A single injection of alpha beta-interferon (alpha beta-IFN) (30000 units/mouse), a major biological modifier of natural killer (NK) cytolytic activity, strongly stimulated NK activity in normal mice, as expected, while the same treatment did not statistically alter the NK response in cyclophosphamide (CY)-suppressed animals. We investigated the possibility of thymosin alpha 1 cooperating with alpha beta-IFN in boosting NK activity in CY-suppressed animals. The results show that treatment with thymosin alpha 1 (200 micrograms/kg) for 4 days, followed by a single injection of alpha beta-IFN 24 h before testing, strongly restored NK activity in CY-suppressed mice. Thymosin alpha 1 was, moreover, able to accelerate the recovery rate of NK activity in bone marrow reconstituted murine chimeras. Taken together the data support the concept that the synergic effect between thymosin alpha 1 and alpha beta-IFN could be the result of effects on differentiation of the NK lineage at different levels.
Spleen cells collected from DBA/2 (H-2d) mice inoculated with the polycythemic variant of Friend-Leukemia Virus Complex (FLV-P) were tested for T-dependent immune functions, such as the in vitro generation of cytotoxic T lymphocytes (CTL) and of non-specific T suppressor lymphocytes (STL). CTL were generated against H-2b splenocytes, and STL were obtained following a 5-day lymphocyte culture without stimulator cells. A progressive and severe impairment of the generation of both CLT and STL was found from 2 weeks onward after infection, being almost totally abolished 3-4 weeks after virus challenge. Suppressor cells (SC) capable of inhibiting CTL generation was detected in FLV-P bearing mice. Suppressor activity was unaffected by anti-Thy 1.2 serum and complement but was removed following iron-magnet depletion or passage through nylon-wool column. Moreover complete recovery of the competence of CTL generation was attained when FLV-P infected splenocytes were passed through nylon-wool column. It is concluded that FLV-P infection depresses T-dependent cytotoxic and suppressor responses in mice, by the appearance of non-T adherent phagocytic cells, capable of impairing CTL generation in vitro.
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