This concerns a patient with severe rheumatoid arthritis (RA) and lymphadenopathy (LA) who showed suboptimal clinical response to antitumor necrosis factor alpha (TNFalpha) antibody (Ab), cA2 therapy. The assessment of TNFalpha and IL-6 mRNA expression in the swollen lymph-node (LN) of the patient by reverse transcription, polymerase chain reaction (RT-PCR) before cA2 treatment, showed only enhanced IL-6 production, but not TNFalpha. Moreover, cA2 failed to inhibit in-vitro spontaneous IL-6 production in the LN block culture from the patient. Taken together, these results indicate that IL-6 production in the swollen LNs of the patient might not depend on TNFalpha. This might partly cause suboptimal clinical response to anti-TNFalpha Ab therapy in the patient.