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Circulating and tissue immune complexes in mercury-treated mice
P Hultman1, T Skogh, S Eneström
1Department of Pathology, Linköping University, Sweden.
The amount of circulating immune complexes (CIC) was determined in mercury-treated Balb/c, SJL and C57BL/6J mice using the conglutinin-binding assay and the modified polyethylene glycol (PEG) precipitation test. SJL mice given mercuric chloride developed a transient increase of CIC by both methods, but the increase was modest compared with aged MRL-lpr/lpr (MRL) mice. Mercury-treated Balb/c mice showed increased levels of CIC by the PEG precipitation test. Blood clearance of intravenously injected preformed soluble IC was not impaired. The mesangial IC-deposits in mercury-treated SJL mice contained significantly more IgG1, but significantly less IgG2a and C3 than the combined mesangial-capillary loop deposits in MRL mice. The MRL mice had a severe proliferative glomerulonephritis, whereas, only a mild mesangial glomerulopathy was seen in the mercury-treated SJL mice. The SJL mice given mercuric chloride showed systemic, granular deposits within the vessel walls of IgG1 but not of C3; a few mice had IgG2 deposits which were accompanied by C3. No histological damage was seen in the vessel walls. The CIC found in mercury-treated SJL and Balb/c mice may be the source of origin of the systemic IC-deposits. One explanation for the mild degree of tissue injury might be that the predominant isotype in the deposits was IgG1, which led to deposition of only small amounts of complement.
The amount of circulating immune complexes (CIC) was determined in mercury-treated Balb/c, SJL and C57BL/6J mice using the conglutinin-binding assay and the modified polyethylene glycol (PEG) precipitation test. SJL mice given mercuric chloride developed a transient increase of CIC by both methods, but the increase was modest compared with aged MRL-lpr/lpr (MRL) mice. Mercury-treated Balb/c mice showed increased levels of CIC by the PEG precipitation test. Blood clearance of intravenously injected preformed soluble IC was not impaired. The mesangial IC-deposits in mercury-treated SJL mice contained significantly more IgG1, but significantly less IgG2a and C3 than the combined mesangial-capillary loop deposits in MRL mice. The MRL mice had a severe proliferative glomerulonephritis, whereas, only a mild mesangial glomerulopathy was seen in the mercury-treated SJL mice. The SJL mice given mercuric chloride showed systemic, granular deposits within the vessel walls of IgG1 but not of C3; a few mice had IgG2 deposits which were accompanied by C3. No histological damage was seen in the vessel walls. The CIC found in mercury-treated SJL and Balb/c mice may be the source of origin of the systemic IC-deposits. One explanation for the mild degree of tissue injury might be that the predominant isotype in the deposits was IgG1, which led to deposition of only small amounts of complement.