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This information is current as Interactions Antigen Presentation through CD 27 / CD 70 Survival and Proliferation Independently of Helper B Cells Promote Cytotoxic T Cell
| Content Provider | Semantic Scholar |
|---|---|
| Author | Deola, Sara Panelli, Monica C. Maric, Dragan S. Selleri, Silvia Dmitrieva, Natalia Iurevna Voss, Ching Y. Klein, Harvey Z. Stroncek, David Wang, Ena Marincola, Francesco M. |
| Copyright Year | 2008 |
| Abstract | * CD8-expressing cytotoxic T cell (CTL) interactions with APCs and helper T cells determine their function and ability to survive. In this study, we describe a novel interaction independent of Ag presentation between activated CTLs and bystander CD19-expressing B lymphocytes. Ag-stimulated CTLs serially engage autologous B lymphocytes through CD27/CD70 contact that promotes their survival and proliferation. Moreover, these interactions induce the release of proinflammatory cytokines that follows two general patterns: 1) an epitope-dependent enhancement of cytokine release, and 2) a previously undiscovered coordinate release of cytokines independent of epitope exposure. The latter includes chemoattractants targeting activated T cells. As a result, activated T cells are attracted to B cells, which exert a " helper " role in lymphatic organs or in areas of inflammation. This observation provides a mechanistic explanation to previously reported experimental observations suggesting that B cells are required for T cell priming in vivo. A ntigen-specific CD8 ϩ T cells mature and expand upon interaction with APCs and CD4 ϩ T lymphocytes (1). Previous reports based on in vivo experimental observations pointed to the possible participation of B cells in the context of some virally (2) or parasite-induced T cell responses (3). Moreover, clinical observations suggest that B cells may modulate T cell effector function in the context of allograft rejection (4) and autoimmune disorders such as multiple sclerosis (5). These findings suggest that B cells sustain T cell function in inflamed tissues although, to date, no mechanistic explanation has been provided. We observed that circulating CTLs induced by melanoma Ag-specific immunization display a quiescent phenotype in vivo that could be reversed in vitro by combined exposure of PBMCs to Ag recall and rIL-2, resulting in their rapid and specific expansion (6). Interestingly, expansion of Ag-specific CD8 T cells in vitro required not only Ag recall and rIL-2, but the whole PBMC population because purified CD8 T cells alone proliferated less efficiently in identical conditions. Additional help by CD4-expressing T cells to CD8 T cell cultures only partially restored the ability of Ag-specific CTLs to proliferate, suggesting that other cells included in the whole PBMC population could play a helper role in CD8 activation/proliferation. This observation revealed the necessity to better understand the kinetics of efficient memory T cell activation. To further explore the requirements for in vitro activation/ex-pansion of CTLs, we studied the kinetics of proliferation of HLA-A*0201-restricted, Flu M1:58-66-specific CTLs as a well-characterized human memory … |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | http://www.jimmunol.org/content/jimmunol/180/3/1362.full.pdf?with-ds=yes |
| Alternate Webpage(s) | http://www.jimmunol.org/content/jimmunol/180/3/1362.full.pdf |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |