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Am. J. Respir. Cell Mol. Biol., Volume 22, Number 3, March, 2000 265-271

B7-1 (CD80) and B7-2 (CD86) Have Complementary Roles in Mediating Allergic Pulmonary Inflammation and Airway Hyperresponsiveness

David A. Mark, Carolyn E. Donovan, George T. De Sanctis, Hong Zhen He, Manuela Cernadas, Lester Kobzik, David L. Perkins, Arlene Sharpe, and Patricia W. Finn

Pulmonary Division, Renal Division, and Department of Pathology, Brigham and Women's Hospital; and Departments of Medicine and Pathology, Harvard Medical School, Boston, Massachusetts

We examined the roles of B7-1 (CD80) and B7-2 (CD86) in a model of allergic pulmonary inflammation and airway hyperresponsiveness (AHR) by using mice with germline deletions of the B7-1 and/or B7-2 molecules. Multiple parameters of the allergic response were affected to varying degrees by the absence of B7-1 and/or B7-2. Mice lacking both B7-1 and B7-2 had no elevation of serum immunoglobulin E, lack of airway eosinophilia, and no AHR. These same disease parameters were also reduced in mice lacking either B7-1 or B7-2. Lack of B7-1 and/or B7-2 resulted in an increase in T-helper 1 cytokine production. Our observations suggest that whereas B7-2 is quantitatively more significant in the induction of this response, B7-1 and B7-2 may have complementary roles in mediating the development of allergic pulmonary inflammation.




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