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Researchers reveal lung's unique innate immune system

ways, such as a new flu strain or bioterrorist agents," said Raz.

The researchers' data outlines a complex circuit in which the alveolar macrophages circumvent the inhibition by TGFb for brief period of time, in order perform their immune task. This is accomplished through regulation of TGFb activity by a set of cell surface receptors, proteins called integrins.

This regulation allows the alveolar macrophages to take on their "killer" function ?the ability of macrophages to engulf invading microorganisms ?but only for a very limited period of time. The mediating role of TGFb, briefly inactivated by the integrin, is then restored by one of the lung's own enzymes, the MMP9.

"Basically, the macrophages wake up for a while, but the system's own enzymes activate the inhibitor that puts them back to sleep," said Kenji Takabayshi, Ph.D., first author of the study.

Other contributors to this paper include Maripat Corr, Tomoko Hayashi, Vanessa Redecke, Lucinda Beck, and Donald Guiney of the Department of Medicine at UCSD School of Medicine; and Dean Sheppard, Lung Biology Center, University of California, San Francisco.


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Source:University of California - San Diego


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