Immunologically mediated macrophage aggregation in monolayers of peritoneal cells from BCG-sensitized mice.

Aggregation of cultured macrophage monolayers derived from BCG-sensitized mice was produced if nonadherent cells and specific antigen (tuberculin) were present, particularly if the antigen was renewed in the form of tubercle bacilli. The evidence indicated that antigen-stimulated BCG-sensitized lymphocytes in these cultures produced a soluble factor, which in the presence of the renewed supply of antigen caused the aggregation. The phenomenon was irreversible and followed by death of the macrophages. The 'overlays' of aggregated monolayers would aggregate normal macrophages, provided that the recipient cultures contain-d their own (normal) lymphocytes as well as antigen; this suggested that cultures of BCG-sensitized peritoneal cells produced a factor able to effect aggregation via the activity of normal lymphocytes. Overlays from aggregated monolayers were able also to inhibit the migration of normal mouse macrophages; this and other evidence suggested a similar origin for the inhibition factor, but the latter's identity with the aggregation factor remains undecided. We conclude that the aggregation factor depends upon the presence of specific antigen both for its formation and its expression.