TITLE: Induction of myasthenia by immunization against muscle-specific kinase
AUTHOR CONTACT:
Kazuhiro Shigemoto
Ehime University School of Medicine, Ehime, Japan
Phone: 81-89-960-5278; Fax: 81-89-960-5279; E-mail: shigemot@m.ehime-u.ac.jp
View the PDF of this article at: https://www.the-jci.org/article.php?id=21545
IMMUNOLOGY
When not to scratch: loss of Itch causes airway inflammation
Immune system T cells are able to tell that the body's own "self" cells are not harmful pathogens like bacteria by the use of a process called tolerance. Although extensive studies have been performed to understand the induction of T cell tolerance, the link between a type of tolerance called Th2 tolerance and the control of allergic inflammation is not well understood. In a study appearing online on March 23 in advance of print publication in the April issue of the Journal of Clinical Investigation, Yun-Cai Liu and colleagues at the La Jolla Institute for Allergy and Immunology in California provide evidence that a cell signaling pathway called MEKK1/JNK converges with another pathway called the Itch-mediated protein modification pathway in the control of Th2 tolerance and allergic asthma. The authors used a MEKK1 mutant and JNK1-deficient mice to demonstrate that, like T cells deficient in an important immune protein called Itch, T cells from MEKK1 mutant or JNK1-deficient mice are also resistant to the induction of tolerance. The authors then linked Th2 tolerance to asthma by combining a tolerance protocol using high-dose soluble antigen with a mouse model of asthma. Although as
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Contact: Brooke Grindlinger
press_releases@the-jci.org
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Journal of Clinical Investigation
23-Mar-2006