Badolato / Sozzani Lymphocyte Trafficking in Health and Disease

1. Auflage 2006
ISBN: 978-3-7643-7442-6
Verlag: Springer
Format: PDF
Kopierschutz: 1 - PDF Watermark

E-Book, Englisch, 253 Seiten, eBook

Reihe: Progress in Inflammation Research

Since the discovery of chemokines and of chemokine receptors it has become evident that expression of chemokines at the site of inflammation may regulate the composition of cellular infiltrate, thereby directing the type of immune response. Recently, the molecular characterization of inherited disorders of immune system, (e.g., Wiskott-Aldrich syndrome, WHIM syndrome, leukocyte adhesion deficiency), which are characterized by cytoskeleton/adhesion defects or by altered response of chemokine receptors has contributed to clarifying the key players of immune response in normal physiology and in disease. This book, which deals with the description of the role of chemokines in immune response and underlines potential targets of therapeutical intervention, offers a series of contributions of the most challenging aspects of lymphocyte migration in homeostasis and in disease.

Zielgruppe

Research

Autoren/Hrsg.

Badolato, Raffaele

Sozzani, Silvano

Inhaltsverzeichnis

Lymphocyte trafficking: from immunology paradigms to disease mechanisms.- Lymphocyte trafficking: from immunology paradigms to disease mechanisms.- Physiology of lymphocyte trafficking.- Biology of chemokines.- Lymphocyte-endothelial cell interaction.- Chemokine receptor expression in effector and memory T cell subsets.- Migration of dendritic cell subsets.- Migration of NK cells.- Immunopathology of lymphocyte trafficking.- Lymphocyte trafficking and chemokine receptors during pulmonary disease.- Lymphocyte migration to the brain.- Lymphocyte migration to the kidney.- Leukocyte migration to pancreatic islets: a critical step in the pathogenesis of type 1 diabetes.- Controlling leukocyte trafficking in disease.- Inherited disorders of lymphocyte trafficking.- Leukocyte adhesion deficiency.- Wiskott-Aldrich syndrome as a model of cytoskeleton defects.- From CXCR4 mutations to WHIM syndrome.