Role of macrophages in the pathogenesis of experimental tick-borne encephalitis in mice.

In vivo phagocytosis activity of macrophages (PAM) was temporarily suppressed in mice by application of a suspension of microscopic from particles. As demonstrated, a reversible block of 70% of PAM was accompanied by a marked increase of the lethality during the acute tick-borne encephalitis (TBE) virus infection. Asymptomatic persistence of TBE virus in the brain was 4 times more frequent in mice with PAM defect than in immuno-competent mice. Suppression of PAM during the first 48 hr post infection (p.i.) did not affect interaction of B-, T-lymphocytes and macrophages. Cytotoxic activity of splenocytes against TBE virus-infected mouse embryo fibroblasts (MEF) was alike irrespective of whether cytotoxic cells were collected from mice inoculated or not inoculated with microscopic iron suspension. Similarly, frequency of seroconversion did not differ in these groups of mice. Adoptively transferred peritoneal macrophages from TBE virus-infected or intact mice did not exert any protective activity. The presence of splenic macrophages was necessary neither in adoptive immunity transfer in vivo nor in cytotoxic activity of T-lymphocytes directed to virus-infected targets in vitro. It was further found that peritoneal macrophages (PM) both from TBE virus immunized and non immunized donors in the presence of antibodies to TBE virus acquired the capability to kill TBE virus-infected target cells. Antibody-dependent cytotoxicity (ADC) of macrophages was associated with population of phagocytic cels.(ABSTRACT TRUNCATED AT 250 WORDS)