Signaling Molecules Affecting Immune Response

Paul J. Hertzog, Jennifer E. Fenner, Ashley Mansell

Research output: Chapter in Book/Report/Conference proceedingChapter (Book)Researchpeer-review

Abstract

This chapter presents broad concepts referenced to recent reviews and examples of signaling molecules that are relevant to each branch of the immune response to different stimuli and examples that are important to human disease. Specifically, the chapter discusses toll-like receptors (TLR) signaling molecules and their response to pathogens. Signal transducing molecules are the intracellular messengers necessary for generating the immune response. Immune responses are driven by stimulation of immune cells from pathogens, antigens, cytokines, and factors affecting growth or survival. These stimuli trigger responses via cellular receptors. Signals are transduced by protein adapters and enzymes leading to modification, cleavage, or release of proteins, activation and nuclear translocation of transcription factors, and up or down modulation of expression of genes whose products are responsible for generating biological responses. Signal transducing molecules are often important points of regulation (positive and negative). Mutations in their genes can lead to human immunodeficiency disease and they are targeted by infectious agents for the purpose of subverting the host immune response. Determination of the levels of activation or translocation of signal transducing molecules such as STATs (signal transducers and activators of transcription) can be a valuable indicator of cell/status/ function and therefore makes an important contribution to measuring immunity. The STATs are predominantly involved in pathways that utilize receptor subunits lacking in intrinsic kinase activity.

Original languageEnglish
Title of host publicationMeasuring Immunity
Subtitle of host publicationBasic Biology and Clinical Assessment
PublisherAcademic Press
Pages62-79
Number of pages18
ISBN (Print)9780124559004
DOIs
Publication statusPublished - 1 Dec 2005

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