PubMed · 10635771
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S Takemura. 1999. [The third component of complement, C3].. https://pubmed.ncbi.nlm.nih.gov/10635771/
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Complement component 3 (C3) is the major opsonin for the pathogenic fungus Cryptococcus neoformans in the non-immune host. However, the efficiency of complement-mediated opsonization varies, depending on the strain, through mechanisms that are not understood. Analysis of complement-mediated phagocytosis for 12 strains grown in Sabouraud medium revealed that phagocytic indices were inversely correlated with capsule volume. In contrast, there was no correlation between phagocytic index and capsule volume for IgG1-opsonized cells. When capsule size was increased, the efficacy of complement-mediated phagocytosis decreased, whereas that of antibody-mediated phagocytosis increased. C3 localized inside the capsule and at the outer capsule edge for poorly phagocytozed and well-phagocytozed strains, respectively. Blocking experiments revealed that complement-mediated phagocytosis occurred through complement receptor 3 (CR3), without significant involvement of CR1 or CR4. Blocking experiments with antibodies to C3 did not completely abrogate yeast cell uptake, consistent with phagocytosis through glucuronoxylomannan-CR3 interactions. Our data explain how some large encapsulated cells avoid phagocytosis and suggest a novel strategy for immune evasion whereby a microbial capsule interferes with phagocytosis by modifying the location of C3 deposition.
OBJECTIVE: To determine the degree to which changes in C3 and C4 precede or coincide with changes in systemic lupus erythematosus (SLE) activity, as measured by 5 global activity indices, the physician's global assessment (PGA), modified SLE Disease Activity Index (M-SLEDAI), modified Lupus Activity Index (M-LAI), Systemic Lupus Activity Measure (SLAM), and the modified British Isles Lupus Assessment Group (M-BILAG), and to evaluate the association between changes in C3 and C4 levels and SLE activity in individual organ systems. METHODS: Fifty-three lupus patients were observed monthly for 1 year in a longitudinal study. Lupus disease activity and complement levels were measured at each visit. Lupus flare was defined as a 1.0 (or greater) increase in the PGA, a 3-point increase in the M-SLEDAI, a 0.1 increase in the M-LAI, a 3-point increase in the SLAM, or a 4-point increase in the M-BILAG within a 1-month period. Flare rates were calculated for subgroups defined by previous (1 month before) or concurrent changes in complement levels. Logistic regression models were used to determine the significance of the association between recent changes in complement levels and flare, controlling for prednisone dosage. Similar models were used to assess the association between changes in C3 or C4 levels and increased SLE activity in specific organ systems. RESULTS: Lupus flares occurred at 12% of visits based on the PGA, 19% based on the M-SLEDAI, 25% based on the M-LAI, 13% based on the SLAM, and 12% based on the M-BILAG. Recent changes in C3 and C4 levels were not associated with flares based on 3 of the 5 activity indices. Flares defined by the M-LAI were more frequent when there was a concurrent decrease in C3 (odds ratio [OR] 1.9, 95% confidence interval [95% CI] 1.1-3.1) or C4 (OR 2.1, 95% CI 1.3-3.6). Higher flare rates, as defined by the SLAM, were associated with previous increases in C3 (OR 1.6, 95% CI 1.0-2.6) and C4 (OR 2.2, 95% CI 1.2-3.9). When individual organ systems were analyzed, decreases in C3 and C4 were associated with a concurrent increase in renal disease activity (OR 2.2, 95% CI 1.4-3.5 and OR 1.9, 95% CI 1.1-3.4, respectively). Decreases in C3 were also associated with concurrent decreases in the hematocrit (OR 4.6, 95% CI 1.7-12.3), platelet (OR 2.5, 95% CI 1.5-4.1), and white blood cell (OR 2.2, 95% CI 1.3-3.6) counts. Previous increases in C3 levels were associated with a decrease in platelets (OR 1.7, 95% CI 1.1-2.7). A decrease in C4 was associated with a concurrent decrease in the hematocrit level (OR 3.2, 95% CI 1.3-7.5) and platelet count (OR 1.6, 95% CI 1.0-2.5). CONCLUSION: Decreases in complement levels were not consistently associated with SLE flares, as defined by global measures of disease activity. However, decreasing complement was associated with a concurrent increase in renal and hematologic SLE activity.
Two cases of hepatic follicular dendritic cell (FDC) tumor are described. Both patients were female, aged 57 and 51 years. They presented with epigastralgia or abdominal fullness and weight loss. The first patient refused surgical resection. She developed progressive polyclonal gammopathy and then bilateral purpura over the legs. Skin biopsy revealed leukocytoclastic vasculitis with granular vascular deposits of IgA and C3. The second patient had marked peripheral blood and tissue eosinophilia. The histological diagnosis was confirmed by positive staining for CD21 and CD23. The stromal lymphocytes were predominantly composed of CD3(+)and CD8(+) cells. In situ hybridization for EBER showed a positive nuclear signal in tumor cells but not in inflammatory cells. Polymerase chain reaction amplification for Exon 3 of the latent membrane protein-1 (LMP-1) gene showed a characteristic 30-bp deletion between nucleotides 168282 and 168253, corresponding to the B95-8 sequence. The unique clinicopathological features of our cases have not been reported for FDC tumors before. The clinical significance of the 30-bp deletion in Exon 3 of the LMP-1 gene in FDC tumor of the liver warrants further investigation.