Psoriasis is an immune-mediated chronic inflammatory skin disease whose etiology is still unclear. Numerous approaches are available to treat psoriasis, but often with limited effectiveness or significant toxicity with long-term use, especially in patients with moderate to severe psoriasis treated with traditional oral medications. Some of the biologics now approved for use in different countries (selectively acting on different stages of the immunogenesis of psoriasis) include alefacept, efalizumab, infliximab, adalimumab, etanercept, and the recently launched Etancercept), and the newly marketed Ustekinumab (Ustekinumab) show different efficacy in the treatment of psoriasis, while the use of these biologics is not accompanied by the dose-limiting organ toxicity of conventional drug therapy for psoriasis. 1. alefacept (alefacept,LFA-3Tip,Amevive): a recombinant protein that acts mainly on CD2 on T cells, consisting of the first extra-membrane region of LFA-3 and the human IgG1Fc fraction. The LFA-3 extracellular region binds to CD2 on the surface of CD2+ cells (mainly activated T cells and CD45RO+ memory T cells), and the Fc part binds to FcγR on the surface of NK cells and then stimulates the release of granzyme B from NK cells, which, together with perforin, causes an intracellular cascade reaction in bridging CD2+ target cells and finally causes apoptosis of the target cells. 2. efalizumab (efalizumab,hull24,Xanelim): a humanized monoclonal antibody against CD11a, a unique alpha chain of LFA-1 on the surface of T cells, which can block the binding of LFA-1 on T cells to ICAMs on antigen-presenting cells, thereby attenuating the necessary co-stimulatory effect of activated T cells. The drug also blocks the migration of activated T cells to the focal area. In addition, the drug blocks the interaction between Tc1 and keratin-forming cells in epidermal lesions. TNF can induce the production of adhesion factor in the skin and promote the infiltration of leukocytes, promote the maturation of Langerhans cells in psoriasis lesions, enhance their ability to activate T cells, and strengthen the proliferation of keratinocytes in psoriasis lesions. The drug binds to TNF, blocking the binding of TNF and its cell surface receptors so as to play a role. 4.Adalimumab: It is a recombinant fully human IgG1 monoclonal antibody that can specifically bind to TNFα, a pro-inflammatory cytokine that plays an important role in the pathogenesis of psoriasis. 5. etanercept (Enbrel): recombinant type II tumor necrosis factor receptor-antibody fusion protein, a fusion protein consisting of the human p75 TNF receptor and the Fc portion of human IgG1. The drug blocks the binding of TNF to TNF receptor, thus blocking the effect of TNF. 6, Ustekinumab: a human interleukin-12 p40 fully human IgG1κ monoclonal antibody, named Ustekinumab (also known as CNTO 1275). ustekinumab can bind with high affinity to the p40 subunit shared by human IL-12 and IL-23, thus preventing it from binding to T cells, natural killer cells and antigenic tissues. natural killer cells and IL-12 receptor β1 (IL-12Rβ1) expressed on the surface of antigen-presenting cells.