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

Int Immunol. 1998 Nov;10(11):1647-55. doi: 10.1093/intimm/10.11.1647.


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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antigens, CD / immunology*
  • Antigens, CD / metabolism
  • Asthma / immunology*
  • Asthma / pathology
  • B7-1 Antigen / immunology*
  • B7-1 Antigen / metabolism
  • B7-2 Antigen
  • Bronchial Hyperreactivity
  • Cytokines / metabolism
  • Disease Models, Animal
  • Eosinophilia
  • Lung / immunology
  • Lung / pathology
  • Lymphocyte Activation
  • Male
  • Membrane Glycoproteins / immunology*
  • Membrane Glycoproteins / metabolism
  • Methacholine Chloride / pharmacology
  • Mice
  • Mice, Inbred BALB C
  • Respiratory Hypersensitivity / immunology*
  • T-Lymphocytes / immunology
  • Th2 Cells / immunology


  • Antigens, CD
  • B7-1 Antigen
  • B7-2 Antigen
  • Cd86 protein, mouse
  • Cytokines
  • Membrane Glycoproteins
  • Methacholine Chloride