Antigen presentation by liver sinusoidal lining cells after antigen exposure in vivo.

The ability of liver sinusoidal lining cells (LSLC), a mixture of Kupffer cells and endothelial cells, to function as antigen-presenting cells (APC) was examined. Guinea pig LSLC were found to present antigen in vitro, albeit somewhat less effectively than a reference population of peritoneal exudate macrophages. The difference in APC function could not be explained by a deficiency of interleukin 1 (IL 1), as LSLC secreted IL 1 and expressed membrane-bound thymocyte stimulatory activity.

Liver sinusoidal lining cells express class II major histocompatibility antigens but are poor stimulators of fresh allogeneic T lymphocytes.

Guinea pig liver sinusoidal lining cells (LSLC), a mixture of Kupffer cells (KC) and sinusoidal endothelial cells (EC), were examined for their capacity to function as antigen-presenting cells (APC). LSLC were extremely poor stimulators of freshly isolated allogeneic T lymphocytes even though a large number of them expressed class II major histocompatibility complex (MHC) antigens (Ia). This deficiency could not be explained by a lack of soluble factor production by LSLC, because an interleukin 1-containing macrophage (M phi) supernatant could not restore the capacity of LSLC to stimulate allogeneic T cells.

Dissection of the functions of antigen-presenting cells in the induction of T cell activation.

The functions of antigen-presenting cells (APC) in the initiation of T cell activation was examined by culturing antigen-bearing guinea pig macrophages (M phi) with T cells obtained from antigen-primed animals. Although such antigen-bearing M phi stimulated primed syngeneic T cell DNA synthesis, as assessed by tritiated thymidine incorporation, paraformaldehyde fixation (0.15% for 1 min at 37 degrees C) abolished this capacity.

Immunologic function of endothelial cells: guinea pig aortic endothelial cells support mitogen-induced T lymphocyte activation, but do not function as antigen-presenting cells.

The possibility that vascular endothelial cells (EC), like macrophages (M phi), can function as accessory cells necessary for mitogen- and antigen-induced T cell activation was examined. EC were enzymatically detached from the luminal surfaces of guinea pig aortas and then propagated in culture. Lymph node T lymphocytes were rigorously depleted of adherent cells, such that they completely lost the capacity to respond to mitogenic stimulation with phytohemagglutinin or concanavalin A.

Pulmonary immune effector cells in guinea pigs with immune complex disease. I. Changes in T- and B-lymphocyte populations after exposure to antigen.

Changes in immunologic effector cell populations in lung tissue, bronchoalveolar spaces, tracheobronchial lymph nodes, spleen, and peripheral blood were evaluated during the course of a pulmonary immune complex disease in guinea pigs. The number of macrophages, lymphocytes, and neutrophils present in each cell population were determined. T and B lymphocytes were identified by E and EAC rosette formation, respectively.

Immune complex disease in guinea pig lungs: elicitation with pigeon serum.

Immune complex- and T cell-mediated reactions to organic antigens appear to contribute to the pathogenesis of hypersensitivity pneumonitis in humans. Because pigeon serum is one of the reagents used by clinicians to diagnose this disease, we assessed its potential to elicit immune complex-mediated pulmonary inflammation in guinea pigs. Animals were immunized with different concentrations of pigeon serum protein emulsified in complete Freund's adjuvant, and serums were collected at 4-day intervals after the booster injection.

Immunologically induced lung disease in guinea pigs. A comparison of ovalbumin and pigeon serum as antigens.

This study was conducted to compare the capacity of pigeon serum (PS), an antigen (Ag) associated with hypersensitivity pneumonitis (HP), and ovalbumin (OA) in the induction of immunologic lung disease in guinea pigs (gp). Whereas OA was very effective in inducing a severe pneumonitis, PS failed to produce significant disease. A determination of the antibody (Ab) responses in OA- or PS-sensitized GP revealed that total Ab activity, as well as specific IgG1, and IgG2 responses, were not significantly different in the two groups.