Autoimmunity--a perspective.

Spleen cells from BALB/c or CAF1 mice released little or no detectable leukemia virus when cultured 2-7 days in vitro. In contrast, spleen cells of CAF1 mice previously inoculated with parental BALB/c spleen cells released leukemia viruses in 10 of 11 cases studied. Cultures of a mixture of spleen cells from normal BALB/c and CAF1 mice also contained leukemia viruses. Phytohemagglutinin induced the transformation of lymphocytes in cultures of CAF1 or BALB/c spleen cells, but this transformation did not activate leukemia viruses. It is concluded that mixed lymphocyte cultures in vitro, just as graft-versus-host reactions in vivo, can activate leukemia viruses that are normally present in a repressed form. This activation is not solely a function of lymphocyte transformation. The activated mouse leukemia virus may subsequently account for the observed high incidence of neoplasia in graft-versus-host disease.

Activation of Leukemia Viruses by Graft-Versus-Host and Mixed Lymphocyte Reactions In Vitro

Extraglomerular immunoglobulin deposits in human nephritis

The incidence of lymphomas in 371 CAF1 mice injected with BALB/c spleen cells was compared with that in 324 control CAF1 mice. A high incidence of lymphomas was found in the treated mice, but not in the control animals. The development of the neoplasms was a function of the number of parental cells administered. Analyses of the injected mice for the presence of donor cells indicated that the majority of the injected parental cells lost antihost activity, probably within 24 hr of their administration. The tumors were of host origin, as judged by transplantation tests and antigenic analysis of tumor cells.

/pdf/chronic-allogeneic-disease-ii-development-of-lymphomas-2rlhpelq2m.pdf

Chronic allogeneic disease. II. Development of lymphomas.

Membranous glomerulonephritis in the mouse

Glomerulonephritis, often accompanied by the nephrotic syndrome, developed in CAF1 mice following the administration of spleen cells from normal BALB/c mice. The renal lesion was membranous glomerulonephritis. When studied with fluorescein-conjugated antisera to either mouse gamma globulin or β1C-globulin, the glomeruli contained beaded and irregular deposits of these immunoproteins. The ultrastructure of the lesion was characterized by thickening of the glomerular basement membranes and the presence of electron-dense subepithelial deposits. Acid eluates of the diseased kidneys contained gamma globulin that failed to bind to sections of normal kidneys. These findings conform to the type of nephritis provoked by immune complexes. They indicate that this type of immune injury can be based on the reaction of intolerant immunocytes to normal antigens.

https://rupress.org/jem/article-pdf/128/4/653/1267731/653.pdf

Asuman Muftuoglu

Papers

Chronic allogeneic disease : i. development of glomerulonephritis