Toll-like receptors, endogenous ligands, and systemic autoimmune disease
- PMID: 15790348
- DOI: 10.1111/j.0105-2896.2005.00239.x
Toll-like receptors, endogenous ligands, and systemic autoimmune disease
Abstract
The critical role of Toll-like receptors (TLRs) as mediators of pathogen recognition by the innate immune system is now firmly established. Such recognition results in the initiation of an inflammatory immune response and subsequent instruction of the adaptive immune system, both of which are designed to rid the host of the invading pathogen. More controversial is the potential role of TLRs in the recognition of endogenous ligands and what effect this might have on the consequent development of autoimmune or other chronic sterile inflammatory disorders. An increasing number of studies implicate TLRs as being involved in the immune response to self-molecules that have in some way been altered from their native state or accumulate in non-physiologic sites or amounts, although questions have been raised about possible contaminants in certain of these studies. In this review, we discuss the evidence for endogenous ligand-TLR interactions with particular emphasis on mammalian chromatin, systemic lupus erythematosus, and atherosclerosis. Overall, the data support the general concept of a role for TLRs in the recognition of endogenous ligands. However, the precise details of the interactions and the extent to which they may contribute to the pathogenesis of human disease remain to be clarified.
Similar articles
-
The role of toll-like receptors in chronic inflammation.Int J Biochem Cell Biol. 2010 Apr;42(4):506-18. doi: 10.1016/j.biocel.2009.10.009. Epub 2009 Oct 29. Int J Biochem Cell Biol. 2010. PMID: 19837184 Review.
-
Mammalian Toll-like receptors: to immunity and beyond.Clin Exp Immunol. 2005 Jun;140(3):395-407. doi: 10.1111/j.1365-2249.2005.02801.x. Clin Exp Immunol. 2005. PMID: 15932500 Free PMC article. Review.
-
Evolution and integration of innate immune recognition systems: the Toll-like receptors.J Endotoxin Res. 2005;11(1):51-5. doi: 10.1179/096805105225006687. J Endotoxin Res. 2005. PMID: 15826379 Review.
-
Role of Toll-like receptor 4 in the initiation and progression of atherosclerotic disease.Eur J Clin Invest. 2004 May;34(5):328-34. doi: 10.1111/j.1365-2362.2004.01338.x. Eur J Clin Invest. 2004. PMID: 15147329 Review.
-
Innate immunity and toll-like receptors: clinical implications of basic science research.J Pediatr. 2004 Apr;144(4):421-9. doi: 10.1016/j.jpeds.2004.01.057. J Pediatr. 2004. PMID: 15069387 Review.
Cited by
-
The metabolic cofactor Coenzyme A enhances alternative macrophage activation via MyD88-linked signaling.bioRxiv [Preprint]. 2024 Mar 31:2024.03.28.587096. doi: 10.1101/2024.03.28.587096. bioRxiv. 2024. PMID: 38585887 Free PMC article. Preprint.
-
Glaucoma: from pathogenic mechanisms to retinal glial cell response to damage.Front Cell Neurosci. 2024 Jan 25;18:1354569. doi: 10.3389/fncel.2024.1354569. eCollection 2024. Front Cell Neurosci. 2024. PMID: 38333055 Free PMC article. Review.
-
The infant gut virome is associated with preschool asthma risk independently of bacteria.Nat Med. 2024 Jan;30(1):138-148. doi: 10.1038/s41591-023-02685-x. Epub 2023 Dec 15. Nat Med. 2024. PMID: 38102298
-
The 1926 novel, "One, no one, one hundred thousand", metaphorizes the potential danger when the immune system is exposed to a repetitive antigen stimulation.Front Immunol. 2023 Sep 13;14:1254853. doi: 10.3389/fimmu.2023.1254853. eCollection 2023. Front Immunol. 2023. PMID: 37771583 Free PMC article.
-
B cell-intrinsic TLR7 expression drives severe lupus in TLR9-deficient mice.JCI Insight. 2023 Aug 22;8(16):e172219. doi: 10.1172/jci.insight.172219. JCI Insight. 2023. PMID: 37606042 Free PMC article.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Medical