Mechanisms responsible for defective human T-lymphocyte sheep erythrocyte rosette function associated with hepatitis B virus infections.

Abstract

A B S T R A C T The expression of selected lymphocyte surface-membrane markers was evaluated in 37 patients with acute viral hepatitis B, 10 of whom were studied serially through the resolving and convalescent phases of disease. Bone marrow-derived (B) lymphocytes were identified by reference to surface immunoglobulin, whereas normal thymus-derived (T) lymphocytes were assayed by their capacity to form spontaneous nonim- Both intrinsic and extrinsic suppression of T lymphocyte ER function commonly occurred during the first 4 wk of acute viral hepatitis B. 9 of the 10 patients followed serially continued to manifest defective ER function at 12 wk. However, the intrinsic defect was observable only in those patients whose liver disease had resolved or was resolving, whereas the extrinsic defect was observed only in two patients with biochemical and histological evidence of unresolved hepatitis at that time.

In vitro antigen-induced antibody responses to hepatitis B surface antigen in man. Kinetic and cellular requirements.

“…The reasons for the disparate results are unclear, but technical differences in studies, including the serum source used for culture, the source, dose, and purity of HBsAg, as well as other experimental parameters, may be relevant. In this regard, the description of a serum protein in the blood of some patients with hepatitis B viral infection that can modulate T lymphocyte receptors (50,51) and the description of an albumin receptor on HBsAg (52, 53) clearly emphasize the unique and complex nature of the interaction between hepatitis B virus and the human host.…”

Tγ cells in systemic lupus erythematosus

“…A possible interference by warm-reactive IgG antibodies (19,20) is more difficult to exclude, but the absence of detectable IgG by direct immunofluorescence on the surface of freshly isolated PBL from patients with SLE renders this possibility unlikely. Special culture techniques to remove lipoprotein rosette inhibitor factor, which has been described in other diseases (12,21,22), did not increase T cell percentages in SLE.…”

Physiologic concentrations of normal human plasma lipoproteins inhibit the immortalization of peripheral B lymphocytes by the Epstein-Barr virus.

“…Following 24-h cultivation in tissue culture plates (Falcon Labware, Div. Becton, Dickinson) to remove adherent cells, PBM were mixed at a ratio of 1:50 with sheep erythrocytes that had been treated with neuraminidase as previously described (18). The mixture was incubated at 37°C for 10 min, centrifuged at 200 g for 5 min, and incubated at room temperature for 1 h at which time it was gently resuspended and sedimented onto a barrier of FicollHypaque as described above.…”

“…Lipoprotein-depleted autologous serum was prepared by a single ultracentrifugation at 1.21 g/ml. The isolations initially used a 45-Ti rotor (Beckman Instruments, Inc., Fullerton, Calif.) at 42,000 rpm and, finally, a 60-Ti rotor at 58,000 rpm for 16- (22) and by double diffusion in gel with rabbit antisera to human albumin and IgG, and if free of contaminating proteins, used and stored sterile at 4°C for no >20 d. HDL infranate, representing all residual nonlipoprotein serum proteins was dialyzed and sterilized as above before and after precipitation of immunoglobulins with 50% ammonium sulfate as described (18). All preparations were analyzed for protein by a modification (23) (Fig.…”