CD1d-restricted immunoglobulin G formation to GPI-anchored antigens mediated by NKT cells

被引：332

作者：

Schofield, L ^{[1
]}

McConville, MJ

Hansen, D

Campbell, AS

Fraser-Reid, B

Grusby, MJ

Tachado, SD

机构：

[1] Royal Melbourne Hosp, Walter & Eliza Hall Inst Med Res, Melbourne, Vic 3050, Australia

[2] Univ Melbourne, Dept Biochem & Mol Biol, Parkville, Vic 3052, Australia

[3] INSMED Pharmaceut, Richmond, VA 23219 USA

[4] Nat Prod & Glycotechnol, Durham, NC 27707 USA

[5] Harvard Univ, Sch Publ Hlth, Dept Immunol & Infect Dis, Boston, MA 02115 USA

[6] Harvard Univ, Sch Med, Dept Med, Boston, MA 02115 USA

来源：

SCIENCE | 1999年 / 283卷 / 5399期

关键词：

D O I：

10.1126/science.283.5399.225

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Immunoglobulin G (IgG) responses require major histocompatibility complex (MHC)-restricted recognition of peptide fragments by conventional CD4(+) helper T cells. Immunoglobulin G responses to glycosylphosphatidylinositol (GPI)-anchored protein antigens, however, were found to be regulated in part through CD1d-restricted recognition of the GPI moiety by thymus-dependent, interleukin-4-producing CD4(+), natural killer cell antigen 1.1 [(NK1.1)(+)] helper T cells. The CD1-NKT cell pathway regulated immunogobulin G responses to the GPI-anchored surface antigens of Plasmodium and Trypanosoma and may be a general mechanism for rapid, MHC-unrestricted antibody responses to diverse pathogens.

引用

页码：225 / 229

页数：5

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