【目的】 明确氯虫苯甲酰胺对斜纹夜蛾Spodoptera litura幼虫细胞免疫的亚致死效应，探究斜纹夜蛾抵御杀虫剂胁迫的机制。【方法】 以斜纹夜蛾4龄幼虫为研究对象，分别用LC₁₀、LC₂₀和LC₃₀的氯虫苯甲酰胺处理，测定并分析幼虫血细胞形态、总数量以及吞噬、结节和包囊作用的变化。【结果】 根据毒力测定结果，氯虫苯甲酰胺对斜纹夜蛾4龄幼虫处理48 h的LC₁₀、LC₂₀和LC₃₀分别为0.190、0.459和0.868 μg/g。亚致死浓度氯虫苯甲酰胺在一定程度上促进幼虫血细胞总数量增加。斜纹夜蛾幼虫的血细胞类型包括原血细胞、浆血细胞、粒血细胞、珠血细胞以及类绛色细胞。在亚致死浓度氯虫苯甲酰胺处理下，斜纹夜蛾幼虫部分血细胞出现细胞皱缩、细胞膜变形、胞质空泡化、粒细胞脱粒及细胞核形变甚至凋亡等形态变化。LC₁₀氯虫苯甲酰胺在48 h后能抑制吞噬作用，LC₂₀氯虫苯甲酰胺在12 h后促进幼虫的吞噬作用，在6、48和72 h显著抑制（P<0.01）吞噬作用，LC₃₀氯虫苯甲酰胺能显著抑制斜纹夜蛾吞噬作用，但随着处理时间增加抑制作用逐渐减弱。LC₁₀、LC₂₀和LC₃₀氯虫苯甲酰胺均能显著（P<0.01）抑制斜纹夜蛾结节作用。LC₁₀氯虫苯甲酰胺能抑制斜纹夜蛾包囊作用，而LC₂₀和LC₃₀在12和24 h会促进包囊作用，在72 h显著（P<0.01）抑制。【结论】 氯虫苯甲酰胺对斜纹夜蛾细胞免疫的亚致死效应表现为改变部分血细胞形态，一定程度上促进血细胞总数量增加，显著抑制结节作用。此外，随着药剂浓度和处理时间增加，亚致死浓度氯虫苯甲酰胺先促进后抑制吞噬和包囊作用。从昆虫免疫作用角度为未来害虫的控制和管理策略提供了理论依据。

[Aim]  To determine the sublethal effects of chlorantraniliprole on the cellular immunity of Spodoptera litura larvae and explore the mechanisms of involved in insecticide resistance. [Methods]  Forth instar S. litura larvae were exposed to LC₁₀, LC₂₀ and LC₃₀ concentrations of chlorantraniliprole. Hemocyte morphology, total hemocyte count, phagocytosis, nodulation, and encapsulation were measured to compare the effect of different sublethal exposure doses of chlorantraniliprole on the cellular immunity of S. litura larvae. [Results]  Based on the bioassay, the LC₁₀, LC₂₀, and LC₃₀ values of chlorantraniliprole for 4th instar S. litura larvae after 48 h of exposure were 0.190, 0.459, and 0.868 μg/g, respectively. A moderate increase in the total hemocyte count was observed following exposure to sublethal concentrations of chlorantraniliprole. S. litura larvae have several types of hemocytes including prohemocytes, plasmatocytes, granulocytes, spherulocytes, and oenocytoids. Exposure to sublethal concentrations of chlorantraniliprole resulted in various morphological changes to some hemocytes such as cell shrinkage, cell membrane deformation, vacuolation, granulocyte degranulation, cell nucleus deformation, cell nucleus apoptosis, among others. Exposure to LC₁₀ chlorantraniliprole for 48 h inhibited phagocytosis. Exposure to LC₂₀ chlorantraniliprole for 12 h promoted phagocytosis, while exposures of 6, 48, and 72 h significantly (P<0.01) inhibited phagocytosis. Exposure to LC₃₀ chlorantraniliprole significantly inhibited phagocytosis, but the inhibitory effect gradually weakened with increasing treatment time. Exposure to LC₁₀, LC₂₀, and LC₃₀ chlorantraniliprole all significantly (P<0.01) inhibited nodulation in S. litura. LC₁₀ chlorantraniliprole exposure inhibited encapsulation, while LC₂₀ and LC₃₀ promoted encapsulation after 12 and 24 h exposure. However, longer exposure times significantlyinhibited encapsulation (P<0.01). [Conclusion]  The results of this study indicate that sublethal doses of chlorantraniliprole affect the hemocyte immunity of  S. litura larvae, causing changes in larval hemocyte morphology, a moderate increase in total hemocyte count, and inhibiting nodulation. Phagocytosis and encapsulation were initially promoted, but then inhibited with increasing chlorantraniliprole concentration and treatment time. This study offers valuable information for future pest control and management strategies from the perspective of insect immunity.