首页    期刊浏览 2024年12月03日 星期二
登录注册

文章基本信息

  • 标题:HIV-1-suppressive factors are secreted by CD4+ T cells during primary immune responses
  • 本地全文:下载
  • 作者:Sayed F. Abdelwahab ; Fiorenza Cocchi ; Kenneth C. Bagley
  • 期刊名称:Proceedings of the National Academy of Sciences
  • 印刷版ISSN:0027-8424
  • 电子版ISSN:1091-6490
  • 出版年度:2003
  • 卷号:100
  • 期号:25
  • 页码:15006-15010
  • DOI:10.1073/pnas.2035075100
  • 语种:English
  • 出版社:The National Academy of Sciences of the United States of America
  • 摘要:CD4+ T cells are required for immunity against many viral infections, including HIV-1 where a positive correlation has been observed between strong recall responses and low HIV-1 viral loads. Some HIV-1-specific CD4+ T cells are preferentially infected with HIV-1, whereas others escape infection by unknown mechanisms. One possibility is that some CD4+ T cells are protected from infection by the secretion of soluble HIV-suppressive factors, although it is not known whether these factors are produced during primary antigen-specific responses. Here, we show that soluble suppressive factors are produced against CXCR4 and CCR5 isolates of HIV-1 during the primary immune response of human CD4+ T cells. This activity requires antigenic stimulation of naive CD4+ T cells. One anti-CXCR4 factor is macrophage-derived chemokine (chemokine ligand 22, CCL22), and anti-CCR5 factors include macrophage inflammatory protein-1 (CCL3), macrophage inflammatory protein-1{beta} (CCL4), and RANTES (regulated upon activation of normal T cells expressed and secreted) (CCL5). Intracellular staining confirms that CD3+CD4+ T cells are the source of the prototype HIV-1-inhibiting chemokines CCL22 and CCL4. These results show that CD4+ T cells secrete an evolving HIV-1-suppressive activity during the primary immune response and that this activity is comprised primarily of CC chemokines. The data also suggest that production of such factors should be considered in the design of vaccines against HIV-1 and as a mechanism whereby the host can control infections with this virus.
国家哲学社会科学文献中心版权所有