2013 Fiscal Year Final Research Report
Analysis of the mechanism of production of pathologic autoantibodies
| Project/Area Number |
23591447
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
膠原病・アレルギー・感染症内科学
|
|---|
| Research Institution | Kitasato University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
NAGAI Tatsuo 北里大学, 医学部, 講師 (60365947)
|
|---|
| Project Period (FY) |
2011 – 2013
|
| Keywords | 自己抗体 / Bリンパ球 / Tリンパ球 / 抗CD３抗体 / クラススイッチ / CTLA4 / CD80 / マクロファージ |
|---|
| Research Abstract |
In order to delineate the mechanism of polyclonal B cell activation, we first explore the mechanism of suppression of B cell by activated T cells using the system with immobilized anti-CD3. Although it was suggested that interactions between CTLA4 on T cells and CD80/86 on B cells might involve in the suppression, we could not get direct evidence.
We also examined whether IgG type autoantibodies might be produced in cultures with immobilized anti-CD3 stimulated mitomycin C-treated T cells and B cells. However, none of IgG anti-DNA, anti-Sm, anti-RNP were produced. Nor could we induce class switch of IgM anti-DNA to IgG anti-DNA with monocytes or alpha-interferon.
Further studies are required to investigate the mechanism of production of IgG anti-DNA.
|
-
-
-
-
-
-
[Journal Article] Serum level of soluble CX3CL1/fractalkine is elevated in patients with polymyositis and dermatomyositis, which is correlated with disease activity2012
Author(s)
Suzuki F, Kubota T, Miyazaki Y, Ishikawa K, Ebisawa M, Hirohata S, Ogura T, Mizusawa H, Imai T, Miyasaka N, Nanki T
-
Journal Title
Arthritis Res Ther
Volume: 14(2)
Pages: R48
DOI
Peer Reviewed
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
