FUNCTIONAL ANALYSES OF B-CELLS IN (NZW X BXSB) F1-MICE

被引：8

作者：

ADACHI, Y ^{[1
]}

INABA, M ^{[1
]}

INABA, K ^{[1
]}

NAGATA, N ^{[1
]}

KOBAYASHI, Y ^{[1
]}

IKEHARA, S ^{[1
]}

机构：

[1] KANSAI MED UNIV,DEPT PATHOL 1,1 FUMIZONO CHO,MORIGUCHI,OSAKA 570,JAPAN

来源：

AUTOIMMUNITY | 1993年 / 15卷 / 02期

关键词：

B-CELLS; HYPERREACTIVITY; AUTOANTIBODY; (NZW X BXSB)F1 MOUSE;

D O I：

10.3109/08916939309043884

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Functions of B cells from (NZW x BXSB)F1 (W/BF1) mice are investigated. The W/BF1 mouse, which is an animal model for systemic lupus erythematosus (SLE) and immune thrombocytopenic purpura (ITP), produces anti-DNA and anti-platelet antibodies; W/BF1 mice show hypergammaglobulinemia (particularly increases in IgG2a and IgG2b). The ratio of small resting B cells to large activated B cells in W/BF1 mice is low compared to normal mice, suggesting that B cells in W/BF1 mice are already activated in vivo. Furthermore, small resting B cells separated by a Percoll density gradient technique show hyper-responsiveness to lipopolysaccharide (LPS) or anti-mu plus IL-4. This suggests that B cells in W/BF1 mice are genetically programmed to be easily activated, resulting in the overproduction of autoantibodies. A significant number of CD5+B cells are found in the lymph nodes of old W/BF1 mice. These findings indicate that all cells in the B cell lineage of W/BF1 mice are already activated in vivo.

引用

页码：99 / 105

页数：7

共 16 条

[1]

Minoda M., Hamada K., Higashikawa M., Sugishima H., Funauchi M., Horiuchi A., Examination of the inhibitory effects of interferon-gamma on interleukin-4-induced stimulation of resting B cells from NZB/NZW F1 mice, Clin exp Immunol, 78, pp. 115-119, (1989)

[2]

Hang L., Izui S., Dixon F.J., (NZW x BXSB)F1 Hybrid. A model of acute lupus and coronary vascular disease with myocardial infarction, J Exp Med, 154, pp. 216-221, (1981)

[3]

Oyaizu N., Yasumizu R., Miyama-lnaba M., Nomura S., Yoshida H., Miyawaki S., (NZW x BXSB)F1 mouse. A new animal model of idiopathic thrombocytopenic purpura, J Exp Med, 167, pp. 2017-2022, (1988)

[4]

Hang L., Stephens-Larson P., Henry J.P., Dixon F.J., The role of hypertension in the vascular disease and myocardinal infarcts associated with murine systemic lupus erythematosus, Arthritis and Rheumatism, 26, pp. 1340-1345, (1983)

[5]

Birkeland L.M., Johnson P., Trowbridge I.S., Pure E., Changes in CD45 isoform expression accompany antigen-induced murine T-cell activation, Proc Natl Acad Sci, 86, pp. 6734-6743, (1989)

[6]

Boom W.H., Liano D., Abbas A.K., Heterogeneity of helper/inducer T lymphocytes. Effects of interleukin 4-and inter-leukin 2-producing T cell clones on resting B lymphocytes, J Exp Med, 167, pp. 1350-1363, (1988)

[7]

Inaba M., Inaba K., Adachi Y., Nango K., Ogata H., Muramatsu S., Functional analyses of thymic CD5<sup>+</sup> B cells. Responsiveness to major histocompatibility complex class II-restricted T blasts but not to lipopolysaccharide or anti-IgM plus interleukin 4, J Exp Med, 171, pp. 321-326, (1990)

[8]

Ikehara S., Good R.A., Nakamura T., Sekita K.-I., Inoue S., Maung Maung O.O., Rationale for bone marrow transplantation in the treatment of autoimmune diseases, Proc Natl Acad Sci, 82, pp. 2483-2487, (1985)

[9]

Theofilopoulos A.N., Dixon F.J., Experimental murine systemic lupus erythematosus, Systemic lupus erythematosus, pp. 121-202, (1987)

[10]

Hardy R.R., Hayakawa K., Development and physiology of Ly-1 B and its human homologue, Leu-1 B, Immunol Rev, 93, pp. 53-80, (1986)

← 1 2 →