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Year : 2013  |  Volume : 58  |  Issue : 3  |  Page : 247
The role of plasmacytoid dendritic cells and interferon-alpha in the immunopathogenesis of psoriasis


Department of Surgery, School of Medical Sciences, University of Marília, Marília, São Paulo, Brazil

Date of Web Publication20-Apr-2013

Correspondence Address:
Rafael Denadai
Department of Surgery, School of Medical Sciences, University of Marília, Marília, São Paulo
Brazil
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0019-5154.110900

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How to cite this article:
Denadai R. The role of plasmacytoid dendritic cells and interferon-alpha in the immunopathogenesis of psoriasis. Indian J Dermatol 2013;58:247

How to cite this URL:
Denadai R. The role of plasmacytoid dendritic cells and interferon-alpha in the immunopathogenesis of psoriasis. Indian J Dermatol [serial online] 2013 [cited 2019 May 27];58:247. Available from: http://www.e-ijd.org/text.asp?2013/58/3/247/110900


Sir,

I read with great interest the recent review by Coondoo, [1] and specifically on the topic immunopathogenesis of psoriasis, I have the following comments to offer:

In addition to overexpression of several pro-inflammatory cytokines such as interleukin-2 (IL-2), IL-6, IL-8, IL-12, interferon-gamma (IFN-γ), and tumor necrosis factor-alpha (TNF-α) by Th1 cells described by the author, [1] interferon-alpha (IFN-α) produced by activated plasmocytoid dendritic cells (pDCs) has been found to contribute to the pathophysiology of psoriasis. [2],[3],[4],[5],[6]

High amounts of IFN-α produced by activated pDCs induce a strong activation of the local immune system (mainly myeloid dendritic cells and potentially autoreactive T cells) that become capable of secreting cytokines that further promote an pathogenic inflammatory cascade. [7] For this to occur, pDCs infiltrate the dermis of psoriasis patients and become active to produce IFN-α early during disease development. [2] The earliest event seems to be the conversion of pro-chemerin into chemerin in psoriatic pre-lesionnal skin leading to the recruitment of ChemR23 expressing pDCs and the antimicrobial peptide LL37 (also known as CAMP) has been identified as the key factor that mediates pDCs activation in psoriasis lesions. [3],[4] Recently, also was demonstrated that the histamine H4 receptor is highly expressed on pDCs in psoriasis and histamine influences cytokine production and migration of pDCs. [5] Other report [6] showed that sun exposure rapidly reduces pDCs in psoriatic lesional dermis preceded clinical improvement. These findings suggest that suninduced clinical benefit may partly be explained by its effect on pDCs and their products. [6]

Moreover, there are other interesting studies that support such close relationship between IFN-α and the onset of psoriatic lesions. [8],[9],[10],[11] There are cases of psoriasis development or exacerbation after injection of recombinant IFN-α or the topical application of imiquimod (a potent IFN-α inducer). [8],[9] Psoriatic lesions induced by anti-TNF-α (pharmacological class with remarkable efficacy in the treatment of the psoriasis) have also been described worldwide. [10],[11] Since pDCs are normally downregulated by TNF-α through the inhibition of the maturation of their hematopoietic precursors, TNF-α inhibition by the biological may determine increased and uncontrolled IFN-α production and generate, as a result, the onset and/or aggravation of psoriasis. [10],[11] A study [10] detected strong production of protein MxA (represents a specific marker for IFN signaling) in the inflammatory cells of skin samples of anti-TNF-α-induced psoriasis. Another report [11] found increased IFN-α expression in the psoriatic lesions of patients under anti-TNF-α therapy.

Finally, these findings [2,[3],[4],[5],[6] suggest that both pDCs and IFN-α may be potential early therapeutic targets in psoriasis treatment.

 
   References Top

1.Coondoo A. The role of cytokines in the pathomechanism of cutaneous disorders. Indian J Dermatol 2012;57:90-6.  Back to cited text no. 1
[PUBMED]  Medknow Journal  
2.Nestle FO, Conrad C, Tun-Kyi A, Homey B, Gombert M, Boyman O, et al. Plasmacytoid predendritic cells initiate psoriasis through interferon-alpha production. J Exp Med 2005;202:135-43.  Back to cited text no. 2
    
3.Albanesi C, Scarponi C, Pallotta S, Daniele R, Bosisio D, Madonna S, et al. Chemerin expression marks early psoriatic skin lesions and correlates with plasmacytoid dendritic cell recruitment. J Exp Med 2009;206:249-58.  Back to cited text no. 3
    
4.Lande R, Gregorio J, Facchinetti V, Chatterjee B, Wang YH, Homey B, et al. Plasmacytoid dendritic cells sense self-DNA coupled with antimicrobial peptide. Nature 2007;449:564-9.  Back to cited text no. 4
    
5.Gschwandtner M, Mommert S, Köther B, Werfel T, Gutzmer R. The histamine H4 receptor is highly expressed on plasmacytoid dendritic cells in psoriasis and histamine regulates their cytokine production and migration. J Invest Dermatol 2011;131:1668-76.  Back to cited text no. 5
    
6.Heier I, Søyland E, Krogstad AL, Rodríguez-Gallego C, Nenseter MS, Jahnsen FL. Sun exposure rapidly reduces plasmacytoid dendritic cells and inflammatory dermal dendritic cells in psoriatic skin. Br J Dermatol 2011;165:792-801.  Back to cited text no. 6
    
7.Nestle FO, Kaplan DH, Barker J. Psoriasis. N Engl J Med 2009;361:496-509.  Back to cited text no. 7
    
8.Funk J, Langeland T, Schrumpf E, Hanssen LE. Psoriasis induced by interferon-alpha. Br J Dermatol 1991;125:463-5.  Back to cited text no. 8
    
9.Patel U, Mark NM, Machler BC, Levine VJ. Imiquimod 5% cream induced psoriasis: A case report, summary of the literature and mechanism. Br J Dermatol 2011;164:670-2.  Back to cited text no. 9
    
10.Seneschal J, Milpied B, Vergier B, Lepreux S, Schaeverbeke T, Taïeb A. Cytokine imbalance with increased production of interferon-alpha in psoriasiform eruptions associated with antitumour necrosis factor-alpha treatments. Br J Dermatol 2009;161:1081-8.  Back to cited text no. 10
    
11.de Gannes GC, Ghoreishi M, Pope J, Russell A, Bell D, Adams S, et al. Psoriasis and pustular dermatitis triggered by TNF-{α} inhibitors in patients with rheumatologic conditions. Arch Dermatol 2007;143:223-31.  Back to cited text no. 11
    




 

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