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Biochim Biophys Acta. 2014 Nov;1843(11):2563-2582. doi: 10.1016/j.bbamcr.2014.05.014. Epub 2014 Jun 2.

Cytokines and chemokines: At the crossroads of cell signalling and inflammatory disease.

Author information

1
Interdisciplinary Biomedical Research Centre, School of Science and Technology, Nottingham Trent University, Clifton, Nottingham NG11 8NS, United Kingdom. Electronic address: mark.turner@ntu.ac.uk.
2
Leukocyte Biology Section, National Heart and Lung Institute, Imperial College, South Kensington, London SW7 2AZ, United Kingdom.
3
Interdisciplinary Biomedical Research Centre, School of Science and Technology, Nottingham Trent University, Clifton, Nottingham NG11 8NS, United Kingdom.
4
Blizard Institute, Barts and The London School of Medicine, Queen Mary University of London, Whitechapel, London E1 2AT, United Kingdom.

Abstract

Inflammation occurs as a result of exposure of tissues and organs to harmful stimuli such as microbial pathogens, irritants, or toxic cellular components. The primary physical manifestations of inflammation are redness, swelling, heat, pain, and loss of function to the affected area. These processes involve the major cells of the immune system, including monocytes, macrophages, neutrophils, basophils, dendritic cells, mast cells, T-cells, and B-cells. However, examination of a range of inflammatory lesions demonstrates the presence of specific leukocytes in any given lesion. That is, the inflammatory process is regulated in such a way as to ensure that the appropriate leukocytes are recruited. These events are in turn controlled by a host of extracellular molecular regulators, including members of the cytokine and chemokine families that mediate both immune cell recruitment and complex intracellular signalling control mechanisms that characterise inflammation. This review will focus on the role of the main cytokines, chemokines, and their receptors in the pathophysiology of auto-inflammatory disorders, pro-inflammatory disorders, and neurological disorders involving inflammation.

KEYWORDS:

Chemotaxis; Innate immunity; Interferon; Interleukin; Tumour necrosis factor

PMID:
24892271
DOI:
10.1016/j.bbamcr.2014.05.014
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