Increased expression of class II antigens of the major histocompatibility complex on alveolar macrophages and alveolar type II cells and interleukin-1 (IL-1) secretion from alveolar macrophages in an animal model of silicosis.

Silicosis is a chronic progressive granulomatous and fibrotic lung disease caused by inhaled silica. Although the causative agent is known, the pathogenesis, especially the immunologic response, is not well understood. We examined two important components of cell-mediated immune responses in the lungs of rats with silica-induced lung disease, i.

Class II molecules on rat alveolar type II epithelial cells.

Class II (Ia) molecules of the major histocompatibility complex are important in the presentation of antigen to T cells and in the regulation of the immune response. Recent studies have suggested that many epithelial cell types can express class II molecules. We examined rat alveolar type II epithelial cells, a cell which can synthesize and secrete pulmonary surface-active material, for the expression of class II antigens.

The isolation and characterization of enriched microvascular endothelial cells from mouse adipose tissue. The induction of class II molecules of the major histocompatibility complex (MHC) by interferon-gamma (IFN-gamma).

Collagenase digestion and selective filtration have been used to establish primary cultures from mouse omentum of cells enriched for microvascular endothelium. In culture these cells exhibit a cobblestone morphology characteristic of endothelial cells, metabolize an acetylated low-density lipoprotein, and exhibit trace levels of angiotensin-converting enzyme activity. In primary cultures, the cells are negative for class II molecules (Ia) of the major histocompatibility complex (MHC) but can be induced to express these molecules by exposure to a supernatant from concanavalin A (ConA)-treated rat spleen cells or by recombinant interferon-gamma (rIFN-gamma).