Background: The incidence and mortality of cervical cancer are increasing, which seriously threatens the life and health of women. Lymph node metastasis is a critical factor involved in the survival rate of patients. Research has shown that the immune system plays a key role in suppressing tumor development and metastasis. Thus, to study the relationship between immunity and tumor metastasis, we explored the mechanism by which Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway promotes lymph node metastasis in cervical cancer based on CD8+T cell senescence. Methods: The level of JAK-STAT protein was detected by collecting cervical cancer tissues and adjacent normal tissues. JAK-STAT protein levels were compared in patients with different Federation International of Gynecology and Obstetrics (FIGO) stages and lymph node metastasis. To analyze the diagnostic value of JAK-STAT level in cervical cancer lymph node metastasis, cervical cancer cell lines were infected with JAK-STAT pathway inhibitors to detect cell viability, migration, and invasion. Concurrently, CD8+ T cells were co-cultured with cervical cancer cell lines to assess CD8+ T cell count, surface molecule expression (CD28, CD27, and CD57), and inflammatory factor levels. The lymphoid metastasis model of cervical cancer in nude mice was constructed to observe changes in the general state and lymph node metastasis of nude mice. Cervical cancer infiltration in lymph nodes was certified by pathological method, and the expression of JAK-STAT in lymph tissues was detected. The expressions of CD8+ T cells and surface molecules (CD28, CD27, and CD57), as well as inflammatory factors in lymph nodes were examined. Result: JAK-STAT signaling pathway was activated in cervical cancer tissues, correlated with different FIGO stages and lymph node metastasis, and exhibited a certain degree of clinical diagnostic value (p < 0.05). After JAK-STAT inhibition, cervical cancer cell viability decreased, and migration and invasion ability weakened (p < 0.05). The co-cultivation of CD8+ T cells with cervical cancer cell lines revealed a time-dependent fluctuation in the cell vitality, initially increasing and subsequently decreasing (p < 0.05). Moreover, the expressions of CD28 and CD27 decreased (p < 0.05), and the expression of CD57 increased (p < 0.05). While the cell vitality in the JAK-STAT inhibition + co-culture group initially increased and then slowly decreased (p < 0.05), with an increase in the expressions of CD28 and CD27 and a decrease in the expression of CD57 (p < 0.05). The lymphatic metastasis model of cervical cancer in nude mice revealed that after JAK-STAT inhibition, the lymph nodes were fewer and smaller, and the cervical invasion in the lymph nodes was reduced (p < 0.05). Podoplanin and p-cytokeratin (p-CK) confirmed cervical cancer metastasis in lymph nodes. The number and function of CD8+ T cells in vitro showed that the expressions of CD28, CD27, and CD57 tended to be normal in the blank and the solvent groups. Nevertheless, inflammatory factors Interleukin (IL)-6, IL-1β, and Tumor Necrosis Factor (TNF)-α exhibited an increase, and inhibiting JAK-STAT led to elevated expressions of CD28 and CD27 (p < 0.05). Conversely, CD57 expressions and levels of inflammatory cytokines IL-6, IL-1β, and TNF-α demonstrated a significant reduction (p < 0.05). Conclusions: The JAK-STAT signaling pathway is activated in cervical cancer, contributing to the growth and metastasis of the disease, and influencing the senescence of CD8+ T cells. Inhibition of the JAK-STAT pathway can delay the senescence of CD8+ T cells, weaken the biological behavior of cervical cancer cells, and inhibit tumor metastasis.