Lee M E, Adams J W, Villinger F, Brar S S, Meadows M, Bucur S Z, Lackey D A, Brice G T, Cruikshank W W, Ansari A A, Hillyer C D
Department of Pathology and Laboratory Medicine and the Winship Cancer Center, Emory University School of Medicine, Atlanta, Georgia 30329, USA.
AIDS Res Hum Retroviruses. 1998 Oct 10;14(15):1323-8. doi: 10.1089/aid.1998.14.1323.
Interleukin 16 (IL-16) has been shown to diminish HIV and SIV replication through inhibition of HIV and SIV mRNA transcription. To evaluate its role further, we compared IL-16 cloned from disease-susceptible rhesus macaques and disease-resistant sooty mangabeys. Recombinant rhesus macaque (rr) IL-16 was compared with recombinant sooty mangabey (rm), human, and other nonhuman primate IL-16 sequences and evaluated for its ability to induce chemotaxis and inhibit the mixed lymphocyte response (MLR). Also, rrIL-16 and rmIL-16 were evaluated for suppression of SIVmac251, which replicates efficiently in T cells and monocyte/macrophages (dual tropic), and cloned SIVmac239, which replicates efficiently in T cells (T tropic). Sequence comparison of rrIL-16 and rmIL-16 with human IL-16 showed >97% amino acid identity. Biocharacterization of rrIL-16 revealed potent induction of chemotaxis (p < 0.05) and marked inhibition of MLR (73 +/- 0.6%,p < 0.05) in rhesus and human cell systems. Using rrIL-16 and rmIL-16, p27 antigen production from PBMCs infected with SIVmac251 was decreased up to 70% (p < 0.05 and p < 0.01, respectively). In similar cultures infected with SIVmac239, rrIL-16 and rmIL-16 reduced p27 levels by 96 and 100%, respectively. These data demonstrate the biologic and antiviral functionality of rrIL-16 and rmIL-16.
白细胞介素16（IL-16）已被证明可通过抑制HIV和SIV mRNA转录来减少HIV和SIV复制。为了进一步评估其作用，我们比较了从疾病易感恒河猴和抗病黑掌卷尾猴克隆的IL-16。将重组恒河猴（rr）IL-16与重组黑掌卷尾猴（rm）、人及其他非人类灵长类动物的IL-16序列进行比较，并评估其诱导趋化性和抑制混合淋巴细胞反应（MLR）的能力。此外，还评估了rrIL-16和rmIL-16对SIVmac251（在T细胞和单核细胞/巨噬细胞中高效复制，即双嗜性）和克隆的SIVmac239（在T细胞中高效复制，即T嗜性）的抑制作用。rrIL-16和rmIL-16与人IL-16的序列比较显示氨基酸同一性>97%。rrIL-16的生物学特性表明，在恒河猴和人类细胞系统中，它能有效诱导趋化性（p<0.05）并显著抑制MLR（73±0.6%，p<0.05）。使用rrIL-16和rmIL-16，感染SIVmac251的PBMC中p27抗原的产生分别降低了70%（分别为p<0.05和p<0.01）。在感染SIVmac239的类似培养物中，rrIL-16和rmIL-16分别使p27水平降低了96%和100%。这些数据证明了rrIL-16和rmIL-16的生物学和抗病毒功能。
