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International Immunology, Vol 10, 1647-1655, Copyright © 1998 by Oxford University Press

ARTICLES

Both CD80 and CD86 co-stimulatory molecules regulate allergic pulmonary inflammation

DA Mark, CE Donovan, GT De Sanctis, SJ Krinzman, L Kobzik, PS Linsley, MH Sayegh, J Lederer, DL Perkins and PW Finn
Pulmonary Division, Brigham and Women's Hospital, Boston, MA 02115, USA.

We examined the roles of CD80 (B7-1) and CD86 (B7-2) in a model of allergic pulmonary inflammation and airway hyper-responsiveness (AHR) by selectively inhibiting either CD80 or CD86. Inhibition of co- stimulation by either CD80 or CD86 affected multiple parameters of the allergic response. Specifically, blockade of either CD80 or CD86 in ovalbumin-sensitized and challenged mice resulted in reduced expression of IL-2Ralpha (CD25) on CD4+ T lymphocytes, decreased airway eosinophilia, lower serum IgE production and diminished AHR. Importantly, blockade of CD80 and CD86 inhibited production of IL-4 and IL-2, and enhanced IFN-gamma production. Our observations support a role for both CD80- and CD86-mediated co-stimulation in development of allergic pulmonary inflammation.
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