title: Biologic therapeutics in the treatment of psoriasis. Part 1: review.
abstract: BACKGROUND
  Psoriasis is a chronic inflammatory skin disease principally mediated by activated T cells, which release proinflammatory cytokines with reactive epidermal changes in the skin, producing the characteristic lesions of psoriasis. New research into possible treatment options has been inspired by increased understanding of the pathophysiology of psoriasis and advances in immunology and molecular biology permitting the development of targeted, highly active biologic agents.
  
  
  OBJECTIVE
  The aim of this article is to review the efficacy and safety of five biologic therapeutics in the treatment of moderate to severe psoriasis and to provide practical guidelines for integration of these agents in the management of psoriasis.
  
  
  METHODS
  We searched MEDLINE (1966-2005) for articles containing the key words: alefacept, efalizumab, etanercept, infliximab, and adalimumab and searched recent conference abstracts.
  
  
  RESULTS
  Emerging immunotherapeutic agents (fusion proteins, recombinant cytokines, fusion toxins, or antibodies) target T cells or cytokines responsible for plaque formation that is characteristic of psoriasis. Alefacept is the first biologic to be approved in both the United States and Canada. More recently, efalizumab and etanercept and infliximab have been approved in the United States and Canada for plaque-type psoriasis. Adalimumab is currently in phase III clinical trials.
  
  
  CONCLUSIONS
  These novel biologics offer an intriguing and effective treatment option for patients with moderate to severe psoriasis.
authors.affiliation: Department of Medicine, Dalhousie University, Halifax, NS, Canada. richard.langley@dal.ca
authors.forename: Richard G
authors.initials: RG
authors.lastname: Langley
authors.forename: Aditya K
authors.initials: AK
authors.lastname: Gupta
authors.forename: Andrea M
authors.initials: AM
authors.lastname: Cherman
authors.forename: Kimberley A
authors.initials: KA
authors.lastname: Inniss
mesh_terms: D000068879:Adalimumab; D000077944:Alefacept; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D001691:Biological Therapy / Q000379:methods*; D018845:CD11 Antigens / Q000627:therapeutic use; D003879:Dermatologic Agents / Q000627:therapeutic use*; D000068800:Etanercept; D006801:Humans; D007074:Immunoglobulin G / Q000627:therapeutic use; D007155:Immunologic Factors / Q000627:therapeutic use; D000069285:Infliximab; D011565:Psoriasis / Q000628:therapy*; D018124:Receptors, Tumor Necrosis Factor / Q000627:therapeutic use; D011993:Recombinant Fusion Proteins / Q000627:therapeutic use; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D018845:CD11 Antigens; D003879:Dermatologic Agents; D007074:Immunoglobulin G; D007155:Immunologic Factors; D018124:Receptors, Tumor Necrosis Factor; D011993:Recombinant Fusion Proteins; D014409:Tumor Necrosis Factor-alpha; D000069285:Infliximab; D000077944:Alefacept; D000068879:Adalimumab; D000068800:Etanercept; C472181:efalizumab