Hultman P, Skogh T, Eneström S
Department of Pathology, Linköping University, Sweden.
J Clin Lab Immunol. 1989 Aug;29(4):175-83.
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.