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Circulating soluble CR1 (CD35). Serum levels in diseases and evidence for its release by human leukocytes
M Pascual1, M A Duchosal, G Steiger
1Laboratory of Immunonephrology, Centre Médical Universitaire, Geneva, Switzerland.
Insights
Soluble complement receptor type 1 (sCR1) levels increase in end-stage renal failure, liver cirrhosis, and some hematologic malignancies. These elevated sCR1 levels are reversible after transplantation or chemotherapy, suggesting a link to disease states.
Area of Science:
- Immunology
- Complement System
- Clinical Chemistry
Background:
- Soluble complement receptor type 1 (sCR1) is a circulating form of CR1 (CD35).
- Understanding sCR1 levels in various diseases is crucial for elucidating its role in immune responses.
Purpose of the Study:
- To measure sCR1 concentrations in healthy individuals and patients with diverse diseases.
- To investigate the reversibility of altered sCR1 levels and potential cellular sources.
Main Methods:
- Enzyme-linked immunosorbent assay (ELISA) was used to quantify sCR1 in serum and plasma.
- sCR1 levels were analyzed in normal donors, patients with renal failure, liver cirrhosis, hematologic malignancies, HIV, and SLE.
- In vitro studies assessed sCR1 release from immune cells, and in vivo studies used SCID mice.
Main Results:
- Elevated sCR1 was observed in end-stage renal failure (54.8 ng/ml), liver cirrhosis (158.3 ng/ml), and certain hematologic malignancies (e.g., Hodgkin's lymphoma, B cell lymphoma).
- sCR1 levels decreased significantly post-liver transplantation and after chemotherapy for myeloproliferative syndromes, indicating reversibility.
- No significant changes in sCR1 were noted in HIV-infected patients or SLE patients, despite reduced CR1 on erythrocytes.
Conclusions:
- Increased sCR1 levels are associated with specific disease states, notably end-stage renal failure, liver cirrhosis, and hematologic malignancies.
- The reversibility of elevated sCR1 suggests its dynamic regulation and potential as a disease biomarker.
- Immune cells like monocytes, lymphocytes, and neutrophils are identified as sources of sCR1, with potential lymphocyte synthesis in vivo.
Abstract:
C receptor type 1 (CR1, CD35) is present in a soluble form in plasma (sCR1). Soluble CR1 was measured with a specific ELISA assay in normal individuals and in patients with different diseases. The mean serum concentration of sCR1 in 31 normal donors was 31.4 +/- 7.8 ng/ml, and was identical in plasma. An increase in sCR1 was observed in 36 patients with end-stage renal failure on dialysis (54.8 +/- 11.7 ng/ml, p < 0.0001), and in 22 patients with liver cirrhosis (158.3 +/- 49.9 ng/ml, p < 0.0001). The mean sCR1 levels dropped from 181 +/- 62.7 to 52.1 +/- 24.0 ng/ml (p < 0.001) in nine patients who underwent liver transplantation, and was 33.5 +/- 7.3 in 10 patients with functioning renal grafts, indicating that the increase in sCR1 was reversible. Soluble CR1 was elevated in some hematologic malignancies (> 47 ng/ml), which included B cell lymphoma (12/19 patients), Hodgkin's lymphoma (4/4), and chronic myeloproliferative syndromes (4/5). By contrast, no increase was observed in acute myeloid or lymphoblastic leukemia (10) or myeloma (5). In two patients with chronic myeloproliferative syndromes, sCR1 decreased rapidly after chemotherapy. The mean concentration of sCR1 was not significantly modified in 181 HIV-infected patients at various stages of the disease (34.8 +/- 14.4 ng/ml), and in 13 patients with active SLE (38.3 +/- 19.6 ng/ml), although in both groups the number of CR1 was diminished on E. There was a weak but significant correlation between sCR1 and CR1 per E in HIV infection and SLE (r = 0.39, p < 0.0001, and r = 0.60, p < 0.03 respectively). In vitro, monocytes, lymphocytes, and neutrophils were found to release sCR1 into culture supernatants. In vivo, sCR1 was detected in the serum of SCID mice populated with human peripheral blood leukocytes. The sCR1 levels correlated with those of human IgG (r = 0.97, p < 0.0001), suggesting synthesis of sCR1 by the transferred lymphocytes. The mechanisms underlining the increased levels of sCR1 and its biologic consequences remain to be defined.
