Modulation of the immunoreactivity of a T-lymphocyte subpopulation by neutrophil-released prostaglandin.
The effect of polymorphonuclear leukocytes (PMNs) on lymphocyte subpopulations and their reactivity was investigated by adding supernatants obtained by culturing PMNs with allogeneic or autologous lymphocytes which had been pre-treated with prostaglandin (PG) synthetase inhibitors. PMNs were obtained from 12 healthy individuals, 7 patients with systemic lupus erythematosus (SLE) and 6 patients with bacterial infections. Freshly prepared normal lymphocytes pretreated with PG synthetase inhibitors were incubated with the above supernatants, and the lymphocyte and T-lymphocyte subpopulations were then quantitated, the responses of lymphocytes to mitogens measured and the generation of helper and suppressor T-cell activities for PWM-stimulated cultures assessed. We also ascertained which T-cell population, i.e. OKT4+ or OKT8+ cells, which had been altered by incubation with supernatants, was responsible for the suppressor T-cell activity. A reduced per cent of OKT4+ cells; depressed responses to Con A, PHA, PWM and allogeneic lymphocytes, impaired helper T-cell activity; and increased suppressor T-cell activity were noted after incubation of lymphocytes with supernatants. The percentage of T lymphocytes and of OKT8+ cells was, however, not affected. Further, enhanced suppressor T-cell activity was obtained when supernatant-incubated OKT4+ cells were cultured with OKT8+ cells, regardless of whether the latter had previously been exposed to supernatants. Addition of PG inhibitors to PMN co-cultures nearly restored the original percentage and reactivity of the T-lymphocyte populations, indicating a role for PG released from PMNs in the effects observed. The amount of PG demonstrated in co-culture supernatants was 30 times more than obtained by sonification of fresh PMNs and 10 times more than found in the culture medium containing PMNs alone. These results suggest that, besides monocytes, other phagocytes, including PMNs, can modulate lymphocyte-mediated immune reactivity by the release of PG. Deceased number of OKT4+ cells, impaired helper T-cell activity and enhanced suppressor cell activity may, at least in part, result from the effect of PG released from PMNs as well as monocytes.
Niwa
Y
Y
Sakane
T
T
Fukuda
Y
Y
Miyachi
Y
Y
Kanoh
T
T
D000293:Adolescent; D000328:Adult; D001424:Bacterial Infections / Q000276:immunology; D002450:Cell Communication; D016861:Cyclooxygenase Inhibitors; D005260:Female; D006801:Humans; D066298:In Vitro Techniques; D008180:Lupus Erythematosus, Systemic / Q000276:immunology; D008297:Male; D008875:Middle Aged; D008934:Mitogens / Q000494:pharmacology; D009504:Neutrophils / Q000276:immunology* / Q000378:metabolism; D011453:Prostaglandins / Q000276:immunology* / Q000378:metabolism; D013601:T-Lymphocytes / Q000145:classification / Q000276:immunology*; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology
D016861:Cyclooxygenase Inhibitors; D008934:Mitogens; D011453:Prostaglandins