In vivo anergized T cells form altered immunological synapses in vitro
| Autor: | E. Zambricki, Tomasz Zal, Dianne B. McKay, Pia P. Yachi, Jonathan Sprent, Nicholas R. J. Gascoigne, Alana A. Shigeoka |
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| Rok vydání: | 2006 |
| Předmět: |
Cell signaling
CD8 Antigens T-Lymphocytes Receptors Antigen T-Cell Antigen-Presenting Cells Mice Transgenic Biology Immunological synapse Mice Antigen Immunology and Allergy Animals Transplantation Homologous Pharmacology (medical) Antigen-presenting cell Clonal Anergy Transplantation Mice Inbred BALB C Clonal anergy Immunological synapse formation Gap Junctions T lymphocyte Immunological Synapses Cell biology Mice Inbred C57BL Transplantation Isogeneic Immunology |
| Zdroj: | American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons. 6(11) |
| ISSN: | 1600-6135 |
| Popis: | T cells contact allogeneic antigen presenting cells (APCs) and assemble, at their contact interface, a molecular platform called the immunological synapse. Synapse-based molecules provide directional signals for the T cell--either positive signals, resulting in T-cell activation, or negative signals causing T-cell inactivation or anergy. To better understand the molecular basis of in vivo T-cell anergy we analyzed the contacts made between in vivo anergized T cells and APCs, and determined which signaling molecules were included or excluded from their immunological synapses. Anergy was induced in TCR transgenic mice by the intravenous injection of semiallogeneic donor spleen cells. T cells from anergized mice were mixed with APCs, the T-cell/APC synapses imaged using deconvolution microscopy, and their molecular compositions were determined. T cells from anergic mice formed unstable immunological synapses in vitro with allogeneic APCs and failed to recruit the signaling proteins necessary to initiate T-cell activation. These findings suggest that T-cell anergy induced by exposure to semiallogeneic donor cells is associated with defects in the earliest events of T-cell activation, immunological synapse formation and recruitment of TCR-mediated signaling proteins. |
| Databáze: | OpenAIRE |
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