Subject(s)
Arsenicals , B-Lymphocyte Subsets/immunology , Immunoglobulin Idiotypes , Animals , Animals, Newborn , Arsenic/immunology , Female , Male , Mice , Models, Biological , Rabbits , Radiation Chimera/immunologyABSTRACT
The normal immune response of A/J mice against arsonate coupled to hemocyanin is characterized by a major recurrent cross-reactive Id, the CRIA. This Id is encoded by a single gene segment combination: VHidcr11-DFL16.1e-JH2 for the H chain and Vkidcr-Jk1 for the L chain. In this report, we show that lethal irradiation of A/J mice followed by reconstitution with autologous or syngeneic lymphoid cells results in loss of major CRIA Id expression in the response to arsonate. Different protocols were performed to repopulate the irradiated mice. First, lethally irradiated A/J mice were reconstituted by the transfer of syngeneic bone marrow cells. Second, A/J mice were lethally irradiated while their hind limbs were partially shielded. Third, lethally irradiated A/J mice received a transfer of syngeneic spleen cells. The three groups of mice produce high titers of antiarsonate antibodies completely devoid of CRIA DH-JH related idiotopes expression. Moreover, a lack of affinity maturation is observed in the secondary antiarsonate response of all irradiated and reconstituted mice. A transfer of syngeneic peritoneal cells or a transfer of primed T cells in irradiated and reconstituted A/J mice do not restore in a significant manner either the recurrent CRIA expression or the affinity maturation of the antiarsonate response. Our data suggest that the choice of this Id is not solely dictated by the Igh locus.
Subject(s)
Antibody Affinity , Antibody Formation/radiation effects , Arsenicals , Immunoglobulin Idiotypes/immunology , Immunologic Memory , Animals , Arsenic/immunology , Bone Marrow Cells , Bone Marrow Transplantation/immunology , Immunoglobulin Heavy Chains/immunology , Mice , Mice, Inbred A , Peritoneal Cavity/cytology , Spleen/cytology , T-Lymphocytes/immunology , Time FactorsABSTRACT
Pulmonary hypertension accompanying portal hypertension is a rare cause of plexogenic pulmonary arteriopathy, which etiopathogenesis is still unknown. The case report presented is that of a young man who underwent surgery at age 8 for ruptured esophageal varices associated with portal thrombosis, and who later developed pulmonary hypertension which led to death at age 21. Hepatic filtration shunt and similarity of this syndrome to pulmonary hypertension subsequent to ingestion of the appetite depressant Aminorex suggest the hypothesis that pressor substances, not detoxified by the liver, are released into the pulmonary circulation.
