Cutting edge:: Essential role of phospholipase C-γ2 in B cell development and function

被引：132

作者：

Hashimoto, A

Takeda, K

Inaba, M

Sekimata, M

Kaisho, T

Ikehara, S

Homma, Y

Akira, S

Kurosaki, T ^{[1
]}

机构：

[1] Kansai Med Univ, Inst Liver Res, Dept Mol Genet, Moriguchi, Osaka 5708506, Japan

[2] Osaka Univ, Microbial Dis Res Inst, Dept Host Def, Osaka, Japan

[3] Kansai Med Univ, Dept Pathol 1, Moriguchi, Osaka 5708506, Japan

[4] Fukushima Med Coll, Dept Biomol Sci, Fukushima, Japan

来源：

JOURNAL OF IMMUNOLOGY | 2000年 / 165卷 / 04期

关键词：

D O I：

10.4049/jimmunol.165.4.1738

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Cross-linking of the B cell Ag receptor (BCR) induces the tyrosine phosphorylation of multiple cellular substrates, including phospholipase C (PLC)-gamma 2, which is involved in the activation of the phosphatidylinositol pathway. To assess the importance of PLC-gamma 2 in murine lymphopoiesis, the PLC-gamma 2 gene was inducibly ablated by using IFN-regulated Cre recombinase. Mice with a neonatally induced loss of PLC-gamma 2 function displayed reduced numbers of mature conventional B cells and peritoneal B1 cells and defective responses in vitro to BCR stimulation and in vivo to immunization with thymus-independent type II Ags. In contrast, T cell development and TCR-mediated proliferation were normal. Taken together, PLC-gamma 2 is a critical component of BCR signaling pathways and is required to promote B cell development.

引用

收藏

页码：1738 / 1742

页数：5

相关论文

共 24 条

[1] INOSITOL TRISPHOSPHATE AND CALCIUM SIGNALING [J].

BERRIDGE, MJ .

NATURE, 1993, 361 (6410) :315-325

[2] The complexity of signaling pathways activated by the BCR [J].

DeFranco, AL .

CURRENT OPINION IN IMMUNOLOGY, 1997, 9 (03) :296-308

[3] Btk/Tec kinases regulate sustained increases in intracellular Ca2+ following B-cell receptor activation [J].

Fluckiger, AC ;

Li, ZM ;

Kato, RM ;

Wahl, MI ;

Ochs, HD ;

Longnecker, R ;

Kinet, JP ;

Witte, ON ;

Scharenberg, AM ;

Rawlings, DJ .

EMBO JOURNAL, 1998, 17 (07) :1973-1985

[4]

GRYNKIEWICZ G, 1985, J BIOL CHEM, V260, P3440

[5] The B cell-restricted adaptor BASH is required for normal development and antigen receptor-mediated activation of B cells [J].

Hayashi, K ;

Nittono, R ;

Okamoto, N ;

Tsuji, S ;

Hara, Y ;

Goitsuka, R ;

Kitamura, D .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (06) :2755-2760

[6] Inactivation of Btk by insertion of lacZ reveals defects in B cell development only past the pre-B cell stage [J].

Hendriks, RW ;

deBruijn, MFTR ;

Maas, A ;

Dingjan, GM ;

Karis, A ;

Grosveld, F .

EMBO JOURNAL, 1996, 15 (18) :4862-4872

[7] BLNK required for coupling Syk to PLCγ2 and Rac1-JNK in B cells [J].

Ishiai, M ;

Kurosaki, M ;

Pappu, R ;

Okawa, K ;

Ronko, I ;

Fu, C ;

Shibata, M ;

Iwamatsu, A ;

Chan, AC ;

Kurosaki, T .

IMMUNITY, 1999, 10 (01) :117-125

[8] Essential role of the tyrosine kinase substrate phospholipase C-gamma 1 in mammalian growth and development [J].

Ji, QS ;

Winnier, GE ;

Niswender, KD ;

Horstman, D ;

Wisdom, R ;

Magnuson, MA ;

Carpenter, G .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (07) :2999-3003

[9] Abnormal development and function of B lymphocytes in mice deficient for the signaling adaptor protein SLP-65 [J].

Jumaa, H ;

Wollscheid, B ;

Mitterer, M ;

Wienands, J ;

Reth, M ;

Nielsen, PJ .

IMMUNITY, 1999, 11 (05) :547-554

[10] IMPAIRED EXPANSION OF MOUSE B-CELL PROGENITORS LACKING BTK [J].

KERNER, JD ;

APPLEBY, MW ;

MOHR, RN ;

CHIEN, S ;

RAWLINGS, DJ ;

MALISZEWSKI, CR ;

WITTE, ON ;

PERLMUTTER, RM .

IMMUNITY, 1995, 3 (03) :301-312