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Immunoregulatory granulocyte factor (GF). II. In vitro features of antibodies against GF+
1Department of Pathophysiology, Institute of Basic Medical Sciences WAM, Lódz.
Activated polymorphonuclear leucocytes (PMNL) secrete a specific factor possessing numerous immunoregulatory properties. The rabbit IgG antibodies against this human granulocyte factor GF (anti-GF-IgG) have significantly changed the regulatory features of GF and the same antibodies alone have also exerted immunoregulatory potency when tested in vitro. Inhibition of mixed lymphocyte reaction (MLR) proliferation after GF treatment was abolished in the presence of anti-GF-IgG. GF displays a potentiating effect on interleukin-1 (IL-1) production by human monocytes in vitro. Anti-GF-IgG did not change the potentiating capacity of GF and these specific antibodies alone also enhanced IL-1 production to the same extent as GF. In peripheral blood mononuclear cell (PBMC) cytotoxicity test, the cytotoxic activity of effector cells was markedly reduced in the presence of GF. Anti-GF-IgG partially abrogated the observed suppression, although their own features indicate a strong inhibitory effect on PBMC cytotoxicity. These contradictory results are difficult to explain but they may enable us to understand the pleiotropic immunoregulatory mechanism of both GF and anti-GF-IgG. The results of the present and recently published studies support the idea that both GF and anti-GF-IgG modify T lymphocyte function at the same receptor level.
Activated polymorphonuclear leucocytes (PMNL) secrete a specific factor possessing numerous immunoregulatory properties. The rabbit IgG antibodies against this human granulocyte factor GF (anti-GF-IgG) have significantly changed the regulatory features of GF and the same antibodies alone have also exerted immunoregulatory potency when tested in vitro. Inhibition of mixed lymphocyte reaction (MLR) proliferation after GF treatment was abolished in the presence of anti-GF-IgG. GF displays a potentiating effect on interleukin-1 (IL-1) production by human monocytes in vitro. Anti-GF-IgG did not change the potentiating capacity of GF and these specific antibodies alone also enhanced IL-1 production to the same extent as GF. In peripheral blood mononuclear cell (PBMC) cytotoxicity test, the cytotoxic activity of effector cells was markedly reduced in the presence of GF. Anti-GF-IgG partially abrogated the observed suppression, although their own features indicate a strong inhibitory effect on PBMC cytotoxicity. These contradictory results are difficult to explain but they may enable us to understand the pleiotropic immunoregulatory mechanism of both GF and anti-GF-IgG. The results of the present and recently published studies support the idea that both GF and anti-GF-IgG modify T lymphocyte function at the same receptor level.