Systemic Lupus Erythematosus. Cryoprecipitation of Sera

Christian, Charles L.; Hatfield, W. B.; Chase, Peter

doi:10.1172/jci104774

Cited by 74 publications

(33 citation statements)

References 20 publications

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“…(Received for publication 21 August 1967) With the observations of immune complexes or antigens in the circulation of patients with rheumatoid arthritis (1,2), systemic lupus erythematosus (3,4), and other diseases, much attention has been drawn to their possible significance in the pathogenesis of the lesions in these disorders. Abundant data derived from experimental models have shown that the presence of complexes in the circulation coincides temporally with the development of the lesions, e.g., acute glomerulonephritis and vasculitis (5,6) and chronic glomerulonephritis (7).…”

Section: Platzs 21 and 22mentioning

confidence: 99%

Studies on Circulating Immune Complexes

Cochrane

Hawkins

1968

The Journal of Experimental Medicine

169

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With the observations of immune complexes or antigens in the circulation of patients with rheumatoid arthritis (1, 2), systemic lupus erythematosus (3, 4), and other diseases, much attention has been drawn to their possible significance in the pathogenesis of the lesions in these disorders. Abundant data derived from experimental models have shown that the presence of complexes in the circulation coincides temporally with the development of the lesions, e.g., acute glomerulonephritis and vasculitis (5, 6) and chronic glomerulonephritis (7). In these studies the complexes were demonstrable in the lesions, and it was reasonably presumed that they reached their destination in the tissues after passage through the circulation.Previous studies in this series have analyzed the mechanisms by which circulating immune complexes are capable of localizing in vessel walls. It was found that complexes localized in blood vessd walls only during an increase in vascular permeability and that the complexes were trapped along the vascular basement membranes during the passage of plasma fluids through the permeable membrane (8). The increase of vascular permeability was brought about in particular by vasoactive amines and histamine that were released from their tissue reservoirs, the mast cells, by the action of the complexes themselves (9). The accompanying article presents data suggesting that this mechanism of localization is instrumental in serum sickness.The present paper deals with the physicochemical properties of complexes and with the concentration of complexes in the plasma required for detectable localization to occur. The validity of these findings is tested in experimental serum sickness of rabbits, a disease known to be caused by deposition of circulating immune complexes. A preliminary report has been presented (10).

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Section: Platzs 21 and 22mentioning

confidence: 99%

Studies on Circulating Immune Complexes

Cochrane

Hawkins

1968

The Journal of Experimental Medicine

169

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“…In active systemic lupus erythematosus (SLE) it may be low and correlated with the total serum complement (5)(6)(7). Precipitation of the serum cryoglobulins which are frequently present in SLE was first shown by Christian, Hatfield, and Chase to be dependent on the presence of Clq (8). In addition, some patients with active chronic "hypocomplementemic' nephritis have reduced sertuni Clq (9).…”

Section: Introductionmentioning

confidence: 99%

Metabolism of Human C1q STUDIES IN HYPOGAMMAGLOBULINEMIA, MYELOMA, AND SYSTEMIC LUPUS ERYTHEMATOSUS

Köhler¹,

Müller‐Eberhard²

1972

J. Clin. Invest.

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A B S T R AC T The in vivo metabolism of radioiodinelabeled Clq was determined in patients with hypogammaglobulinemia, multiple myeloma, systemic lupus erythematosus (SLE), and in healthy controls. Marked differences in metabolic behavior were observed with a much more rapid disappearance of plasma radioactivity in patients as compared with controls. Estimated plasma volumes at 10 min after injection (time 0) were normal in controls and the SLE patient, mean 40 ml/kg, whereas they were grossly elevated, 57-82 ml/kg, in the hypogammaglobulinemic and myeloma patients, indicating significant loss of Clq-l"I during the initial mixing period. Absence of a distinct initial equilibration phase of radioactivity loss from the plasma suggested significant reversible interaction of the labeled Clq with plasma proteins and density gradient studies provided evidence for in vivo uptake into the circulating trimolecular first component complex (Clq, r, s). In controls and the SLE patient 0.51-0.75 of the Clq was retained in the plasma space while only 0.28 or less was in the others. The daily plasma pool fractional Clq catabolism was 0.65-0.67 in controls compared with 0.95-4.80 in the patients. Clq synthetic rates in controls were 4.64 and 4.34 mg/kg per day while higher rates, 4.94-37.40 occurred in the patients.These experiments clearly indicate that the metabolism of Clq is markedly influenced by serum IgG concentrations, probably related to the reversible interPresented in part at the Western Section of the American Federation for Clinical Research, Carmel, Calif., January 1970 (Clin. Res. 18: 135. 1970

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“…For cryoprecipitation to occur, a heat-labile serum factor is required. This factor is present in normal human serum and has been identified as 11 S material (11 S) (6) or the C'lq fraction of the first component of complement (7).…”

Section: Introductionmentioning

confidence: 99%

“…"Mixed" cryoglobulins, in contrast, consist of IgG and IgM in varying proportions and have been described primarily in SLE (6), in a syndrome of purpura, weakness, and arthralgias (8,9), and in other patients with varying clinical pictures (10)(11)(12)(13).…”

Section: Introductionmentioning

confidence: 99%