Interleukin 4 and human immunodeficiency virus stimulate LFA-1-ICAM-1-mediated aggregation of monocytes and subsequent giant cell formation.
Interleukin 4 and human immunodeficiency virus stimulate LFA-1-ICAM-1-mediated aggregation of monocytes and subsequent giant cell formation.
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白细胞介素 4 和人类免疫缺陷病毒刺激 LFA-1-ICAM-1 介导的单核细胞聚集以及随后的巨细胞形成。
DOI：
10.1099/0022-1317-75-10-2795
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Anthony L. Cunningham
中科院分区：
文献类型：
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作者：
Farhad Kazazi;Joon Chang;Angel F. Lopez;M. Vadas;Anthony L. Cunningham
检测重组白介素4(IL-4)对人类免疫缺陷病毒(HIV)感染和未感染单核细胞的细胞团和多核巨细胞(MGC)形成的影响。通过离心洗脱和单抗补体依赖的残存T细胞裂解分离人血单核细胞，并感染低传代HIV毒株。单核细胞接种HIV后，持续给予重组IL-4(1~20 ng/ml)。IL-4对单核细胞ICAM-1的表达有明显的促进作用，但对LFA-1无明显影响，但底物黏附的刺激作用更强。经Giemsa固定和染色后，对单核细胞簇和MGC的形成进行定量。在IL-4刺激后4-7天，HIV感染和未感染的单核细胞群持续显著增加。HIV和IL-4的结合比单独使用任何一种治疗都更具刺激性。在5个未感染的单核细胞中有2个和7个感染艾滋病毒的单核细胞中有3个，在刺激后10到14天，MGC的形成也显著增加。与抗LFA-1(抗CD11a、抗CD18)和抗ICAM-1(抗CD54)单抗共同孵育可减少IL-4刺激的单核细胞聚集，从而减少MGC的形成。抗ICAM-1在抑制HIV感染的单核细胞聚集方面不如抗CD11a或抗CD18，在这些培养物中抗ICAM-2也具有抑制作用。抗CD11a或抗ICAM-1不能持续降低细胞外HIV抗原浓度。因此，IL-4显著增强了HIV感染和未感染单核细胞的单核细胞聚集性，可能是通过增强所有培养物中LFA-1-ICAM-1的相互作用和感染单核细胞中LFA-1-ICAM-2的相互作用，导致某些培养物中MGC的形成。
The effects of recombinant interleukin 4 (IL-4) on cell cluster and multinucleated giant cell (MGC) formation from human immunodeficiency virus (HIV)-infected and uninfected monocytes were examined. Human blood monocytes were isolated by centrifugal elutriation and monoclonal antibody-complement-dependent lysis of residual T cells, and infected with low passage HIV strains. Monocytes were exposed to recombinant IL-4 (1 to 20 ng/ml), continuously after inoculation with HIV. Monocyte expression of ICAM-1 but not LFA-1 was significantly enhanced by IL-4 although substrate adherence was a more potent stimulus. Monocyte cluster and MGC formation was quantified after fixation and staining with Giemsa. Clusters of HIV-infected and uninfected monocytes were consistently and significantly increased at 4 to 7 days after IL-4 stimulation. The combination of HIV and IL-4 was more stimulatory than either treatment alone. In two out of five uninfected and three out of seven HIV-infected monocyte cultures, MGC formation was also markedly increased at 10 to 14 days after stimulation. Incubation with anti-LFA-1 (anti-CD11a, anti-CD18) and anti-ICAM-1 (anti-CD54) monoclonal antibodies reduced IL-4-stimulated aggregation in HIV-infected and uninfected monocytes and subsequently reduced MGC formation. Anti-ICAM-1 was not as effective as anti-CD11a or anti-CD18 in inhibiting aggregation of HIV-infected monocytes and in these cultures anti-ICAM-2 was also inhibitory. Extracellular HIV antigen concentrations were not consistently reduced by anti-CD11a or anti-ICAM-1. Hence IL-4 markedly enhanced monocyte aggregation in both HIV-infected and uninfected monocytes, probably through enhanced LFA-1-ICAM-1 interactions in all cultures and LFA-1-ICAM-2 interactions in infected monocytes, leading subsequently to MGC formation in some cultures.