Both CD80 and CD86 co-stimulatory molecules regulate allergic pulmonary inflammation
| Autor: | G. T. De Sanctis, Lester Kobzik, S J Krinzman, Mohamed H. Sayegh, Carolyn E. Donovan, David L. Perkins, D A Mark, Peter S. Linsley, James A. Lederer, Patricia W. Finn |
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| Rok vydání: | 1998 |
| Předmět: |
Male
Allergy T-Lymphocytes Immunology chemical and pharmacologic phenomena Lymphocyte Activation medicine.disease_cause Immunoglobulin E Mice Th2 Cells Antigens CD Aldesleukin Eosinophilia Lymphocyte costimulation Respiratory Hypersensitivity medicine Animals Immunology and Allergy Lung Methacholine Chloride Interleukin 4 Mice Inbred BALB C Membrane Glycoproteins biology Chemistry hemic and immune systems General Medicine respiratory system medicine.disease Asthma Blockade Disease Models Animal Allergic response B7-1 Antigen biology.protein Cytokines B7-2 Antigen Bronchial Hyperreactivity medicine.symptom |
| Zdroj: | International Immunology. 10:1647-1655 |
| ISSN: | 1460-2377 |
| DOI: | 10.1093/intimm/10.11.1647 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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