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

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Critical role of the Toll-like receptor signal adaptor protein MyD88 in acute allograft rejection.

The Toll-like receptors (TLRs) are recently discovered germline-encoded receptors on APCs that are critically important in innate immune recognition of microbial pathogens. However, their role in solid-organ transplantation is unknown. To explore this role, we employed a skin allograft model using mice with targeted deletion of the universal TLR signal adaptor protein, MyD88. We report that minor antigen-mismatched (HY-mismatched) allograft rejection cannot occur in the absence of MyD88 signaling. Furthermore, we show that the inability to reject these allografts results from a reduced number of mature DCs in draining lymph nodes, leading to impaired generation of anti-graft-reactive T cells and impaired Th1 immunity. Hence, this work demonstrates that TLRs can be activated in a transplant setting and not solely by infections. These results link innate immunity to the initiation of the adaptive alloimmune response.[1]

References

  1. Critical role of the Toll-like receptor signal adaptor protein MyD88 in acute allograft rejection. Goldstein, D.R., Tesar, B.M., Akira, S., Lakkis, F.G. J. Clin. Invest. (2003) [Pubmed]
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