| First Author | Sabatos CA | Year | 2008 |
| Journal | Immunity | Volume | 29 |
| Issue | 2 | Pages | 238-48 |
| PubMed ID | 18674934 | Mgi Jnum | J:140042 |
| Mgi Id | MGI:3811671 | Doi | 10.1016/j.immuni.2008.05.017 |
| Citation | Sabatos CA, et al. (2008) A Synaptic Basis for Paracrine Interleukin-2 Signaling during Homotypic T Cell Interaction. Immunity 29(2):238-48 |
| abstractText | T cells slow their motility, increase adherence, and arrest after encounters with antigen-presenting cells (APCs) bearing peptide-MHC complexes. Here, we analyzed the cell-cell communication among activating T cells. In vivo and in vitro, activating T cells associated in large clusters that collectively persisted for >30 min, but they also engaged in more transient interactions, apparently distal to APCs. Homotypic aggregation was driven by LFA-1 integrin interactions. Ultrastructural analysis revealed that cell-cell contacts between activating T cells were organized as multifocal synapses, and T cells oriented both the microtubule-organizing complex and interleukin-2 (IL-2) secretion toward this synapse. T cells engaged in homotypic interactions more effectively captured IL-2 relative to free cells. T cells receiving paracrine synaptic IL-2 polarized their IL-2 signaling subunits into the synaptic region and more efficiently phosphorylated the transcription factor STAT5, likely through a synapse-associated signaling complex. Thus, synapse-mediated cytokine delivery accelerates responses in activating T cells. |
