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    • Letter to the Editor
      Open Access

      Complement C3 Exacerbates Imiquimod-Induced Skin Inflammation and Psoriasiform Dermatitis

      Journal of Investigative Dermatology
      Vol. 137Issue 3p760–763Published online: November 19, 2016
      • Chiara Giacomassi
      • Norzawani Buang
      • Guang Sheng Ling
      • Greg Crawford
      • H. Terence Cook
      • Diane Scott
      • and others
      Cited in Scopus: 13
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        The complement system is pivotal in protection against pathogens, but it also plays important roles in bridging innate and adaptive immune responses (Scott and Botto, 2016) and in modulating local and systemic inflammation (Markiewski and Lambris, 2007). Activation of complement occurs through three different pathways (classical, alternative, and lectin), converges at C3 cleavage, and culminates in the formation of the membrane attack complex. The anaphylatoxic fragments, C3a and C5a, generated during the proteolytic cascade, recruit immune cells that can promote the removal of debris and pathogens, but they can also cause tissue damage (Markiewski and Lambris, 2007).
        Complement C3 Exacerbates Imiquimod-Induced Skin Inflammation and Psoriasiform Dermatitis
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