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First Department of Internal Medicine, Kumamoto University School of Medicine, Kumamoto, Japan; and
Pulmonary Center, Boston University School of Medicine, Boston, MA 02118
Hypersensitivity pneumonitis (HP) is characterized by an
inflammatory lymphocytic alveolitis comprised of both CD8+
and CD4+ T cells. Animal models suggest that HP is
facilitated by overproduction of IFN-
, and that IL-10 ameliorates
severity of the disease, indicating a Th1-type response. To determine
whether a Th1 phenotype in HP also exists clinically, bronchoalveolar
lavage (BAL) and peripheral blood (PB) T cells were obtained from HP
individuals and analyzed for Th1 vs Th2 cytokine profiles. It was
determined that soluble OKT3-stimulated BAL T cells cocultured with
alveolar macrophages produced more IFN- and less IL-10 than PB T
cells cocultured with monocytes, but no difference was observed in IL-4
production. The monocytic cells did not account for this difference, as
CD80 and CD86 expressions were similar, and coculturing PB T cells with
alveolar macrophages resulted in no difference in IFN- production.
Similarly, there was no difference in IL-12 production between
stimulated BAL or PB T cells; however, addition of rIL-12 significantly
increased production of IFN- by BAL T cells, but not by PB T cells.
This effect was due to a difference in IL-12R expression. High affinity
IL-12R were only present in association with BAL T cells. These studies
indicate that clinical HP is characterized by a predominance of
IFN--producing T cells, perhaps resulting from a reduction in IL-10
production and an increase in high affinity IL-12R compared with blood
T cells.
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