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Critical Reviews™ in Immunology
IF: 1.352 5-Year IF: 3.347 SJR: 0.657 SNIP: 0.55 CiteScore™: 2.19

ISSN Print: 1040-8401
ISSN Online: 2162-6472

Critical Reviews™ in Immunology

DOI: 10.1615/CritRevImmunol.v30.i1.40
pages 53-67

Induction of Cytokines and Chemokines by Toll-like Receptor Signaling: Strategies for Control of Infammation

Ahmet Zeytun
Biosciences Division, Los Alamos National Laboratory, Los Alamos, New Mexico, USA
Anu Chaudhary
Biosciences Division, Los Alamos National Laboratory, Los Alamos, New Mexico, USA
Paige Pardington
Biosciences Division, Los Alamos National Laboratory, Los Alamos, New Mexico, USA
R. Bruce Cary
Mesa Tech International, Inc. Santa Fe, New Mexico, USA
Goutam Gupta
Biosciences Division, Los Alamos National Laboratory, Los Alamos, NM 87545, USA

ABSTRACT

Recognition of the pathogen-associated molecular pattern (PAMP) by host Toll-like receptors (TLR) is an important component of the innate immune response for countering against invading viruses, bacteria, and fungi. Upon PAMP recognition, the TLR induces intracellular signaling cascades that involve adapter, signalosome, and transcription factor complexes and result in the production of both pro- and anti-inflammatory cytokines and chemokines. An inflammatory response for a short duration can be beneficial because it helps to clear the infectious agent. However, prolonged inflammation can be detrimental because it may cause host toxicity and tissue damage. Indeed, excessive production of inflammatory cytokines and chemokines via TLR pathways is often associated with many inflammatory and autoimmune diseases. Therefore, fine control of inflammation in the TLR pathway is highly desirable for effective host defense. In this article, we review intrinsic control mechanisms that include a balance between pro-inflammatory and anti-inflammatory cytokines and chemokines, production of host effectors, and regulation at the level of adapter, signalosome, and transcription factor complexes in the TLR pathways. We also discuss how understanding of the TLR signaling steps leads to the development of small-molecule drugs that can interfere with the formation of active adapter, signalosome, and adapter complexes.


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