期刊
JOURNAL OF CLINICAL INVESTIGATION
卷 111, 期 10, 页码 1571-1578出版社
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI200317573
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资金
- NIAID NIH HHS [K08 AI001732, KO8 AI1732] Funding Source: Medline
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.
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