From these in situ analysis of TNFR expression, it is interesting to note that while TNF antagonists such as soluble TNFRII-Fc fusion protein (Enbrel) and anti-TNFα mAbs have become main stakes in the treatment of autoimmune diseases, the involvement of TNFR expressing cell types seemed to be strikingly different, with immune infiltrates in RA and keratinocytes in psoriasis being the major source of cell types over-expressing TNF receptors. This evidence concerns the gene TNFRSF1B and psoriasis.