2000年8月
Generation, expansion, migration and activation of mouse B1 cells
IMMUNOLOGICAL REVIEWS
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- 巻
- 176
- 号
- 開始ページ
- 205
- 終了ページ
- 215
- 記述言語
- 英語
- 掲載種別
- 書評論文,書評,文献紹介等
- 出版者・発行元
- MUNKSGAARD INT PUBL LTD
We have studied the expansion, activation, homing and antibody production of B1 cells in two different mouse models. One is the Hi transgenic mouse, which carries Ig genes encoding the anti-red blood cell autoantibody (4C8) and develops autoimmune hemolytic anemia by the activation of autoreactive B1 cells that escape from clonal deletion and expand in the peritoneal cavity (PEC). The other model is represented by alymphoplasia (aly) mice, which carry a point mutation in the gene encoding NF-kappa B-inducing kinase (NIK) and have drastically reduced immunoglobulin serum levels, in spite of their peritoneal cavity containing a large number of B1 cells. We have found that a) expression levels of the B-cell antigen receptor (BCR) influence the size of the B1-cell compartment and efficiency of allelic exclusion and BZ-cell deletion; b) antibody production of B1 cells is closely related with their migration from PEC to other lymphoid organs and is dependent on NIK; and c) infection, lipopolysaccharide stimulation, cytokine administration or T-cell activation by noncanonical antigens induces migration and differentiation of peritoneal B1 cells into antibody-producing cells. We describe a scenario where most of B1 and BZ differences are due to a distinct activation threshold of BCR and antigen repertoire.
- リンク情報
- ID情報
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- ISSN : 0105-2896
- Web of Science ID : WOS:000089376400017