Skip to main content
Figure 1 | Arthritis Res Ther

Figure 1

From: SLE - Complex cytokine effects in a complex autoimmune disease: tumor necrosis factor in systemic lupus erythematosus

Figure 1

In the afferent limb of the (auto)immune response, tumor necrosis factor (TNF) acts as a growth factor for B cells and may promote dendritic cell (DC) maturation, but leads to T-cell hyporesponsiveness and to the expression of anti-apoptotic molecules. Its inhibition by TNF-blocking agents here could influence the immune response in several ways. First, by better activation of T cells, including help for B cells and influences in the T helper type 1/T helper type 2 cell balance (via IL-6). Second, by reduced TNF effects (but increased IFN-α effects) on DCs, and thus a divergence in DC maturation and activation steps. Finally, by effects of B-cell activation via interference with B-cell proliferation and (IL-6-mediated) class switching. All these changes could modulate autoimmunity, particularly when paralleled by effects on apoptosis (induction or inhibition). In the efferent limb, TNF is induced by immune complexes (IC), and promotes inflammation and secondary tissue destruction; liberation of autoantigens during necrosis could fuel autoimmunity. TNF blockade therefore rapidly reduces TNF-induced inflammation, but may also block immunomodulatory and anti-apoptotic activities of TNF. Taken together, TNF blockade can interfere in a beneficial way with tissue destruction, but in the afferent limb it may in part foster autoimmunity. Ag, antigen; Ab, antibodies; M0, monocytes/macrophages; T, T cells; B, B cells.

Back to article page