Monocyte-derived interferon-alpha primed dendritic cells in the pathogenesis of psoriasis: New pieces in the puzzle

Árpád Farkas, Lajos Kemény

Research output: Contribution to journalReview article

19 Citations (Scopus)


Psoriasis is a common chronic inflammatory skin disorder with serious clinical, psychosocial, and economic consequences. There is much evidence that different dendritic cell (DC) subsets, various proinflammatory cytokines and Toll-like receptors (TLRs) have a central role in the pathogenesis of the disease. One of the early events in psoriatic inflammation is the secretion of interferon (IFN)-α by activated plasmacytoid DCs, a special DC subset present in symptomless psoriatic skin. Secreted IFN-α along with other proinflammatory cytokines can lead to monocyte-derived DC (moDC) development, which might contribute to T-helper (Th)1 and Th17 lymphocyte differentiation/activation and to keratinocyte proliferation. Recently it was proven that interleukin (IL)-12 and IL-23 play a critical role in this process. Additionally in psoriatic lesions, Th1 and Th17 lympocytes can interact with monocytes and instruct these cells to differentiate into Th1- and Th17-promoting moDCs, further governing the formation and function of specialized moDC subsets. The concept we present here focuses on the initial and central role of IFN-α, on the importance of other proinflammatory cytokines, on TLR stimulation and on the effect of T lymphocytes in priming moDCs, which may play an important role in initiating and maintaining psoriasis.

Original languageEnglish
Pages (from-to)215-218
Number of pages4
JournalInternational Immunopharmacology
Issue number2
Publication statusPublished - Jun 1 2012


  • Dendritic cell
  • Interferon-alpha
  • Monocyte
  • Psoriasis
  • T lymphocytes
  • Toll-like receptors

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Pharmacology

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