Inhibition of lymphocyte transformation by pregnancy-associated plasma protein-A (PAPP-A).

A third trimester pregnancy plasma pool was divided into 2 aliquots, one of them was depleted of pregnancy-associated plasma protein-A (PAPP-A) by absorption onto a monospecific antiserum to PAPP-A. These plasmas as well as pure PAPP-A (isolated from pregnancy plasma) were tested for their ability to inhibit mitogen induced lymphocyte transformation. Pregnancy plasma containing PAPP-A exerted a significantly higher inhibition of phytohemagglutinin (PHA) induced lymphoblastogenesis than did pregnancy plasma devoid of PAPP-A. Pure PAPP-A added to normal human AB serum was also inhibitory. Since PAPP-A (pregnancy plasma with PAPP-A) is inhibitory even if it is preincubated in absence of PHA (and this mitogen added after washing the cells) one can conclude that the inhibitory effect of PAPP-A is specific and is not due to the binding of PHA to PAPP-A (glycoprotein). The fact that PAPP-A is active on prestimulated cells in absence of PHA seems to indicate that PAPP-A inhibits lymphoblastogenesis by acting on the secretion products of lymphocytes.

Analysis of cell-mediated hypersensitivity, immune complexes and monocyte-released factor(s) in allergic alveolitis and asymptomatic exposed subjects.

Patients with allergic alveolitis to various antigens, asymptomatic exposed individuals and healthy control subjects were studied. The lymphocyte transformation test and the formation of two lymphokines were shown to be positive in almost all affected subjects and only rarely in asymptomatic exposed individuals. In most symptomatic subjects and only rarely in asymptomatic exposed individuals. In most symptomatic subjects, the presence of antigen-antibody complexes could be demonstrated. However, such complexes were also present in six of the nine asymptomatic exposed individuals having precipitating antibodies. Factor(s) released from sensitized monocytes strongly facilitate the in vitro formation of specific antibodies but are poorly effective when incubated with cells from asymptomatic exposed subjects or normal individuals.

Effects of long-term administration of clonidine on plasma renin activity.

Plasma renin activity (PRA) was studied before and during long-term treatment with moderate oral doses (0.2 or 0.3 mg/d) of clonidine. Nine outpatients with essential hypertension received clonidine for 12 weeks; a significant decrease in blood pressure was evident in all patients. Except for a nonsignificant increase after 12 weeks of treatment, PRA values were not notably changed by clonidine therapy. No correlation was found between individual blood pressure changes and PRA variation during the study. The absence of a net effect on PRA in this study does not exclude more complex interactions of clonidine with the renin-angiotensin system. Nonetheless, clonidine cannot generally be classified as a "renin-inhibiting" drug.