Skip to main content Accessibility help
×
Hostname: page-component-78c5997874-s2hrs Total loading time: 0 Render date: 2024-11-05T16:45:22.433Z Has data issue: false hasContentIssue false

13 - Cytokines and Chemokines in Inflammation

from PART III - CHEMICAL MEDIATORS

Published online by Cambridge University Press:  05 April 2014

Dennis M. Lindell
Affiliation:
University of Washington
Nicholas W. Lukacs
Affiliation:
Research Faculty Ann Arbor, Michigan
Charles N. Serhan
Affiliation:
Harvard Medical School
Peter A. Ward
Affiliation:
University of Michigan, Ann Arbor
Derek W. Gilroy
Affiliation:
University College London
Get access

Summary

SUMMARY

Mediators produced during inflammatory/immune responses dictate the type of response, as well as its magnitude (“quality and quantity”). The profile of cytokines and chemokines produced are responsible for the cell-to-cell communication that facilitates initial recognition of infection or damage. These signals, in turn, communicate with primary lymphoid tissues (the thymus and bone marrow) to mobilize inflammatory cells to the bloodstream. At the tissue site, chemokines and cytokines orchestrate leukocyte adhesion to vascular endothelium, extravasation, and localization of leukocytes at the site of inflammation. Recruitment of leukocyte populations into inflamed tissues is initiated by cytokine-induced expression of adhesion molecules on vascular endothelium. These adhesion molecules play an essential role in capturing and tethering circulating leukocytes from the bloodstream. Chemokines promote the tight adherence of leukocytes to activated endothelium, as well as direct the extravasation of cells into inflamed tissue. Cytokines and chemokines further coordinate the response of inflammatory effector cells as they arrive in inflamed tissues. The sequential activation and cellular recruitment cascades mediated by cytokines and chemokines are essential for successful resolution of infection or other tissue damage. However, overproduction or dysregulation of these inflammatory mediators can also lead to destructive, pathological consequences. This chapter will examine the role played by cytokines and chemokines in the initiation, amplification, and shaping of inflammatory responses.

Type
Chapter
Information
Publisher: Cambridge University Press
Print publication year: 2010

Access options

Get access to the full version of this content by using one of the access options below. (Log in options will check for institutional or personal access. Content may require purchase if you do not have access.)

References

1. Shuai, K., and Liu, B. 2003. Regulation of JAK-STAT signaling in the immune system. Nat Rev Immunol 3(11):900–911.CrossRefGoogle ScholarPubMed
2. Chang, F., Steelman, L.S., Lee, J.T., et al. 2003. Signal transduction mediated by the Ras/Raf/MEK/ERK pathway from cytokine receptors to transcription factors: potential targeting for therapeutic intervention. Leukemia 17(7):1263–1293.CrossRefGoogle ScholarPubMed
3. Tamura, M., Gu, J., Matsumoto, K., Aota, S., Parsons, R., and Yamada, K.M. 1998. Inhibition of cell migration, spreading, and focal adhesions by tumor suppressor PTEN. Science 280(5369):1614–1617.CrossRefGoogle ScholarPubMed
4. Janeway, C.A. Jr. and Medzhitov, R. 2002. Innate immune recognition. Annu Rev Immunol 20:197–216.CrossRefGoogle ScholarPubMed
5. Trinchieri, G., and Sher, A. 2007. Cooperation of Tolllike receptor signals in innate immune defense. Nat Rev Immunol 7(3):179–190.CrossRefGoogle Scholar
6. Mosmann, T.R., and Coffman, R.L. 1989. TH1 and TH2 cells: different patterns of lymphokine secretion lead to different functional properties. Annu Rev Immunol 7:145–173.CrossRefGoogle ScholarPubMed
7. Weaver, C.T., Harrington, L.E., Mangan, P.R., Gavrieli, M., and Murphy, K.M. 2006. Th17: an effector CD4 T cell lineage with regulatory T cell ties. Immunity 24(6):677–688.CrossRefGoogle ScholarPubMed
8. Schubert, L.A., Jeffery, E., Zhang, Y., Ramsdell, F., and Ziegler, S.F. 2001. Scurfin (FOXP3) acts as a repressor of transcription and regulates T cell activation. J Biol Chem 276(40):37672–37679.CrossRefGoogle ScholarPubMed
9. Hori, S., Nomura, T., and Sakaguchi, S. 2003. Control of regulatory T cell development by the transcription factor Foxp3. Science 299(5609):1057–1061.CrossRefGoogle ScholarPubMed
10. Sallusto, F., and Lanzavecchia, A. 2000. Understanding dendritic cell and T-lymphocyte traffic through the analysis of chemokine receptor expression. Immunol Rev 177:134–140.CrossRefGoogle ScholarPubMed
11. Ward, S.G., and Marelli-Berg, F.M. 2009. Mechanisms of chemokine and antigen-dependent T-lymphocyte navigation. Biochem J 418(1):13–27.CrossRefGoogle ScholarPubMed
12. Cyster, J.G. 2003. Lymphoid organ development and cell migration. Immunol Rev 195:5–14.CrossRefGoogle ScholarPubMed
13. Li, M.O., Wan, Y.Y., Sanjabi, S., Robertson, A.K., and Flavell, R.A. 2006. Transforming growth factor-beta regulation of immune responses. Annu Rev Immunol 24:99–146.CrossRefGoogle ScholarPubMed
14. Border, W.A., and Ruoslahti, E. 1992. Transforming growth factor-beta in disease: the dark side of tissue repair. J Clin Invest 90(1):1–7.CrossRefGoogle ScholarPubMed

Save book to Kindle

To save this book to your Kindle, first ensure [email protected] is added to your Approved Personal Document E-mail List under your Personal Document Settings on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part of your Kindle email address below. Find out more about saving to your Kindle.

Note you can select to save to either the @free.kindle.com or @kindle.com variations. ‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi. ‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.

Find out more about the Kindle Personal Document Service.

Available formats
×

Save book to Dropbox

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Dropbox.

Available formats
×

Save book to Google Drive

To save content items to your account, please confirm that you agree to abide by our usage policies. If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account. Find out more about saving content to Google Drive.

Available formats
×