Toll-like receptors in the pathogenesis of inflammatory diseases

Jun K. Lee; Daniel H. Hwang; Joo Y. Lee

doi:10.1080/17471060701200410

Toll-like receptors in the pathogenesis of inflammatory diseases

Jun K. Lee
, Daniel H. Hwang
, Joo Y. Lee

Gwangju Institute of Science and Technology
University of California at Davis

Research output: Contribution to journal › Review article › peer-review

1 Scopus citations

Abstract

Toll-like receptors (TLRs) are newly established immune receptors which are critical for host defense through the activation of both innate and adaptive immunity. TLRs can recognize molecules with both microbial and non-microbial origins. Emerging evidence now suggests that TLRs are implicated in the pathogenesis of many chronic diseases, including sepsis, atherosclerosis, ischemia/reperfusion-mediated organ dysfunction, rheumatoid arthritis, diabetes, and cancer. Therefore, an understanding of the role of TLRs in inducing chronic inflammation will provide new insights to help design an effective intervention strategy for inflammatory diseases.

Original language	English
Pages (from-to)	119-128
Number of pages	10
Journal	Journal of Organ Dysfunction
Volume	5
Issue number	2
DOIs	https://doi.org/10.1080/17471060701200410
State	Published - 2009

Bibliographical note

Funding Information:
This work was supported by grants from the Korea Health 21 R&D Project, Ministry of Health & Welfare, South Korea (No. A060501) and the Korea Research Foundation funded by the Korean Government (MOEHRD, Basic Research Promotion Fund; No. KRF-2006-331-E00425) to Joo Y. Lee, and by grants DK064007, DK41868 and CA75613 from the National Institutes of Health, grant (2001-35200-10721) from the United States Department of Agriculture (USDA), grant (01A095Rev) from the American Institute for Cancer Research, and program funds from the Western Human Nutrition Research Center/ARS/USDA to Daniel H. Hwang.

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

Immunity
Inflammation
Myeloid differentiation factor 88
TRIF
Toll-like receptors

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10.1080/17471060701200410

Cite this

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title = "Toll-like receptors in the pathogenesis of inflammatory diseases",

abstract = "Toll-like receptors (TLRs) are newly established immune receptors which are critical for host defense through the activation of both innate and adaptive immunity. TLRs can recognize molecules with both microbial and non-microbial origins. Emerging evidence now suggests that TLRs are implicated in the pathogenesis of many chronic diseases, including sepsis, atherosclerosis, ischemia/reperfusion-mediated organ dysfunction, rheumatoid arthritis, diabetes, and cancer. Therefore, an understanding of the role of TLRs in inducing chronic inflammation will provide new insights to help design an effective intervention strategy for inflammatory diseases.",

keywords = "Immunity, Inflammation, Myeloid differentiation factor 88, TRIF, Toll-like receptors",

author = "Lee, \{Jun K.\} and Hwang, \{Daniel H.\} and Lee, \{Joo Y.\}",

note = "Funding Information: This work was supported by grants from the Korea Health 21 R\&D Project, Ministry of Health \& Welfare, South Korea (No. A060501) and the Korea Research Foundation funded by the Korean Government (MOEHRD, Basic Research Promotion Fund; No. KRF-2006-331-E00425) to Joo Y. Lee, and by grants DK064007, DK41868 and CA75613 from the National Institutes of Health, grant (2001-35200-10721) from the United States Department of Agriculture (USDA), grant (01A095Rev) from the American Institute for Cancer Research, and program funds from the Western Human Nutrition Research Center/ARS/USDA to Daniel H. Hwang.",

year = "2009",

doi = "10.1080/17471060701200410",

language = "English",

volume = "5",

pages = "119--128",

journal = "Journal of Organ Dysfunction",

issn = "1747-1060",

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number = "2",

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TY - JOUR

T1 - Toll-like receptors in the pathogenesis of inflammatory diseases

AU - Lee, Jun K.

AU - Hwang, Daniel H.

AU - Lee, Joo Y.

N1 - Funding Information: This work was supported by grants from the Korea Health 21 R&D Project, Ministry of Health & Welfare, South Korea (No. A060501) and the Korea Research Foundation funded by the Korean Government (MOEHRD, Basic Research Promotion Fund; No. KRF-2006-331-E00425) to Joo Y. Lee, and by grants DK064007, DK41868 and CA75613 from the National Institutes of Health, grant (2001-35200-10721) from the United States Department of Agriculture (USDA), grant (01A095Rev) from the American Institute for Cancer Research, and program funds from the Western Human Nutrition Research Center/ARS/USDA to Daniel H. Hwang.

PY - 2009

Y1 - 2009

N2 - Toll-like receptors (TLRs) are newly established immune receptors which are critical for host defense through the activation of both innate and adaptive immunity. TLRs can recognize molecules with both microbial and non-microbial origins. Emerging evidence now suggests that TLRs are implicated in the pathogenesis of many chronic diseases, including sepsis, atherosclerosis, ischemia/reperfusion-mediated organ dysfunction, rheumatoid arthritis, diabetes, and cancer. Therefore, an understanding of the role of TLRs in inducing chronic inflammation will provide new insights to help design an effective intervention strategy for inflammatory diseases.

AB - Toll-like receptors (TLRs) are newly established immune receptors which are critical for host defense through the activation of both innate and adaptive immunity. TLRs can recognize molecules with both microbial and non-microbial origins. Emerging evidence now suggests that TLRs are implicated in the pathogenesis of many chronic diseases, including sepsis, atherosclerosis, ischemia/reperfusion-mediated organ dysfunction, rheumatoid arthritis, diabetes, and cancer. Therefore, an understanding of the role of TLRs in inducing chronic inflammation will provide new insights to help design an effective intervention strategy for inflammatory diseases.

KW - Immunity

KW - Inflammation

KW - Myeloid differentiation factor 88

KW - TRIF

KW - Toll-like receptors

UR - https://www.scopus.com/pages/publications/70849121897

U2 - 10.1080/17471060701200410

DO - 10.1080/17471060701200410

M3 - Review article

AN - SCOPUS:70849121897

SN - 1747-1060

VL - 5

SP - 119

EP - 128

JO - Journal of Organ Dysfunction

JF - Journal of Organ Dysfunction

IS - 2

ER -

Toll-like receptors in the pathogenesis of inflammatory diseases

Abstract

Bibliographical note

UN SDGs

Keywords

Access to Document

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