Schofield L, McConville M J, Hansen D, Campbell A S, Fraser-Reid B, Grusby M J, Tachado S D
Walter and Eliza Hall Institute of Medical Research, Post Office, Royal Melbourne Hospital, Victoria 3050, Australia.
Science. 1999 Jan 8;283(5399):225-9. doi: 10.1126/science.283.5399.225.
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.
免疫球蛋白G(IgG)反应需要传统的CD4(+)辅助性T细胞对肽片段进行主要组织相容性复合体(MHC)限制的识别。然而,发现对糖基磷脂酰肌醇(GPI)锚定蛋白抗原的免疫球蛋白G反应部分是通过胸腺依赖性、产生白细胞介素-4的CD4(+)、自然杀伤细胞抗原1.1 [(NK1.1)+]辅助性T细胞对GPI部分的CD1d限制识别来调节的。CD1-NKT细胞途径调节对疟原虫和锥虫GPI锚定表面抗原的免疫球蛋白G反应,并且可能是对多种病原体进行快速、不受MHC限制的抗体反应的一般机制。