Erythrocytic Receptors for the Third Complement Component in Patients with Systemic Lupus Erythematosus.
Project/Area Number |
60570295
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Research Category |
Grant-in-Aid for General Scientific Research (C)
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Allocation Type | Single-year Grants |
Research Field |
内科学一般
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Research Institution | Kyushu University |
Principal Investigator |
YOKOTA Eisuke Faculty of Medicine, Kyushu University , Assistant, 医学部, 助手 (60167723)
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Project Period (FY) |
1985 – 1986
|
Project Status |
Completed (Fiscal Year 1986)
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Budget Amount *help |
¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1986: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1985: ¥900,000 (Direct Cost: ¥900,000)
|
Keywords | SLE / CRI |
Research Abstract |
Erythrocytic receptors for the third complement component (CR1) were measured by the use of an immune-adherence hemagglutination (IAHA) reaction. The erythrocytes were obtained from 112 patients with definite systemic lupus erythematosus (SLE), and 162 normal controls in Fukuoka population. Apparently healthy 685 subjects residing in Yonaguni and Hateruma Islands were also studied. The CR1 activities on erythrocyte membraines were deficient in 65% of the patients with SLE in Fukuoka population, as compared to the 77 individuals (9.1%) among 847 normal controls. Pedigree analysis indicated that the deficiency was determined by an autosomal recessive mode of inheritance, except for 4 families for which an autosomal recessive gene was unlikely to be involved. To clarify the mode of inheritance of defective CR1 activity, we assessed CR1 activities in 25 families among normal controls in Okinawa. Family study in this population revealed that the deficiency was determined by an autosomal recessive gene. The CR1 activities both in patients with SLE and in healthy individuals, were genetically determined by an autosomal recessive gene. Some acquired factors, such as disease activity of SLE, were thought to involve in the variability of CR1 activities.
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Report
(1 results)
Research Products
(2 results)