期刊
IMMUNOLOGIC RESEARCH
卷 34, 期 1, 页码 33-48出版社
HUMANA PRESS INC
DOI: 10.1385/IR:34:1:33
关键词
toll-like receptor (TLR); phosphoinositide 3-kinase (PI3K); Rho GTPase
类别
资金
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [T32HL007195] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI035947] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [P01GM037696] Funding Source: NIH RePORTER
- NHLBI NIH HHS [5T32 HL07195] Funding Source: Medline
- NIAID NIH HHS [5R01 AI035947] Funding Source: Medline
- NIGMS NIH HHS [1P01 GM037696] Funding Source: Medline
Toll-like receptors (TLRs) play a crucial role in the innate immune system as a first line of defense against pathogens. TLR activation In phagocytes produces pro-inflammatory cytokines and chemokines that contribute directly to elimination of infectious agents and activation of adaptive immune responses. However, a Sustained inflammatory response can result in tissue damage and generalized sepsis. This review summarizes the complex and sometimes conflicting links of TLR signaling with two important regulators of immune cells functions: phosphoinositide 3-kinases (PI3Ks) and small GTPases of the Rho family. A unified model of hierarchical organization of these signaling participants is still premature. given that the tools for delineating how control of TLR-mediated pathways is achieved are just emerging. Critical progress in our understanding of spatial-temporal propagation of TLR signaling will certainly be provided in the near future by pharmacoloaical targeting of PI3KS using recently characterized, second-generation PI3K inhibitors in combination with gene-targeting strategies for PI3K Subunits and Rho GTPases targeted to the murine myeloid compartment.
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