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Mediators of Inflammation
Volume 2009, Article ID 819408, 9 pages
http://dx.doi.org/10.1155/2009/819408
Research Article

Linking Innate and Adaptive Immunity: Human V 9V 2 T Cells Enhance CD40 Expression and HMGB-1 Secretion

Division of Infectious Diseases, Departments of Medicine, Microbiology and Immunology, University of British Columbia and Vancouver Hospital Coastal Health Research Institute, Vancouver, BC, Canada V5Z 3J5

Received 23 June 2009; Accepted 17 July 2009

Academic Editor: Magdalena Klink

Copyright © 2009 Shirin Kalyan and Anthony W. Chow. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Linked References

  1. L. Wang, H. Das, A. Kamath, L. Li, and J. F. Bukowski, “Human Vγ2Vδ2 T cells augment migration-inhibitory factor secretion and counteract the inhibitory effect of glucocorticoids on IL-1β and TNF-α production,” The Journal of Immunology, vol. 168, no. 10, pp. 4889–4896, 2002. View at Google Scholar
  2. M. Lahn, A. Kanehiro, K. Takeda et al., “?d T cells as regulators of airway hyperresponsiveness,” International Archives of Allergy and Immunology, vol. 125, no. 3, pp. 203–210, 2001. View at Publisher · View at Google Scholar
  3. S. Kalyan and A. W. Chow, “Human peripheral γδ T cells potentiate the early proinflammatory cytokine response to staphylococcal toxic shock syndrome toxin-1,” Journal of Infectious Diseases, vol. 189, no. 10, pp. 1892–1896, 2004. View at Publisher · View at Google Scholar
  4. S. R. Carding and P. J. Egan, “The importance of γδT cells in the resolution of pathogen-induced inflammatory immune responses,” Immunological Reviews, vol. 173, pp. 98–108, 2000. View at Publisher · View at Google Scholar
  5. P. J. Egan and S. R. Carding, “Downmodulation of the inflammatory response to bacterial infection by γδ T cells cytotoxic for activated macrophages,” Journal of Experimental Medicine, vol. 191, no. 12, pp. 2145–2158, 2000. View at Publisher · View at Google Scholar
  6. J. Jameson, K. Ugarte, N. Chen et al., “A role for skin ?d T cells in wound repair,” Science, vol. 296, no. 5568, pp. 747–749, 2002. View at Publisher · View at Google Scholar
  7. P. Constant, F. Davodeau, M.-A. Peyrat et al., “Stimulation of human ?d T cells by nonpeptidic mycobacterial ligands,” Science, vol. 264, no. 5156, pp. 267–270, 1994. View at Google Scholar
  8. J. F. Bukowski, C. T. Morita, Y. Tanaka, B. R. Bloom, M. B. Brenner, and H. Band, “Vγ2Vδ2 TCR-dependent recognition of non-peptide antigens and Daudi cells analyzed by TCR gene transfer,” The Journal of Immunology, vol. 154, no. 3, pp. 998–1006, 1995. View at Google Scholar
  9. C. T. Morita, E. M. Beckman, J. F. Bukowski et al., “Direct presentation of nonpeptide prenyl pyrophosphate antigens to human ?d T cells,” Immunity, vol. 3, no. 4, pp. 495–507, 1995. View at Publisher · View at Google Scholar
  10. C. T. Morita, H. K. Lee, D. S. Leslie, Y. Tanaka, J. F. Bukowski, and E. Märker-Hermann, “Recognition of nonpeptide prenyl pyrophosphate antigens by human γδ T cells,” Microbes and Infection, vol. 1, no. 3, pp. 175–186, 1999. View at Publisher · View at Google Scholar
  11. M. Kistowska, E. Rossy, S. Sansano et al., “Dysregulation of the host mevalonate pathway during early bacterial infection activates human TCR ?d cells,” European Journal of Immunology, vol. 38, no. 8, pp. 2200–2209, 2008. View at Publisher · View at Google Scholar
  12. T. Krakauer, “Immune response to staphylococcal superantigens,” Immunologic Research, vol. 20, no. 2, pp. 163–173, 1999. View at Google Scholar
  13. T. Ferry, D. Thomas, T. Perpoint et al., “Analysis of superantigenic toxin Vß T-cell signatures produced during cases of staphylococcal toxic shock syndrome and septic shock,” Clinical Microbiology and Infection, vol. 14, no. 6, pp. 546–554, 2008. View at Publisher · View at Google Scholar
  14. S. Kalyan and A. W. Chow, “Staphylococcal toxic shock syndrome toxin-1 induces the translocation and secretion of high mobility group-1 protein from both activated T cells and monocytes,” Mediators of Inflammation, vol. 2008, Article ID 512196, 7 pages, 2008. View at Publisher · View at Google Scholar
  15. H. Wang, O. Bloom, M. Zhang et al., “HMG-1 as a late mediator of endotoxin lethality in mice,” Science, vol. 285, no. 5425, pp. 248–251, 1999. View at Publisher · View at Google Scholar
  16. U. Andersson, H. Wang, K. Palmblad et al., “High mobility group 1 protein (HMG-1) stimulates proinflammatory cytokine synthesis in human monocytes,” Journal of Experimental Medicine, vol. 192, no. 4, pp. 565–570, 2000. View at Publisher · View at Google Scholar
  17. W. W. S. Kum, K. B. Laupland, R. H. See, and A.W. Chow, “Improved purification and biologic activities of staphylococcal toxic shock syndrome toxin 1,” Journal of Clinical Microbiology, vol. 31, no. 10, pp. 2654–2660, 1993. View at Google Scholar
  18. W. W. S. Kum, R. W. Y. Hung, S. B. Cameron, and A. W. Chow, “Temporal sequence and functional implications of Vβ-specific T cell receptor down-regulation and costimulatory molecule expression following in vitro stimulation with the staphylococcal superantigen toxic shock syndrome toxin-1,” Journal of Infectious Diseases, vol. 185, no. 4, pp. 555–560, 2002. View at Publisher · View at Google Scholar
  19. A. Rouhiainen, J. Kuja-Panula, E. Wilkman et al., “Regulation of monocyte migration by amphoterin (HMGB1),” Blood, vol. 104, no. 4, pp. 1174–1182, 2004. View at Publisher · View at Google Scholar
  20. J. E. Dalton, J. Pearson, P. Scott, and S. R. Carding, “The interaction of γδ T cells with activated macrophages is a property of the Vγ1 subset,” The Journal of Immunology, vol. 171, no. 12, pp. 6488–6494, 2003. View at Google Scholar
  21. J. Ismaili, V. Olislagers, R. Poupot, J.-J. Fournié, and M. Goldman, “Human γδ T cells induce dendritic cell maturation,” Clinical Immunology, vol. 103, no. 3, pp. 296–302, 2002. View at Publisher · View at Google Scholar
  22. S.-I. Fujii, K. Liu, C. Smith, A. J. Bonito, and R. M. Steinman, “The linkage of innate to adaptive immunity via maturing dendritic cells in vivo requires CD40 ligation in addition to antigen presentation and CD80/86 costimulation,” Journal of Experimental Medicine, vol. 199, no. 12, pp. 1607–1618, 2004. View at Publisher · View at Google Scholar
  23. J. K. H. Tan and H. C. O'Neill, “Maturation requirements for dendritic cells in T cell stimulation leading to tolerance versus immunity,” Journal of Leukocyte Biology, vol. 78, no. 2, pp. 319–324, 2005. View at Publisher · View at Google Scholar
  24. F. Dieli, N. Caccamo, S. Meraviglia et al., “Reciprocal stimulation of ?d T cells and dendritic cells during the anti-mycobacterial immune response,” European Journal of Immunology, vol. 34, no. 11, pp. 3227–3235, 2004. View at Publisher · View at Google Scholar
  25. L. Conti, R. Casetti, M. Cardone et al., “Reciprocal activating interaction between dendritic cells and pamidronate-stimulated ?d T cells: role of CD86 and inflammatory cytokines,” The Journal of Immunology, vol. 174, no. 1, pp. 252–260, 2005. View at Google Scholar
  26. M. Eberl, G. W. Roberts, S. Meuter, J. D. Williams, N. Topley, and B. Moser, “A rapid crosstalk of human γδ T cells and monocytes drives the acute inflammation in bacterial infections,” PLoS Pathogens, vol. 5, no. 2, Article ID e1000308, 2009. View at Publisher · View at Google Scholar
  27. C. Semino, J. Ceccarelli, L. V. Lotti, M. R. Torrisi, G. Angelini, and A. Rubartelli, “The maturation potential of NK cell clones toward autologous dendritic cells correlates with HMGB1 secretion,” Journal of Leukocyte Biology, vol. 81, no. 1, pp. 92–99, 2007. View at Publisher · View at Google Scholar
  28. V. Urbonaviciute, B. G. Furnrohr, S. Meister et al., “Induction of inflammatory and immune responses by HMGB1-nucleosome complexes: implications for the pathogenesis of SLE,” Journal of Experimental Medicine, vol. 205, no. 13, pp. 3007–3018, 2008. View at Publisher · View at Google Scholar
  29. P. Rovere, E. Clementi, M. Ferrarini et al., “CD95 engagement releases calcium from intracellular stores of long term activated, apoptosis-prone ?d T cells,” The Journal of Immunology, vol. 156, no. 12, pp. 4631–4637, 1996. View at Google Scholar
  30. M. Ferrarini, S. Heltai, E. Toninelli, M. G. Sabbadini, C. Pellicciari, and A. A. Manfredi, “Daudi lymphoma killing triggers the programmed death of cytotoxic Vγ9/Vδ2 T lymphocytes,” The Journal of Immunology, vol. 154, no. 8, pp. 3704–3712, 1995. View at Google Scholar
  31. P. Rovere-Querini, A. Capobianco, P. Scaffidi et al., “HMGB1 is an endogenous immune adjuvant released by necrotic cells,” EMBO Reports, vol. 5, no. 8, pp. 825–830, 2004. View at Publisher · View at Google Scholar
  32. B. Moser, D. D. Desai, M. P. Downie et al., “Receptor for advanced glycation end products expression on T cells contributes to antigen-specific cellular expansion in vivo,” The Journal of Immunology, vol. 179, no. 12, pp. 8051–8058, 2007. View at Google Scholar
  33. I. E. Dumitriu, P. Baruah, B. Valentinis et al., “Release of high mobility group box 1 by dendritic cells controls T cell activation via the receptor for advanced glycation end products,” The Journal of Immunology, vol. 174, no. 12, pp. 7506–7515, 2005. View at Google Scholar
  34. D. Messmer, H. Yang, G. Telusma et al., “High mobility group box protein 1: an endogenous signal for dendritic cell maturation and Th1 polarization,” The Journal of Immunology, vol. 173, no. 1, pp. 307–313, 2004. View at Google Scholar
  35. M.-C. Devilder, S. Maillet, I. Bouyge-Moreau, E. Bonnadieu, M. Bonneville, and E. Scotet, “Potentiation of antigen-stimulated Vγ9Vδ2 T cell cytokine production by immature dendritic cells (DC) and reciprocal effect on DC maturation,” The Journal of Immunology, vol. 176, no. 3, pp. 1386–1393, 2006. View at Google Scholar
  36. D. S. Leslie, M. S. Vincent, F. M. Spada et al., “CD1-mediated ?/d T cell maturation of dendritic cells,” Journal of Experimental Medicine, vol. 196, no. 12, pp. 1575–1584, 2002. View at Publisher · View at Google Scholar