Tomasi, T. B.

Abstract Pretreatment of peritoneal exudate cells (PEC) for 24 to 48 hr with mouse amniotic fluid (MAF) results in a marked reduction in their ability to present antigen in a macrophage-T cell dependent antigen-induced lymphocyte proliferative assay. Since we showed that MAF did not inhibit the uptake of antigen by the antigen-presenting cells, presumably the site of action is either on "processing," T-macrophage interactions and/or on the secretion of soluble factors by macrophages. Whether suppression is the result of a direct effect on MAF on the antigen-presenting cell or indirectly via another cell type present in the PEC preparations was not established by this study. However, our data suggest that a major (although perhaps not sole) site of action of the suppressive factor(s) in MAF is at the level of the antigen-presenting cell. The biologic relevance of these in vitro observations is discussed in regard to the defects of immune function in fetal and neonatal animals.

Abstract A lymphocyte surface glycoprotein designated urinary acidic antigen (UA) has been isolated from normal urine by a combination of preparative isoelectric focusing and ammonium sulfate precipitation. It has an m.w. of 14,000 to 17,500 daltons, and is approximately 60% carbohydrate and 40% amino acid in content. The protein exhibited the following physical properties: S20,omega = 1.24; v = 0.693 ml/g; E1%1 cm, 278 nm = 2.08; and pI-2.5. It appears to be unrelated to beta 2-microglobulin, protein HC, urinary proteose, microglobulin, or any previously described normal urine or human serum protein.

Abstract A protein component present in normal human urine has been found on the surface of epidermal cells and lymphocytes. This protein, called urinary acidic antigen (UA), can not be detected in concentrated fractions of normal human serum by double immunodiffusion, suggesting that it is quickly cleared from the circulation. It is readily detected, however, in sera of patients with renal failure. Although it can be eliminated from the cell surface by repeated washings with PBS, it was shown to cap with anti-UA-specific antiserum. Anti-UA suppresses PWM-induced proliferation, but not the lymphocyte response to PHA, Con A, or allogeneic cells. Thus UA appears to have a specific relationship to the pokeweed response. Whether it is a structural component of the PWM receptor is uncertain.