The innate resistance of CBA mice to endogenous murine leukaemia virus infection.

The incidence of lymphomata in CBA mice is low and furthermore is unaltered by transplantation at the early blastocyst stage and being born from the lymphoma-prone AKR. The number of C-type murine leukaemia virus particles in CBA derived in this manner and milk-fostered by AKR mice in no way differs from normal CBA. The results suggest that the oncogenic Gross virus does not pass through either the transplacental or transmammary routes, or alternatively that viral replication in the CBA was in some way inhibited. Both possibilities have still to be distinguished

Failure to induce autoimmune disease with neonatal bursectomy in chickens

To assess the effect of abnormal control of bursa-derived B cell function upon the development of spontaneous autoimmune disease, newly hatched chicks were surgically bursectomized or sham-bursectomized and studied up to 4 months of age. The presence of autoimmune disease was assessed by direct Coombs' test, measurement of antinuclear antibody, total hemoglobin, packed cell volume, plasma bilirubin, red cell survival, and immunofluorescence studies on frozen kidney sections. Despite abnormal immunoglobulin levels detected in bursectomized chickens, no significant differences in terms of autoimmune activity could be demonstrated between the two groups. This suggests that primary B cell control is an unlikely factor in the etiology of autoimmune disease and supports earlier studies which imply that a major factor leading to progressive autoimmune disease is the failure of a normal T cell suppression function. </jats:p

Increased surface expression of a newly identified 150-kDa dimer early after human T lymphocyte activation.

Abstract Lymphocyte activation induces or increases the expression of several surface structures, some of which are directly involved in cell growth such as receptors for IL-2 or transferrin. In order to identify new structures characteristic of activated lymphocytes, we developed a series of mAb against functionally defined human T cell clones. In the present study we report the isolation of a mAb termed BB18 recognizing, at the cell surface, a novel 150-kDa glycoprotein dimer whose expression on T lymphocytes increases readily after their activation with various stimuli including lectins. In contrast, in the presence of PMA, cell-surface expression of this 150-kDa structure is down-regulated even earlier than CD3 molecules. Biochemical studies as well as phenotypic analysis revealed that this structure is different from all previously identified molecules on the lymphocyte cell surface. Furthermore, functional studies showed that triggering this disulfide-linked dimer through BB18 epitope in the presence of submitogenic concentrations of PMA induced strong lymphocyte proliferation. This proliferative response require E+ cells and accessory cells, and this even after immobilization of BB18 mAb.</jats:p