𝔖 Bobbio Scriptorium
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III. Chemokines and other mediators, 8. Chemokines and their receptors in cell-mediated immune responses in the lung

✍ Scribed by Akihiro Matsukawa; Nicholas W. Lukacs; Cory M. Hogaboam; Stephen W. Chensue; Steven L. Kunkel


Publisher
John Wiley and Sons
Year
2001
Tongue
English
Weight
222 KB
Volume
53
Category
Article
ISSN
1059-910X

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✦ Synopsis


Abstract

Chemokines constitute a large family of chemotactic cytokines that belong to a super‐gene family of 8–10 kDa proteins. The chemokines are considered to be primarily beneficial in host defense against invading pathogens. However, the reactions induced by chemokines can be occasionally excessive, resulting in a harmful response to the host. Recent studies in chemokine biology have elucidated that chemokines are involved in the initiation, development, and maintenance of numbers of diseases including lung diseases. In addition to its chemotactic activity, evidence suggests that chemokines can modify the outcome of the cell‐mediated immune responses by altering the Th1/Th2 cytokine profile. Chemokines are also capable of dictating the direction of specific immune responses. Chemokine action is mediated by a large super‐family of G‐protein coupled receptors, and the receptors are preferentially expressed on Th1/Th2 cells. Certain chemokine receptors are constitutively expressed in immune surveying cells such as dendritic cells and naive T cells. The corresponding chemokines are present in normal lymphoid tissues, suggesting a role of chemokines/receptors in cell homing and cell‐cell communication in lymphoid tissue that can be an initial step for immune recognition. Thus, comprehension of the chemokine biology in immune responses appears to be fundamental for understanding the pathogenesis of T cell–mediated immune responses. The following review will highlight the current insight into the role of chemokines and their receptors in the cell‐mediated immune response, with a special focus on lung diseases. Microsc. Res. Tech. 53:298–306, 2001. © 2001 Wiley‐Liss, Inc.


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