Studies were undertaken to determine whether rheumatoid factor (RF) was present in immune human and Aotus trivirgatus monkey sera which inhibited Plasmodium falciparum schizonts in vitro and to determine whether RF could be responsible for or contribute to merozoite agglutination in the parasite inhibition test. Additional studies were conducted to determine the effect of exogenous RF on schizont inhibition when used alone or in conjunction with immune or normal sera. RF was not detected in any of the 11 immune monkey sera or the 3 immune human sera which were tested. However, when RF was added to immune human or Aotus sera, levels of schizont inhibition increased significantly over levels obtained with immune serum alone. When RF was used alone or in conjunction with normal sera, levels of schizont inhibition were comparable to those obtained with normal serum. Furthermore, adsorption of the RF with immunoglobulin G-coated erythrocytes removed the enhancing activity. The results of this study indicate that RF, which is sometimes produced during acute or chronic malarial infection, may contribute nonspecifically to the enhanced clearance of plasmodia in vivo.
Acute-phase serum (APS) collected from Plasmodium berghei-infected rats inhibited phagocytosis of trypsinized rat erythrocytes and of erythrocytes from P. berghei-infected rats. Macrophages (M phi) incubated with APS or heat-aggregated acute-phase serum (HAAPS) for 6 h, followed by 18 h incubation in serum-free medium, exhibited significantly higher levels of phagocytosis than M phi similarly cultured but with normal rat serum. When APS was present at the time of assay, it inhibited erythrophagocytosis by M phi which had been in culture for 0 or 24 h. M phi activation by HAAPS was inhibited by 2-deoxy-D-glucose, which suggests that activation by HAAPS is Fc-receptor mediated. Adsorption of APS with staphylococcal protein A abrogated the ability of APS to inhibit phagocytosis and that of HAAPS to effect M phi activation, suggesting that immune complexes are involved in both processes. Surface-bound immunoglobulins eluted from erythrocytes of P. berghei-infected rats promoted phagocytosis of trypsinized erythrocytes by HAAPS-activated M phi but not by resting M phi. These results indicate that the immunoglobulins which bind to infected or damaged erythrocytes during malarial infections promote erythrophagocytosis by activated M phi and that the immune complexes in serum from rats with acute malaria may inhibit erythrophagocytosis early in the infection but may, over time, induce changes in the M phi which later facilitate erythrophagocytosis.
Bacterial lipopolysaccharide (LPS) stimulates pulmonary macrophages from BCG immune-rechallenged hamsters to kill tumor cells in vitro. However, pulmonary macrophages from BCG immune and from untreated hamsters cannot be activated for tumor cytotoxicity by in vitro treatment with LPS. Pulmonary macrophages from the nonimmune hamsters acquire tumoricidal capacity after 3 hr of coculture with T cells from BCG immune-rechallenged hamsters or when incubated with Con-A-stimulated spleen cell supernatant fluid. A heterogeneous population of pulmonary lavage cells from BCG immune and from BCG immune-rechallenged hamsters destroys the tumor cells more effectively than a homogeneous population of pulmonary macrophages from the same animals. LPS significantly augments the cytotoxic activity of the heterogeneous population of pulmonary lavage cells.
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