Expression of B7–1, B7–2, and Interleukin–12 in Anti–Fas Antibody–Induced Pulmonary Fibrosis in Mice

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Abstract
Background: We have previously reported that the inhalation of anti–Fas antibody induced pulmonary fibrosis in mice. To induce an effective immune response, antigen–presenting cells have to not only present antigenic peptide with MHC molecules to T lymphocytes, but also express B7 costimulating molecules. The purpose of this study is to investigate whether B7 family costimulating molecules and interleukin–12 (IL–12), which primarily promote cellular immunity, are associated with anti–Fas antibody–induced pulmonary fibrosis. Methods: We examined the expression of B7–1, B7–2, and IL–12 using the revese transcription–polymerase chain reaction (RT–PCR), RT–in situ PCR, and immunohistochemistry. Results: We observed the upregulation of B7–1, B7–2, and IL–12 p40 mRNA after anti–Fas antibody inhalation. B7–2 and IL–12 p40 mRNA appeared to be expressed in mononuclear cells, while B7–1 mRNA and protein were expressed in bronchiolar epithelial cells as well as macrophages. Conclusion: These findings indicate that the T–cell–mediated immune response in this model involved the upregulation of B7–1, B7–2, and IL–12, and that the aberrant expression of B7–1 in bronchiolar epithelial cells may induce autoreactive T cell proliferation against themselves.