PubMed · 51166
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A E Stitzel, R E Spitzer. 1975-08-23. Letter: C3 standards.. https://doi.org/10.1016/s0140-6736(75)92804-4
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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 investigate peroxisome proliferator-activated receptor gamma (PPAR-gamma) expressions in patients with actively proliferating glomerulonephritis such as type IV lupus nephritis (LN) and cellular crescentic glomerulonephritis (RPGN). METHODS: All patients were divided into 4 groups as follows: RPGN (17 cases); LN type IV (15 cases); mild mesangial proliferative IgA nephropathy (IgAN, 7 cases) and minimal change disease (MCD, 10 cases). Clinical parameters, immunohisto-chemistry stain and in situ hybridization of renal biopsy specimens were performed. RESULTS: Clinically, proteinuria and hematouria were increased and Ccr were decreased in LN and RPGN patients, and increased ESR and decreased complement C3 were found in group LN. Active index of renal specimens were significantly higher in LN and RPGN groups than in IgAN and MCD groups. Renal specimens of MCD patients showed no positive PPAR-gamma staining in all sections; little immunoreactivity was detected in sections of glomerular, tubular and interstitial cells from IgAN patients. Glomerular positive staining of PPAR-gamma in renal sections in LN and RPGN patients[(3.3 +/- 1.8) and (2.8 +/- 1.2) cells per section of glomerulus, respectively] were significantly increased compared with that in IgAN patients [(0.7 +/- 0.5) cells per section of glomerulus]. Similarly, tubular positive staining of PPAR-gamma in LN and RPGN patients (27.38 +/- 12.46, 23.36 +/- 10.55) were also elevated compared with that in IgAN and MCD patients(6.51 +/- 3.49, 1.72 +/- 0.31). The relevance assay results showed positive relationship between active index and glomerular or tubular PPAR-gamma immunohisto-chemistry staining cell numbers (0.478, P < 0.01; 0.513, P < 0.01). Tubular PPAR-gamma mRNA expression in LN and RPGN patients was upregulated by in situ hybridization. CONCLUSION: Our results demonstrate in vivo that PPAR-gamma expression was increased in active glomerulonephritis patients accompanied with clinical and pathological active inflammation. These data suggest that increase of PPAR-gamma expression in renal cells may play an important role in response to inflammatory stress.