Skip to main content
padlock icon - secure page this page is secure

Regulation of Innate Immunity Signaling and its Connection with Human Diseases

Buy Article:

$68.00 + tax (Refund Policy)

Human innate immunity can respond to diverse microbial products, as well as other substances such as heat shock proteins, taxol, and unsaturated fatty acids. Mediated largely by a family of Toll-like-receptors (TLR) and associated intracellular downstream signaling molecules, human innate immune response serves multiple functions ranging from providing the first line of defense to coordinating cellular growth as well as other cellular functions. To date, about 10 distinct human TLR receptors have been identified in the human genome. Biochemical studies and genetic analyses using transgenic mice have revealed specific ligands for several TLR receptors. TLR intracellular domains could then specifically recruit several adaptor proteins including MyD88, TIRAP / MAL, TRIF, and TOLLIP. These adaptor proteins subsequently associate with a family of interleukin-1 receptor-associated kinases (IRAK1, 2, M, and 4). Recruitments of numerous downstream signaling proteins lead to activation of a range of transcription factors such as NFκB, AP-1, and IRFs, which are responsible for specific gene transcriptions.

Human innate immunity is manifested in diverse cells and tissues. Well-coordinated innate immunity signaling enables human cells and tissues to properly respond to various substances. Improper regulations of such event have been shown to cause various diseases including asthma, atherosclerosis, and cancer. TLR receptors as well as other intracellular signaling proteins can potentially serve as therapeutic targets for numerous human diseases. This review will discuss at the molecular level, regulation of innate immunity signaling as well as its intricate connection with human diseases.
No References
No Citations
No Supplementary Data
No Article Media
No Metrics

Keywords: cell growth; innate immunity; signaling; toll-like receptors

Document Type: Review Article

Affiliations: Department of Medicine, Wake Forest University School of Medicine, Winston Salem, NC27157, USA;

Publication date: March 1, 2004

  • Access Key
  • Free content
  • Partial Free content
  • New content
  • Open access content
  • Partial Open access content
  • Subscribed content
  • Partial Subscribed content
  • Free trial content
Cookie Policy
Cookie Policy
Ingenta Connect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more