| Project/Area Number |
60570305
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
内科学一般
|
|---|
| Research Institution | Kanazawa Medical University, Department of Hematology and Immunolgy Medicine |
|---|
Principal Investigator |
SUGAI Susumu Kanazawa Medical University, Department of Hematology and Immunology Medicine, Associate Professor, 医学部, 助教授 (20064537)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
SHIMIZU Shiro Kanazawa Medical University, Department of Hematology and Immunology Medicine, L, 血液免疫内科, 講師 (50097432)
|
|---|
| Project Period (FY) |
1985 – 1986
|
| Project Status |
Completed (Fiscal Year 1986)
|
| Budget Amount *help |
¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 1986: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1985: ¥1,300,000 (Direct Cost: ¥1,300,000)
|
|---|
| Keywords | Sjogren's syndrome / Rheumatoid factor / Cross-reactive idiotype / Monoclonal anti-idiotypic antibody / Cell surface membrane idiotype / B細胞分化 |
|---|
| Research Abstract |
It is important to study autoantibody idiotype (Id) to clarify the mechanism of autoantibody production and suppression. Rheumatoid factor (RF) is a most common autoantibody seen in many autoimmune diseases. We produced monoclonal anti-Id antisera (mA-Id) by the cell hybridization technique against 3 monoclonal RFs (IgM-K, IgA-L and IgA-K) in patients with Sjogren's syndrome (SS) and one monoclonal RF (IgM-K) in a patient with Waldenstrom's macroglobulinemia. These mA-Id were site-specific antibodies against RFs. The Id determinant was studied by Western blot analysis and identified on the kappa chain (2 IgM-K), mu, kappa and alpha (?) chain (IgA-L) and mu and alpha-kappa chain (IgA-K), respectively. One mA-Id against IgA-K RF detected small nuclear RNPs in the proliferating lymphoid cells. Cross-reactive Id (CRI) was examined among 50 M proteins and 50 sera containing polyclonal RFs by dot and agar gel electrophoresis immunoblot analyses; CRI was found in 40-90% of 7 monoclonal RFs, 10 M proteins and 10 cryoglobulins in SS patients. Some M proteins without RF activity, a few of sera containing polyclonal RFs and even some normal sera showed CRI. These results suggest that there is a RF V gene family or families shared in common in patients and normal persons and these are highly expressed in autoimmune diseases such as SS. Cell surface Id (SmId) and SmIg of peripheral blood lymphocyts (PBL) were examined by the double immunofluorescence method. B cells bearing SmId (0.3-11.8%) were identified in PBL of 4 SS patients with monoclonal RF. B cell differentiation to plasma cells containing cytoplasmic Id was observed in 3 patients by PWM stimulation. These results indicate that monoclonal B cells are pressent in PBL of patients with RF and differentiate to plasma cells in vivo by some stimulations and there might be some controlling mechanism to stimulate or suppress the differentiation of these monoclonal B cells.
|
