Differential regulation of HIV-1 fusion cofactor expression by CD28 costimulation of CD4(+) T cells

被引:175
作者
Carroll, RG
Riley, JL
Levine, BL
Feng, Y
Kaushal, S
Ritchey, DW
Bernstein, W
Weislow, OS
Brown, CR
Berger, EA
June, CH
StLouis, DC
机构
[1] HENRY M JACKSON FDN ADVANCEMENT MIL MED,ROCKVILLE,MD 20850
[2] USN,MED RES INST,IMMUNE CELL BIOL PROGRAM,BETHESDA,MD 20889
[3] WALTER REED ARMY INST RES,DIV RETROVIROL,ROCKVILLE,MD 20850
[4] NIAID,VIRAL DIS LAB,NIH,BETHESDA,MD 20889
[5] SRA TECHNOL,ROCKVILLE,MD 20850
[6] NIAID,INFECT DIS LAB,NIH,ROCKVILLE,MD 20852
关键词
D O I
10.1126/science.276.5310.273
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 [理学]; 0710 [生物学]; 09 [农学];
摘要
Activation of CD4(+) T lymphocytes from human immunodeficiency virus-type 1 (HIV-1)-infected donors with immobilized antibodies to CD3 and CD28 induces a virus-resistant state. This effect is specific for macrophage-tropic HIV-I, Transcripts encoding CXCR4/Fusin, the fusion cofactor used by T cell line-tropic isolates, were abundant in CD3/CD28-stimulated cells, but transcripts encoding CCR5, the fusion cofactor used by macrophage-tropic viruses, were not detectable. Thus, CD3/CD28 costimulation induces an HIV-1-resistant phenotype similar to that seen in some highly exposed and HIV-uninfected individuals.
引用
收藏
页码:273 / 276
页数:4
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