Robbins P A, Roderiquez G L, Peden K W, Norcross M A
Laboratory of Cell and Viral Regulation, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, Maryland 20892, USA.
AIDS Res Hum Retroviruses. 1998 Nov 1;14(16):1397-406. doi: 10.1089/aid.1998.14.1397.
The effect of macrophage (M)-tropic and T cell line (T)-tropic human immunodeficiency virus type 1 (HIV-1) infection on antigen-specific CD4 cytotoxic T lymphocytes (CTLs) has been studied using a CD4 CTL line specific for a peptide from influenza B virus hemagglutinin. In the absence of antigen presentation, the production of CC chemokines was low. Both the M-tropic HIV-1 strain (HIV-1AD) and the T-tropic HIV-1 strain (HIV-1LAI) established productive infections in the CD4 CTLs, decreasing antigen-specific cytotoxicity. Peptide presented to the CD4 CTLs increased their secretion of RANTES and MIP-1beta, suppressed M-tropic HIV-1 replication, downmodulated CCR5 expression, and preserved CTL recognition. The suppression of M-tropic HIV-1 replication and downmodulation of the CCR5 receptor likely resulted from CC chemokine secretion since antibodies to CC chemokines restored M-tropic HIV-1 replication. Antigen presentation did not protect CD4 CTLs from T-tropic HIV-1 infection or preserve their CTL recognition. Thus, these CD4 CTLs do not make suppressor factors that inhibit the T-tropic HIV-1LAI isolate. The results indicate that these CD4 CTLs can either harbor or suppress M-tropic HIV-1 infection, depending on whether antigen is present. CD4 CTLs might therefore provide some protection in the early stages of HIV-1 infection when M-tropic isolates are present.
利用一种对乙型流感病毒血凝素肽具有特异性的CD4细胞毒性T淋巴细胞（CTL）系，研究了巨噬细胞（M）嗜性和T细胞系（T）嗜性1型人类免疫缺陷病毒（HIV-1）感染对抗原特异性CD4 CTL的影响。在没有抗原呈递的情况下，CC趋化因子的产生较低。M嗜性HIV-1毒株（HIV-1AD）和T嗜性HIV-1毒株（HIV-1LAI）均在CD4 CTL中建立了有效感染，降低了抗原特异性细胞毒性。呈递给CD4 CTL的肽增加了它们的RANTES和MIP-1β分泌，抑制了M嗜性HIV-1复制，下调了CCR5表达，并保留了CTL识别能力。M嗜性HIV-1复制的抑制和CCR5受体的下调可能是由于CC趋化因子的分泌，因为针对CC趋化因子的抗体恢复了M嗜性HIV-1复制。抗原呈递并不能保护CD4 CTL免受T嗜性HIV-1感染或保留其CTL识别能力。因此，这些CD4 CTL不会产生抑制T嗜性HIV-1LAI分离株的抑制因子。结果表明，这些CD4 CTL根据是否存在抗原，既可以容纳也可以抑制M嗜性HIV-1感染。因此，当存在M嗜性分离株时，CD4 CTL可能在HIV-1感染的早期阶段提供一些保护。
