Toll-like Receptors in Host Defense and Immune Disorders

被引：0

作者：

Lee, Joo Y. ^{[1
]}

机构：

[1] Gwangju Inst Sci & Technol, Dept Life Sci, Gwangju 500712, South Korea

来源：

TOXICOLOGICAL RESEARCH | 2007年 / 23卷 / 02期

关键词：

Toll-like receptor; Immune dysfunction; Inflammation; Infection; Innate and Adaptive immunity;

D O I：

10.5487/TR.2007.23.2.097

中图分类号：

R99 [毒物学（毒理学）];

学科分类号：

100405 ;

摘要：

Toll-like receptors (TLRs) play a crucial role in initiating and regulating innate and adaptive immune responses by detecting invading microbial pathogens. TLRs can also respond to non-microbial molecules derived from damaged tissue. Accumulating evidence suggests that deregulation of TLRs results in the dysfunction of immune system and ultimately increases the risk of many immune and inflammatory diseases including infectious diseases, allergy, and autoimmune diseases. Therefore, understanding how the immune system is controlled by TLRs will provide new insight to find the way to prevent or treat infectious diseases and immune disorders.

引用

页码：97 / 105

页数：9

共 73 条

[1] Human toll-like receptor 4 mutations but not CD14 polymorphisms are associated with an increased risk of gram-negative infections [J].

Agnese, DM ;

Calvano, JE ;

Hahm, SJ ;

Coyle, SM ;

Corbett, SA ;

Calvano, SE ;

Lowry, SF .

JOURNAL OF INFECTIOUS DISEASES, 2002, 186 (10) :1522-1525

[2] Recognition of double-stranded RNA and activation of NF-κB by Toll-like receptor 3 [J].

Alexopoulou, L ;

Holt, AC ;

Medzhitov, R ;

Flavell, RA .

NATURE, 2001, 413 (6857) :732-738

[3] Toll-like receptor 2 Arg677Trp polymorphism is associated with susceptibility to tuberculosis in Tunisian patients [J].

Ben-Ali, M ;

Barbouche, MR ;

Bousnina, S ;

Chabbou, A ;

Dellagi, K .

CLINICAL AND DIAGNOSTIC LABORATORY IMMUNOLOGY, 2004, 11 (03) :625-626

[4] Inferences, questions and possibilities in toll-like receptor signalling [J].

Beutler, B .

NATURE, 2004, 430 (6996) :257-263

[5] Cutting edge: A toll-like receptor 2 polymorphism that is associated with lepromatous leprosy is unable to mediate mycobacterial signaling [J].

Bochud, PY ;

Hawn, TR ;

Aderem, A .

JOURNAL OF IMMUNOLOGY, 2003, 170 (07) :3451-3454

[6] Environmental exposure to endotoxin and its relation to asthma in school-age children [J].

Braun-Fahrländer, C ;

Riedler, J ;

Herz, U ;

Eder, W ;

Waser, M ;

Grize, L ;

Maisch, S ;

Carr, D ;

Gerlach, F ;

Bufe, A ;

Lauener, RP ;

Schierl, R ;

Renz, H ;

Nowak, D ;

von Mutius, E .

NEW ENGLAND JOURNAL OF MEDICINE, 2002, 347 (12) :869-877

[7] IFN-α/β receptor interactions to biologic outcomes:: Understanding the circuitry [J].

Brierley, MM ;

Fish, EN .

JOURNAL OF INTERFERON AND CYTOKINE RESEARCH, 2002, 22 (08) :835-845

[8] Synthetic toll-like receptor 4 agonists stimulate innate resistance to infectious challenge [J].

Cluff, CW ;

Baldridge, JR ;

Stöver, AG ;

Evans, JT ;

Johnson, DA ;

Lacy, MJ ;

Clawson, VG ;

Yorgensen, VM ;

Johnson, CL ;

Livesay, MT ;

Hershberg, RM ;

Persing, DH .

INFECTION AND IMMUNITY, 2005, 73 (05) :3044-3052

[9] Poxvirus protein N1L targets the I-κB kinase complex, inhibits signaling to NF-κB by the tumor necrosis factor superfamily of receptors, and inhibits NF-κB and IRF3 signaling by Toll-like receptors [J].

DiPerna, G ;

Stack, J ;

Bowie, AG ;

Boyd, A ;

Kotwal, G ;

Zhang, ZN ;

Arvikar, S ;

Latz, E ;

Fitzgerald, KA ;

Marshall, WL .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2004, 279 (35) :36570-36578

[10] Toll-like receptor 2-deficient mice are highly susceptible to Streptococcus pneumoniae meningitis because of reduced bacterial clearing and enhanced inflammation [J].

Echchannaoui, H ;

Frei, K ;

Schnell, C ;

Leib, SL ;

Zimmerli, W ;

Landmann, R .

JOURNAL OF INFECTIOUS DISEASES, 2002, 186 (06) :798-806

← 1 2 3 4 5 6 7 8 →