Impaired tumour necrosis factor-a (TNF-α) production and abnormal B cell response to TNF-α in patients with systemic lupus erythematosus (SLE).

We examined the TNF-α activity in culture supernatants of monocytes isolated from the peripheral blood of patients with SLE and of normal individuals. The monocytes from patients with SLE stimulated with silica particles, lipopolysaccharide or Staphylococcus aureus Cowan 1 secreted significantly lower amounts of TNF-α than did normal monocytes. A decreased TNF mRNA expression was observed in peripheral blood mononuclear cells stimulated by trtitogens from patients with SLE. Furthermore, we examined the effect of recombinant TNP-α (rTNF-α) on the B cell function in SLE patients. rTNF-α inhibited the spontaneous B cell proliferation of SLE, but tended to enhance the normal B cell proliferation. Spontaneous IgM production from SLE B cells was inhibited by rTNF-α but that from normal B cells was not. Spontaneous IgG production was unaffected by rTNF-α. Also. rTNF-α did not affect the viability of B cells. These findings suggest that an impaired TNF-α production and an abnormal B cell response to TNF-α play a role in the immunological dysfunction in patients with SLE. [ABSTRACT FROM AUTHOR]