Acta pathologica, microbiologica, et immunologica Scandinavica. Section C, Immunology最新文献

Lymphocytes from healthy blood donors were exposed to temperatures between 37 degrees C and 42 degrees C for up to three hours and then tested for natural killer (NK) activity using K562 cells as targets in a 3-h 51Cr-release assay. For a given level of hyperthermia a semilogarithmic decrease in NK activity relative to the treatment period was seen. NK effectors exposed to 42 degrees C for one hour lost 90% of their cytotoxic capacity compared to effectors kept at 37 degrees C. The depression in NK activity could Not be repaired by overnight incubation at 37 degrees C or by interferon treatment. Heating also inhibited the induction of NK-like cells during mixed lymphocyte culture (MLC), while exposure of either responder or stimulator cells to hyperthermia did not affect the degree of MLC-proliferation. The heating only slightly decreased lymphocyte viability--as determined by trypan blue exclusion--whereas a marked and permanent reduction in the number of cells bearing Fc-receptors for IgG occurred. The content of E-rosetting cells decreased initially, but was normalized after overnight incubation. The findings indicate that NK cells and T cells are differentially sensitive to in vitro hyperthermic treatment.

The present study describes the T lymphocytosis in infectious mononucleosis (IM), using rosette techniques, lymphocyte transformation tests, Con A suppressor tests, and chromosomal analysis. Blood was drawn from twelve patients with IM during acute illness and during convalescence. We found a T lymphocytosis with a normal sheep erythrocyte receptor affinity of T cells, using three different E-rosette techniques. The percentage of T cells with Fc receptors for IgM (T mu) was reduced during acute illness, but normal in convalescence. The percentage of T cells with Fc receptors for IgC (T gamma) was normal during illness and slightly reduced afterwards. Owing to the T lymphocytosis the total number of T gamma lymphocytes was significantly increased during IM. The lymphocyte reactivity in vitro after mitogen stimulation (PHA, Con A, PWM) was in the lower end of the normal range. We found no evidence of increased suppressor-cell activity activity during IM, using a Con A suppressor cell assay. No chromosomaL defects were observed in lymphocytes from blood.

A direct plaque forming cell (PFC) assay for the detection of complement fixing IgM-rheumatoid factor (RF) secreting lymphocytes was evaluated. The specificity of the RF-PFC assay was demonstrated by the inhibitory action of exogenous human IgG. The sensitivity of the RF-PFC assay was similar to that of a reverse PFC assay detecting all cells secreting IgM (IgM-PFC). In blood from 75% of seropositive patients with rheumatoid arthritis (RA) RF-PFC were demonstrated, median value 6.8 (range: 0.4-1477) RF-PFC/10(6) mononuclear cells. Practically no RF-PFC were detected in seronegative RA patients and controls. Despite the fact that most IgM-RF undoubtedly is produced outside the blood, a positive correlation was found between the number of RF-PFC and the Waaler-Rose titer in serum. The number of circulating IgM secreting cells did not differ significantly between seropositive RA patients, seronegative RA patients and controls. Comparison of RF-PFC and IgM-PFC in seropositive patients revealed that in mean 7% of IgM-secreting cells in blood secrete IgM-RF.

Four different Aleutian disease virus (ADV) isolates were coated to 1/4" polystyrene balls. The binding capacity of these balls against different mouse hybridoma antibodies prepared against each of the ADV isolates was investigated in two ways. The different ADV-coated balls were either mixed in a tube (competition between balls for antibody), or they were allowed to react separately with antibody (no competition). The difference in competitive and non-competitive binding values allows a comparison of antibody affinity against the four ADV isolates. Examples are given, where two hybridoma antibodies react better with the Danish isolate than with the three American isolates.

The pathophysiology, histology and immunohistology of acute and chronic heterologous immune complex glomerulonephritis were investigated in a long-term study in male Wistar rats. The glomerulonephritis showed 3 phases: an initial nephrotic syndrome, a latent phase with stable proteinuria (40 mg/24 h), and a terminal phase with increasing proteinuria and blood pressure, and declining serum protein concentration and creatinine clearance. Antiserum doses of 1.0, 1.5 and 2.0 ml induced maximal proteinuria (112, 257 and 272 mg/24 h respectively) after 14 days whereas normal rabbit serum and 0.5 ml antiserum gave no proteinuria. After 100 days, the rats injected with 1.0 ml of antiserum did not show physiological signs of renal disease; in the rats injected with 1.5 ml of antiserum the disease run a chronic course. Equal amounts of rabbit IgG, rat IgG and rat C3 were found in 10 glomeruli from rats 100 days after injection of 0.5, 1.0 and 2.0 ml (p greater than 0.10). Intramembranous deposits and spike formation were observed in all groups. All changes increased with greater antiserum doses. Chronically diseased animals observed from 500 to 750 days showed deposits of rabbit IgG in the basement membrane, and in most animals small amounts of rat IgG and rat C3 were also observed. This is compatible with a sustained stimulus for antibody formation throughout the course of this type of glomerulonephritis.

The function of polymorphonuclear neutrophils from blood (B-PMN) and from exudates (E-PMN) was studied in healthy volunteers. The E-PMNs were isolated from skin windows with chambers and the chemotactic, phagocytic and Nitro Blue Tetrazolium (NBT) reducing activity measured and compared to that of simultaneously obtained B-PMNs. The chemotactic and random migration of E-PMNs in Boyden chambers measured by the leading front and by the chemotactic index were reduced compared with B-PMNs (p less than 0.01). Serum independent phagocytosis of paraffin oil emulsions was significantly increased (p less than 0.01) by E-PMNs after 12, 24 and 48 hours and not correlated to the function of B-PMNs. Opsonization with autologous serum increased the phagocytosis by both E-PMNs and B-PMNs, but mainly the latter. The NBT reduction by E-PMNs was increased (p less than 0.01) and positively correlated to the NBT reduction by resting B-PMNs. In contrast, there was no difference in NBT reduction between phagocytosing E-PMNs and B-PMNs. Mobilization of PMNs to an inflammatory focus in healthy subjects induces marked changes in the function, and B-PMN function cannot always be assumed to reflect the function of PMNs from inflammatory sites.