In this study, we first confirmed that IgG interacted with TLR4 after lipopolysaccharide (LPS) stimulation and enhanced its expression in cervical cancer cells that significantly strengthened LPS-induced activities of NF-κB and MAPK including extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38, which in turn increased the production of proinflammatory cytokines including TNF-α, IL-6, and IL-1β. This evidence concerns the gene TLR4 and cervical carcinoma.