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Biomedical subjects

P Urso

Publications and source records attributed to P Urso.

4 recordsLinked to original sources

Immunological consequences from exposure to benzo(a)pyrene during pregnancy.

Progeny and maternal immune status after benzo(a)pyrene (BP) exposure of mothers at mid-pregnancy is disrupted in fetal liver (FL), in spleen and in thymus during pregnancy and postnatally. Mice suffer deficiencies in splenic and thymic mixed lymphocyte responses (MLR), and disorientations of T antigen expressing cells, punctuated by exorbitant increases in Lyt2, especially in FL. FL Lyt2 do not suppress an MLR, while Lyt1 mediate suppression. Isolated Thy1 show a weak response to Concanavalin A; FL Thy1 weakly express an MLR. Maternal macrophages and progeny B cells are also functionally abnormal. Thus, BP induces generalized immune deficiency that may affect ontogeny and which is potentially deleterious to health.

Animals

Immune competence of splenic lymphocytes following graft-vs-host disease in mouse allogeneic radiation chimeras.

The abnormal immune response of long-term mouse allogeneic chimeras is reflected by qualitative deficiencies in either T or B lymphocytes. The present study was undertaken to determine if a relationship existed between the severity of graft-vs-host disease (GVHD) that these animals had experienced and a functional defect in either the T or B cell population. The in vitro PFC response of chimera spleen cells to sheep red blood cells (SRBC) was evaluated in the presence of normal T or B lymphocytes 4 to 8 months after marrow transplantation and well beyond the GVHD period. In an analysis of several different allogeneic radiation chimeras, our results showed no relationship between the severity of GVHD experienced and the immunologic capacity of either T or B cells. Thus, different chimera combinations showing similar degrees of GVHD were functionally deficient in one or the other of these two cells types or both with no apparent predilection for abnormality in either population. In examining the quantitative in vitro PFC response to sheep RBC by spleen cells from individual chimeras, we found that the number of PFC formed was related to the severity of GVHD experienced by that animal. A general relationship between severity of GVHD and PFC capacity may also exist between chimeras of different genetic combinations. However, this relationship is not precise since gross exceptions occur. Our results, although documenting further the qualitative abnormalities in T and/or B lymphocytes of radiation chimeras, do not reveal the factor or mechanisms by which these cells are made unresponsive. It is suggested that the tolerance-inducing mechanism of these animals, whether it be humoral blocking factors or suppressor cells, is in some way interfering with the collaboration of T and B cells for antibody production.

Animals