BOTH CD80 AND CD86 COSTIMULATORY MOLECULES REGULATE ALLERGIC PULMONARY INFLAMMATION

We examined the roles of CD80 (B7-1) and CD86 (B7-2) in a model of all ergic pulmonary inflammation and airway hyper-responsiveness (AHR) by selectively inhibiting either CD80 or CD86. Inhibition of co-stimulati on 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-2R alpha (CD25) on CD4(+) T lymphocytes, decreased airway eosinophilia, lower serum IgE production and diminished AHR. Importantly, blockade o f CD80 and CD86 inhibited production of IL-4 and IL-2, and enhanced IF N-gamma production. Our observations support a role for both CD80- and CD86-mediated co-stimulation in development of allergic pulmonary inf lammation.