LACK OF INTERFERON-GAMMA RECEPTOR-BETA CHAIN AND THE PREVENTION OF INTERFERON-GAMMA SIGNALING IN T(H)1 CELLS

被引：265
作者：
PERNIS, A
GUPTA, S
GOLLOB, KJ
GARFEIN, E
COFFMAN, RL
SCHINDLER, C
ROTHMAN, P
机构：
[1] COLUMBIA UNIV COLL PHYS & SURG, DEPT MED, NEW YORK, NY 10032 USA
[2] COLUMBIA UNIV COLL PHYS & SURG, DEPT MICROBIOL, NEW YORK, NY 10032 USA
[3] DNAX RES INST MOLEC & CELLULAR BIOL INC, PALO ALTO, CA 94304 USA
来源：
SCIENCE | 1995年 / 269卷 / 5221期
关键词：
D O I：
10.1126/science.7618088
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：
The ability of interferon gamma (IFN-gamma) to inhibit the proliferation of type 2 T helper cells (T(H)2), but not that of type 1 (T(H)1) cells, suggests that helper cell subsets might differ in their activation of the IFN-gamma signaling pathway. The IFN-gamma-inducible signal transducing factor (STF-IFN gamma) was activated in murine T(H)2 but not in T(H)1 cell clones, because in the latter the second chain of the IFN-gamma receptor (accessory factor 1 or IFN-gamma R beta) was absent. Thus, T(H)1 cells use receptor modification to prevent the activation of STF-IFN gamma and achieve an IFN-gamma-resistant state.
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页码：245 / 247
页数：3
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