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Inhibition of the in vitro growth of Plasmodium falciparum. I. The effects of immune serum and purified immunoglobulin from owl monkeys.

Sera from Aotus sp. monkeys (karyotypes II, III, and IV) which were immune to Plasmodium falciparum have been used to inhibit the in vitro growth of this human malaria parasite. Culture conditions used for the assays allowed 50- to 100-fold increases in the number of A+ erythrocytes infected in a 96-hr period in control cultures. Although normal monkey serum did not support growth as well as normal human serum, mixtures of normal monkey and human serum were found that did. Compared to such controls, as little as 3.5% immune monkey serum was found to cause approximately 56% inhibition in 4 days (2 replicative cycles). Purified globulin from immune monkeys inhibited 40% at 2 mg/ml and 75% at 7 mg/ml after a single replicative cycle. These data suggest that serum antibody is likely to play a major role in providing Aotus monkeys with protective immunity to P. falciparum.

Animals↗

Serum immune complexes in membranoproliferative and other glomerulonephritides.

Immune complexes were detected in the serum of patients with membranoproliferative glomerulonephritis (MPGN) Types I and II, systemic lupus erythematosus (SLE), and acute poststreptococcal glomerulonephritis (AGN) by sucrose gradient ultracentrifugation and by measurement of Clq binding activity (Clq-BA). Clq-BA was more sensitive in detecting complexes than was gradient ultracentrifugation. By gradient ultracentrifugation, the sedimentation velocities of the complexes in the three diseases were similar, ranging from 13S to 19S. This range corresponds to that observed by others in experimental chronic serum sickness nephritis. The complexes isolated by gradient ultracentrifugation always contained C3, usually IgG and C4, and in some patients with SLE and AGN, IgM. In MPGN, IgM and IgA could be present in glomerular deposits when not present in circulating complexes. In this disease also, serum complement levels were poor predictors of the presence of complexes. With increased Clq-BA, the levels of Clq, C4, and C2 could be normal or reduced and there was no correlation with C3 levels. With few exceptions, the clinical status of the patients with MPGN correlated well with Clq-BA.

Acute Disease↗

Cerebrospinal fluid and serum immune complex in acute inflammatory polyneuritis. Detection by Clq binding assay.

Immune complexes (IC) were assessed in serum and CSF from 11 patients with acute inflammatory polyneuritis (AIP). An 125 I-labeled Clq binding assay (Clq BA) was used. IC were present in the sera of four patients and in the CSF of six. CSF-Clq BA of AIP (Group 1) were compared with 12 patients with other inflammatory neurological diseases (Group 2) and 22 patients with non-inflammatory neurological diseases (Group 3). There was only a significant difference between Group 1 compared to Group 3 (p less than 0.05). Serum and CSF IC did not correlate either with blood-brain barrier lesions or with immunoglobulin deposits in sural nerve biopsy.

Acute Disease↗