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Hapten‐immune pulmonary interstitial fibrosis (HIPIF) in mice requires both CD4 + and CD8 + T lymphocytes
Author(s) -
Hu Hui,
SteinStreilein Joan
Publication year - 1993
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.54.5.414
Subject(s) - immune system , immunology , pulmonary fibrosis , biology , fibrosis , antigen , hydroxyproline , hapten , inflammation , cd8 , adoptive cell transfer , t cell , pathology , medicine , endocrinology
We present a description and analysis of a mouse model for pulmonary interstitial fibrosis that is induced by a specific immune response to a small reactive chemical group called trinitrophenyl. We describe the model, and then we examine the cellular mechanism for the induction of the fibrosis. The specific increase in hydroxyproline reached a peak by day 7 and persisted through day 28 in all animals that were sensitized to and challenged with the hapten. Distinct patterns of fibrosis that were seen histologically correlated with antigenic pretreatment and were dependent on T lymphocytes. We also report that the inflammatory and fibrotic responses could be adoptively transferred with immune lymphocytes but not with immune serum. In vivo administration of anti‐CD4 and anti‐CD8 monoclonal antibodies to sensitized mice prevented the development of immune‐ mediated lung inflammation and was effective in reducing hydroxyproline deposition. We conclude that (activated) T lymphocytes contribute to the pathogenesis of pulmonary fibrotic diseases. The possibility arises that haptens in the environment may promote sensitization of individuals via their skin or lungs and cell‐mediated immune responses to haptenated antigens within the lung may promote pulmonary fibrosis.