blockade of antigen-induced cell death. Blood 97:1134–1137.
  • Daumke, O., M. Weyand, P. P. Chakrabarti, I. R. Vetter, and A. Wittinghofer. 2004. The GTPase-activating protein Rap1GAP uses a catalytic asparagine. Nature 429:197–201.
  • de Bruyn, K. M., S. Rangarajan, K. A. Reedquist, C. G. Figdor, and J. L. Bos. 2002. The small GTPase Rap1 is required for Mn2+- and antibody-induced LFA-1- and VLA-4-mediated cell adhesion. J. Biol. Chem. 277:29468–29476.
  • Dillon, T. J., V. Karpitski, S. A. Wetzel, D. C. Parker, A. S. Shaw, and P. J. Stork. 2003. Ectopic B-Raf expression enhances extracellular signal-regulated kinase (ERK) signaling in T cells and prevents antigen-presenting cell-induced anergy. J. Biol. Chem. 278:35940–35949.
  • Ebinu, J. O., S. L. Stang, C. Teixeira, D. A. Bottorff, J. Hooton, P. M. Blumberg, M. Barry, R. C. Bleakley, H. L. Ostergaard, and J. C. Stone. 2000. RasGRP links T-cell receptor signaling to Ras. Blood 95:3199–3203.
  • Fraser, J. H., M. Rincon, K. D. McCoy, and G. Le Gros. 1999. CTLA4 ligation attenuates AP-1, NFAT and NF-κB activity in activated T cells. Eur. J. Immunol. 29:838–844.
  • Gatta, L., G. Calviello, F. Di Nicuolo, L. Pace, V. Ubaldi, G. Doria, and C. Pioli. 2002. Cytotoxic T lymphocyte-associated antigen-4 inhibits integrin-mediated stimulation. Immunology 107:209–216.
  • Iezzi, G., K. Karjalainen, and A. Lanzavecchia. 1998. The duration of antigenic stimulation determines the fate of naive and effector T cells. Immunity 8:89–95.
  • Ishida, D., H. Yang, K. Masuda, K. Uesugi, H. Kawamoto, M. Hattori, and N. Minato. 2003. Antigen-driven T cell anergy and defective memory T cell response via deregulated Rap1 activation in SPA-1-deficient mice. Proc. Natl. Acad. Sci. USA 100:10919–10924.
  • Katagiri, K., M. Hattori, N. Minato, and T. Kinashi. 2002. Rap1 functions as a key regulator of T-cell and antigen-presenting cell interactions and modulates T-cell responses. Mol. Cell. Biol. 22:1001–1015.
  • Kaye, J., N. J. Vasquez, and S. M. Hedrick. 1992. Involvement of the same region of the T cell antigen receptor in thymic selection and foreign peptide recognition. J. Immunol. 148:3342–3353.
  • Krummel, M. F., and J. P. Allison. 1995. CD28 and CTLA-4 have opposing effects on the response of T cells to stimulation. J. Exp. Med. 182:459–465.
  • Krummel, M. F., and J. P. Allison. 1996. CTLA-4 engagement inhibits IL-2 accumulation and cell cycle progression upon activation of resting T cells. J. Exp. Med. 183:2533–2540.
  • Krummel, M. F., T. J. Sullivan, and J. P. Allison. 1996. Superantigen responses and co-stimulation: CD28 and CTLA-4 have opposing effects on T cell expansion in vitro and in vivo. Int. Immunol. 8:519–523.
  • Lee, K. M., E. Chuang, M. Griffin, R. Khattri, D. K. Hong, W. Zhang, D. Straus, L. E. Samelson, C. B. Thompson, and J. A. Bluestone. 1998. Molecular basis of T cell inactivation by CTLA-4. Science 282:2263–2266.
  • Mandelbrot, D. A., A. J. McAdam, and A. H. Sharpe. 1999. B7-1 or B7-2 is required to produce the lymphoproliferative phenotype in mice lacking cytotoxic T lymphocyte-associated antigen 4 (CTLA-4). J. Exp. Med. 189:435–440.
  • Masteller, E. L., E. Chuang, A. C. Mullen, S. L. Reiner, and C. B. Thompson. 2000. Structural analysis of CTLA-4 function in vivo. J. Immunol. 164:5319–5327.
  • Meng, J., J. L. Glick, P. Polakis, and P. J. Casey. 1999. Functional interaction between Gαgz and Rap1GAP suggests a novel form of cellular cross-talk. J. Biol. Chem. 274:36663–36669.
  • Nakaseko, C., S. Miyatake, T. Iida, S. Hara, R. Abe, H. Ohno, Y. Saito, and T. Saito. 1999. Cytotoxic T lymphocyte antigen 4 (CTLA-4) engagement delivers an inhibitory signal through the membrane-proximal region in the absence of the tyrosine motif in the cytoplasmic tail. J. Exp. Med. 190:765–774.
  • Okumura, N., M. Okada, and H. Nakagawa. 1994. Depolarization-induced tyrosine phosphorylation in PC12h cells. J. Biochem. 116:346–350.
  • Reedquist, K. A., and J. L. Bos. 1998. Costimulation through CD28 suppresses T cell receptor-dependent activation of the Ras-like small GTPase Rap1 in human T lymphocytes. J. Biol. Chem. 273:4944–4949.
  • Saito, T., and S. Yamasaki. 2003. Negative feedback of T cell activation through inhibitory adapters and costimulatory receptors. Immunol. Rev. 192:143–160.
  • Salomon, B., and J. A. Bluestone. 2001. Complexities of CD28/B7: CTLA-4 costimulatory pathways in autoimmunity and transplantation. Annu. Rev. Immunol. 19:225–252.
  • Schmitt, J. M., and P. J. S. Stork. 2000. β2-adrenergic receptor activates extracellular regulated kinases (ERKs) via the small G protein Rap1 and the serine/threonine kinase B-Raf. J. Biol. Chem. 275:25342–25350.
  • Schneider, H., S. D. Dias, H. Hu, and C. E. Rudd. 2001. A regulatory role for cytoplasmic YVKM motif in CTLA-4 inhibition of TCR signaling. Eur. J. Immunol. 31:2042–2050.
  • Schneider, H., D. A. Mandelbrot, R. J. Greenwald, F. Ng, R. Lechler, A. H. Sharpe, and C. E. Rudd. 2002. Cutting edge: CTLA-4 (CD152) differentially regulates mitogen-activated protein kinases (extracellular signal-regulated kinase and c-Jun N-terminal kinase) in CD4+ T cells from receptor/ligand-deficient mice. J. Immunol. 169:3475–3479.
  • Sebzda, E., M. Bracke, T. Tugal, N. Hogg, and D. A. Cantrell. 2002. Rap1A positively regulates T cells via integrin activation rather than inhibiting lymphocyte signaling. Nat. Immunol. 3:251–258.
  • Suga, K., K. Katagiri, T. Kinashi, M. Harazaki, T. Iizuka, M. Hattori, and N. Minato. 2001. CD98 induces LFA-1-mediated cell adhesion in lymphoid cells via activation of Rap1. FEBS Lett. 489:249–253.
  • Tivol, E. A., F. Borriello, A. N. Schweitzer, W. P. Lynch, J. A. Bluestone, and A. H. Sharpe. 1995. Loss of CTLA-4 leads to massive lymphoproliferation and fatal multiorgan tissue destruction, revealing a critical negative regulatory role of CTLA-4. Immunity 3:541–547.
  • Tivol, E. A., S. D. Boyd, S. McKeon, F. Borriello, P. Nickerson, T. B. Strom, and A. H. Sharpe. 1997. CTLA4Ig prevents lymphoproliferation and fatal multiorgan tissue destruction in CTLA-4-deficient mice. J. Immunol. 158:5091–5094.
  • Vijayakrishnan, L., J. M. Slavik, Z. Illes, R. J. Greenwald, D. Rainbow, B. Greve, L. B. Peterson, D. A. Hafler, G. J. Freeman, A. H. Sharpe, L. S. Wicker, and V. K. Kuchroo. 2004. An autoimmune disease-associated CTLA-4 splice variant lacking the B7 binding domain signals negatively in T cells. Immunity 20:563–575.
  • Walunas, T. L., D. J. Lenschow, C. Y. Bakker, P. S. Linsley, G. J. Freeman, J. M. Green, C. B. Thompson, and J. A. Bluestone. 1994. CTLA-4 can function as a negative regulator of T cell activation. Immunity 1:405–413.
  • Wetzel, S. A., T. W. McKeithan, and D. C. Parker. 2002. Live cell dynamics and the role of costimulation in immunological synapse formation. J. Immunol. 169:6092–6101.
  • Whitehurst, C. E., and T. D. Geppert. 1996. MEK1 and the extracellular signal-regulated kinases are required for the stimulation of IL-2 gene transcription in T cells. J. Immunol. 156:1020–1029.
  • Zhao, H., Y. Y. Li, R. V. Fucini, S. E. Ross, J. E. Pessin, and G. A. Koretzky. 1997. T cell receptor-induced phosphorylation of Sos requires activity of CD45, Lck, and protein kinase C, but not ERK. J. Biol. Chem. 272:21625–21634.

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