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A water-soluble extract of Nocardia markedly increased in vitro [(3)H]thymidine incorporation by mouse spleen lymphocytes. The blastogenic activity of the extract and lipopolysaccharide was studied comparatively on various mouse lymphocyte subpopulations. The data obtained by [(3)H]thymidine incorporation and by electron microscopy have demonstrated that this preparation stimulates selectively mouse bone-marrow-derived cortisone-sensitive lymphocytes. This stimulation is related neither to a natural infection of mice with Nocardia organisms nor to the presence in Nocardia water-soluble mitogen of a lipopolysaccharide contaminant or of a lipopolysaccharide-like material.

Concanavalin A (Con A) and phytohemagglutinin (PHA) released histamine from hamster mast cells incubated in a serum-free medium. Concentrations of Con A and PHA approximating those optimal for transforming lymphocytes also released maximal amounts of histamine without apparent cytotoxicity. Higher concentrations of mitogen inhibited both lymphocyte transformation and histamine release. Incubation at 37 C for 15 min released histamine, although longer times were more effective. Supernatants from cultured hamster splenocytes stimulated with Con A also released histamine from added mast cells. However, the effect could be inhibited by the addition of 0.1 M methyl alpha-D-mannoside or by passing the spleen cell culture supernatants through Sephadex G-75 to remove Con A. This mitogen-induced release of mast cell histamine is therefore not mediated by a lymphokine but probably results from a direct interaction of mitogens with receptors on mast cells.

Immunohistological and elution studies of the human placenta revealed the presence of IgG on the trophoblastic basement membrane (TBM) which demonstrated specificity for placental but not lung, thyroid, or kidney basement membranes, suggesting the presence of a placenta-specific antigen in TBM. IgG comprised the bulk of immunoglobulin in eluates, and small amounts of IgA, trace amounts of IgM, but no IgE or IgD were identified in eluates. The distribution of IgG subclasses in eluate was not unusual as compared to maternal and neonatal sera, and Gm and Inv typing of eluates indicated that it was of maternal origin. Small amounts of eluate-IgG effectively inhibited the blastogenic response of unrelated lymphocytes to old tuberculin, phytohemagglutinin, and in one- or two-way mixed lymphocyte culture reactions. The inhibition was distinct from nonspecific inhibitors, and dose-response analysis indicated that eluate was very much more potent as an inhibitor than were the nonspecific inhibitors. Inhibition was shown to not be due to anti-HL-A activity, and was probably not due to aggregated IgG or immune complexes. Binding of eluate to lymphocytes was very loose as shown by washing experiments, and no binding could be shown by immunofluorescence. The capacity of eluate IgG to inhibit MLC was retained after pepsin digestion to F(ab')(2), suggesting that the inhibition reactions were immunological. It is suggested that eluate-IgG is maternal blocking antibody to a hitherto uncharacterized trophoblast antigen, and it is speculated that either abnormal antigen or aberrant responses to antigen could result in fetal wastage.