Rapid proliferation of activated lymph node CD4plus T cells is achieved by greatly curtailing the duration of gap phases in cell cycle progression

• Autorzy: Mishima T. , Toda S. , Ando Y. , Matsunaga T. , Inobe M.
• Języki publikacji: EN

Abstrakty

EN

Peripheral T cells are in G0 phase and do not proliferate. When they encounter an antigen, they enter the cell cycle and proliferate in order to initiate an active immune response. Here, we have determined the first two cell cycle times of a leading population of CD4+ T cells stimulated by PMA plus ionomycin in vitro. The first cell cycle began around 10 h after stimulation and took approximately 16 h. Surprisingly, the second cell cycle was extremely rapid and required only 6 h. T cells might have a unique regulatory mechanism to compensate for the shortage of the gap phases in cell cycle progression. This unique feature might be a basis for a quick immune response against pathogens, as it maximizes the rate of proliferation.

Słowa kluczowe

EN

rapid proliferation; lymph node; CD4plus T cell; gap phase; cell cycle progression; cell cycle; cell activity

• Wydawca: -
• Czasopismo: Cellular and Molecular Biology Letters
• Rocznik: 2014
• Tom: 19
• Numer: 4
• Opis fizyczny: p.638-648,fig.,ref.

Twórcy

autor

Mishima T.

• Laboratory of Human Molecular Genetics, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kakuma-machi, Kanazawa, 920-1192, Japan

autor

Toda S.

• Laboratory of Human Molecular Genetics, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kakuma-machi, Kanazawa, 920-1192, Japan

autor

Ando Y.

• Laboratory of Human Molecular Genetics, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kakuma-machi, Kanazawa, 920-1192, Japan

autor

Matsunaga T.

• Laboratory of Human Molecular Genetics, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kakuma-machi, Kanazawa, 920-1192, Japan

autor

Inobe M.

• Laboratory of Human Molecular Genetics, Institute of Medical, Pharmaceutical and Health Sciences, Kanazawa University, Kakuma-machi, Kanazawa, 920-1192, Japan

Bibliografia

• 1. Lea, N.C., Orr, S.J., Stoeber, K., Williams, G.H., Lam, E.W.F., Ibrahim, M.A.A., Ghulam, J.M. and Thomas, N.S.B. Commitment point during G0-->G1 that controls entry into the cell cycle. Mol. Cell. Biol. 23 (2003) 2351–2361.
• 2. Jenkins, M.K. and Moon, J.J. The role of naive T cell precursor frequency and recruitment in dictating immune response magnitude. J. Immunol. 188 (2012) 4135–4140.
• 3. Yarke, C.A., Dalheimer, S.L., Zhang, N., Catron, D.M., Jenkins, M.K. and Mueller, D.L. Proliferating CD4+ T cells undergo immediate growth arrest upon cessation of TCR signaling in vivo. J. Immunol. 180 (2008) 156–162.
• 4. Inobe, M. and Schwartz, R.H. CTLA-4 engagement acts as a brake on CD4+ T cell proliferation and cytokine production but is not required for tuning T cell reactivity in adaptive tolerance. J. Immunol. 173 (2004) 7239–7248.
• 5. Singh, N.J. and Schwartz, R.H. The strength of persistent antigenic stimulation modulates adaptive tolerance in peripheral CD4+ T cells. J. Exp. Med. 198 (2003) 1107–1117.
• 6. Ando, Y., Yasuoka, C., Mishima, T., Ikematsu, T., Uede, T., Matsunaga, T. and Inobe, M. Concanavalin A-mediated T cell proliferation is regulated by herpes virus entry mediator costimulatory molecule. In Vitro Cell. Dev. Biol. Anim. 50 (2014) 313–320.
• 7. Abe, R., Vandenberghe, P., Craighead, N., Smoot, D.S., Lee, K.P. and June, C.H. Distinct signal transduction in mouse CD4+ and CD8+ splenic T cells after CD28 receptor ligation. J. Immunol. 154 (1995) 985–997.
• 8. Unkeless, J.C. Characterization of a monoclonal antibody directed against mouse macrophage and lymphocyte Fc receptors. J. Exp. Med. 150 (1979) 580–596.
• 9. Hirata, A., Inada, K-I., Tsukamoto, T., Sakai, H., Mizoshita, T., Yanai, T., Masegi, O., Goto, H., Inagaki, M. and Tatematsu, M. Characterization of a monoclonal antibody, HTA28, recognizing a histone H3 phosphorylation site as a useful marker of M-phase cells. J. Histochem. Cytochem. 52 (2004) 1503–1509.
• 10. Goto, H., Tomono, Y., Ajiro, K., Kosako, H., Fujita, M., Sakurai, M. Okawa, K., Iwamatsu, A., Okigaki, T., Takahashi, T. and Inagaki, M. Identification of a novel phosphorylation site on histone H3 coupled with mitotic chromosome condensation. J. Biol. Chem. 274 (1999) 25543–25549.
• 11. Toba, K., Winton, E.F., Koike, T. and Shibata, A. Simultaneous three-color analysis of the surface phenotype and DNA-RNA quantitation using 7-amino-actinomycin D and pyronin Y. J. Immunol. Methods 182 (1995) 193–207.
• 12. Crissman, H.A., Darzynkiewicz, Z., Tobey, R.A. and Steinkamp, J.A. Correlated measurements of DNA, RNA, and protein in individual cells by flow cytometry. Science 228 (1985) 1321–1324.
• 13. Buck, S.B., Bradford, J., Gee, K.R., Agnew, B.J., Clarke, S.T. and Salic, A. Detection of S-phase cell cycle progression using 5-ethynyl-2“-deoxyuridine incorporation with click chemistry, an alternative to using 5-bromo-2- ”deoxyuridine antibodies. BioTechniques 44 (2008) 927–929.
• 14. Sojka, D.K., Bruniquel, D., Schwartz, R.H. and Singh, N.J. IL-2 secretion by CD4+ T cells in vivo is rapid, transient, and influenced by TCR-specific competition. J. Immunol. 172 (2004) 6136–6143.
• 15. Kirschner, M., Newport, J. and Gerhart, J. The timing of early developmental events in Xenopus. Trends Genet. 1 (1985) 41–47.
• 16. Onoyama, I., Tsunematsu, R., Matsumoto, A., Kimura, T., de Alborán, I.M., Nakayama, K. and Nakayama, K.I. Conditional inactivation of Fbxw7 impairs cell-cycle exit during T cell differentiation and results in lymphomatogenesis. J. Exp. Med. 204 (2007) 2875–2888.
• 17. Li, G., Domenico, J., Lucas, J.J. and Gelfand, E.W. Identification of multiple cell cycle regulatory functions of p57Kip2 in human T lymphocytes. J. Immunol. 173 (2004) 2383–2391.
• 18. Mohapatra, S., Agrawal, D. and Pledger, W.J. p27Kip1 regulates T cell proliferation. J. Biol. Chem. 276 (2001) 21976–2183.

Identyfikatory

DOI

10.2478/s11658-014-0219-z