Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Höpken, U.E. et al.

Höpken, Droese, Li, Joergensen, Breitfeld, Zerwes, Lipp,

The chemokine receptor CCR7 controls lymph node-dependent cytotoxic T cell priming in alloimmune responses.

The chemokine receptor CCR7 and its ligands regulate migration and colocalization of T cells and mature dendritic cells to and within secondary lymphoid organs. The requirement of CCR7 in efficient priming of allospecific cytotoxic CD8(+) T cells is poorly characterized. Here, we demonstrate a role for CCR7 in the initiation of an alloimmune response and in the development of transplant rejection. Remarkably, in a model of acute allogeneic tumor rejection, CCR7(-/-) mice completely failed to reject subcutaneously injected MHC class I mismatched tumor cells and cytotoxic activity of allospecific T cells was severely compromised. When solid tumors derived from wild-type mice were transplanted, recipient CCR7(-/-) mice were capable of rejecting the allografts. In contrast, tumor allografts transplanted from CCR7(-/-) donors onto CCR7(-/-) recipients showed allograft survival up to 28 days, suggesting a critical function of CCR7 on donor-type passenger leukocytes in the initiation of cytotoxic CD8(+) T cell responses. In a heterotopic heart transplantation model CCR7 deficiency resulted in significantly prolonged but not indefinite allograft survival. Additional prolongation of graft survival was observed when hearts from CCR7(-/-) mice were used as donor organs. Our results define a key role for CCR7 in allogeneic T cell priming within the context of draining lymph nodes.[1]

References

The chemokine receptor CCR7 controls lymph node-dependent cytotoxic T cell priming in alloimmune responses. Höpken, U.E., Droese, J., Li, J.P., Joergensen, J., Breitfeld, D., Zerwes, H.G., Lipp, M. Eur. J. Immunol. (2004) [Pubmed]

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