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. The gene discussed is TNFRSF1B; the disease is autoimmune disease.