Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2008 Aug;13(4):358-65.
doi: 10.1097/MOT.0b013e3283061149.

Toll-like receptor signaling in transplantation

Maria-Luisa Alegre  1 , Daniel R Goldstein, Anita S Chong
Affiliations
Review

Toll-like receptor signaling in transplantation

Maria-Luisa Alegre et al. Curr Opin Organ Transplant. 2008 Aug.

Abstract

Purpose of review: This review summarizes recent advances in the role of endogenous and exogenous Toll-like receptor ligands in the activation and inhibition of immune responses in transplantation.

Recent findings: During an alloresponse, Toll-like receptors can be engaged by both damage-induced endogenous ligands or microbial-associated molecular patterns. The damage-induced molecule high mobility group box 1 protein and its binding to Toll-like receptor 4 have been identified as major initiators of antitumor and antitransplant immune responses. Type I interferon signaling plays an important role in the pro-rejection effect mediated by Toll-like receptor agonists and some bacteria. Similar pathways, however, in neonates can result in inhibition rather than activation of alloimmune responses.

Summary: The consequences of Toll-like receptor engagement by endogenous and exogenous ligands in transplantation may depend on the relative induction of inflammatory and regulatory pathways and the stage of development of the immune system.

PubMed Disclaimer

References

    1. Goldstein DR, Tesar BM, Akira S, Lakkis FG. Critical role of the Toll-like receptor signal adaptor protein MyD88 in acute allograft rejection. J Clin Invest. 2003;111:1571–1578. - PMC - PubMed
    1. McKay D, Shigeoka A, Rubinstein M, Surh C, Sprent J. Simultaneous deletion of MyD88 and Trif delays major histocompatibility and minor antigen mismatch allograft rejection. Eur J Immunol. 2006;36:1994–2002. - PubMed
    1. Tesar BM, Zhang J, Li Q, Goldstein DR. TH1 immune responses to fully MHC mismatched allografts are diminished in the absence of MyD88, a toll-like receptor signal adaptor protein. Am J Transplant. 2004;4:1429–1439. - PubMed
    1. Walker WE, Nasr IW, Camirand G, Tesar BM, Booth CJ, Goldstein DR. Absence of innate MyD88 signaling promotes inducible allograft acceptance. J Immunol. 2006;177:5307–5316. - PubMed
    1. Chen L, Wang T, Zhou P, Ma L, Yin D, Shen J, Molinero L, Nozaki T, Phillips T, Uematsu S, et al. TLR engagement prevents transplantation tolerance. Am J Transplant. 2006;6:2282–2291. - PubMed

Publication types

MeSH terms