Both CD80 and CD86 co-stimulatory molecules regulate allergic pulmonary inflammation.
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.
Mark
D A
DA
Pulmonary Division, Brigham and Women's Hospital, Boston, MA 02115, USA.
Donovan
C E
CE
De Sanctis
G T
GT
Krinzman
S J
SJ
Kobzik
L
L
Linsley
P S
PS
Sayegh
M H
MH
Lederer
J
J
Perkins
D L
DL
Finn
P W
PW
D000818:Animals; D015703:Antigens, CD / Q000276:immunology* / Q000378:metabolism; D001249:Asthma / Q000276:immunology* / Q000473:pathology; D018122:B7-1 Antigen / Q000276:immunology* / Q000378:metabolism; D051940:B7-2 Antigen; D016535:Bronchial Hyperreactivity; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D004802:Eosinophilia; D008168:Lung / Q000276:immunology / Q000473:pathology; D008213:Lymphocyte Activation; D008297:Male; D008562:Membrane Glycoproteins / Q000276:immunology* / Q000378:metabolism; D016210:Methacholine Chloride / Q000494:pharmacology; D051379:Mice; D008807:Mice, Inbred BALB C; D012130:Respiratory Hypersensitivity / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
D015703:Antigens, CD; D018122:B7-1 Antigen; D051940:B7-2 Antigen; C497965:Cd86 protein, mouse; D016207:Cytokines; D008562:Membrane Glycoproteins; D016210:Methacholine Chloride