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Transient Induction of Fever in the Imiquimod C57BL/6 Mouse Model of Psoriasis-Like Disease Involves IL-1 and IL-6 but Not IL-36

  • Shuang Sun
    Affiliations
    Center for Inflammation and Lung Research, Department of Microbiology, Immunology and Inflammation, Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania, USA
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  • Laurie E. Kilpatrick
    Affiliations
    Center for Inflammation and Lung Research, Department of Microbiology, Immunology and Inflammation, Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania, USA
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  • Liselotte E. Jensen
    Correspondence
    Corresponding author
    Affiliations
    Center for Inflammation and Lung Research, Department of Microbiology, Immunology and Inflammation, Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania, USA
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      Psoriasis embodies a number of related chronic inflammatory skin conditions. Plaque psoriasis is the most common form and affects 1–3% of the population in many Western countries, whereas generalized pustular psoriasis (GPP) is a much rarer severe form. In addition to skin manifestations, patients with GPP also exhibit several signs of systemic disease, including fever, elevated serum CRP levels, and general malaise (
      • Marrakchi S.
      • Guigue P.
      • Renshaw B.R.
      • Puel A.
      • Pei X.Y.
      • Fraitag S.
      • et al.
      Interleukin-36-receptor antagonist deficiency and generalized pustular psoriasis.
      ;
      • Onoufriadis A.
      • Simpson M.A.
      • Pink A.E.
      • Di Meglio P.
      • Smith C.H.
      • Pullabhatla V.
      • et al.
      Mutations in IL36RN/IL1F5 are associated with the severe episodic inflammatory skin disease known as generalized pustular psoriasis.
      ). GPP is associated with mutations in the gene encoding the IL-36Ra (
      • Marrakchi S.
      • Guigue P.
      • Renshaw B.R.
      • Puel A.
      • Pei X.Y.
      • Fraitag S.
      • et al.
      Interleukin-36-receptor antagonist deficiency and generalized pustular psoriasis.
      ;
      • Onoufriadis A.
      • Simpson M.A.
      • Pink A.E.
      • Di Meglio P.
      • Smith C.H.
      • Pullabhatla V.
      • et al.
      Mutations in IL36RN/IL1F5 are associated with the severe episodic inflammatory skin disease known as generalized pustular psoriasis.
      ). IL-36Ra is a classical receptor antagonist that inhibits the activity of the IL-36 cytokines—IL-36α, IL-36β, and IL-36γ—through competitive binding to the receptor IL-1RL2 (
      • Jensen L.E.
      Interleukin-36 cytokines may overcome microbial immune evasion strategies that inhibit interleukin-1 family signaling.
      ).

      Abbreviation:

      GPP (generalized pustular psoriasis)
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      References

        • Alvarez P.
        • Jensen L.E.
        Imiquimod treatment causes systemic disease in mice resembling generalized pustular psoriasis in an IL-1 and IL-36 dependent manner.
        Mediators Inflamm. 2016; 2016: 6756138
        • Berglöf E.
        • Andre R.
        • Renshaw B.R.
        • Allan S.M.
        • Lawrence C.B.
        • Rothwell N.J.
        • et al.
        IL-1Rrp2 expression and IL-1F9 (IL-1H1) actions in brain cells.
        J Neuroimmunol. 2003; 139: 36-43
        • Grine L.
        • Steeland S.
        • Van Ryckeghem S.
        • Ballegeer M.
        • Lienenklaus S.
        • Weiss S.
        • et al.
        Topical imiquimod yields systemic effects due to unintended oral uptake.
        Sci Rep. 2016; 6: 20134
        • Hawkes J.E.
        • Gudjonsson J.E.
        • Ward N.L.
        The snowballing literature on imiquimod-induced skin inflammation in mice: a critical appraisal.
        J Invest Dermatol. 2017; 137: 546-549
        • Jensen L.E.
        Interleukin-36 cytokines may overcome microbial immune evasion strategies that inhibit interleukin-1 family signaling.
        Sci Signal. 2017; 10eaan3589
        • Lien E.
        • Means T.K.
        • Heine H.
        • Yoshimura A.
        • Kusumoto S.
        • Fukase K.
        • et al.
        Toll-like receptor 4 imparts ligand-specific recognition of bacterial lipopolysaccharide.
        J Clin Invest. 2000; 105: 497-504
        • Marrakchi S.
        • Guigue P.
        • Renshaw B.R.
        • Puel A.
        • Pei X.Y.
        • Fraitag S.
        • et al.
        Interleukin-36-receptor antagonist deficiency and generalized pustular psoriasis.
        N Engl J Med. 2011; 365: 620-628
        • McColl A.
        • Thomson C.A.
        • Nerurkar L.
        • Graham G.J.
        • Cavanagh J.
        TLR7-mediated skin inflammation remotely triggers chemokine expression and leukocyte accumulation in the brain.
        J Neuroinflammation. 2016; 13: 102
        • Onoufriadis A.
        • Simpson M.A.
        • Pink A.E.
        • Di Meglio P.
        • Smith C.H.
        • Pullabhatla V.
        • et al.
        Mutations in IL36RN/IL1F5 are associated with the severe episodic inflammatory skin disease known as generalized pustular psoriasis.
        Am J Hum Genet. 2011; 89: 432-437
        • Shao S.
        • Fang H.
        • Dang E.
        • Xue K.
        • Zhang J.
        • Li B.
        • et al.
        Neutrophil extracellular traps promote inflammatory responses in psoriasis via activating epidermal TLR4/IL-36R crosstalk.
        Front Immunol. 2019; 10: 746
        • Uribe-Herranz M.
        • Lian L.H.
        • Hooper K.M.
        • Milora K.A.
        • Jensen L.E.
        IL-1R1 signaling facilitates Munro’s microabscess formation in psoriasiform imiquimod-induced skin inflammation.
        J Invest Dermatol. 2013; 133: 1541-1549
        • van der Fits L.
        • Mourits S.
        • Voerman J.S.
        • Kant M.
        • Boon L.
        • Laman J.D.
        • et al.
        Imiquimod-induced psoriasis-like skin inflammation in mice is mediated via the IL-23/IL-17 axis.
        J Immunol. 2009; 182: 5836-5845
        • Wang P.
        • Meinhardt B.
        • Andre R.
        • Renshaw B.R.
        • Kimber I.
        • Rothwell N.J.
        • et al.
        The interleukin-1-related cytokine IL-1F8 is expressed in glial cells, but fails to induce IL-1beta signalling responses.
        Cytokine. 2005; 29: 245-250

      Supplementary References

        • Alvarez P.
        • Jensen L.E.
        Imiquimod treatment causes systemic disease in mice resembling generalized pustular psoriasis in an IL-1 and IL-36 dependent manner.
        Mediators Inflamm. 2016; 2016: 6756138
        • Jensen L.E.
        • Etheredge A.J.
        • Brown K.S.
        • Mitchell L.E.
        • Whitehead A.S.
        Maternal genotype for the monocyte chemoattractant protein 1 A(-2518)G promoter polymorphism is associated with the risk of spina bifida in offspring.
        Am J Med Genet A. 2006; 140: 1114-1118
        • Milora K.A.
        • Fu H.
        • Dubaz O.
        • Jensen L.E.
        Unprocessed interleukin-36α regulates psoriasis-like skin inflammation in cooperation with interleukin-1.
        J Invest Dermatol. 2015; 135: 2992-3000
        • Milora K.A.
        • Uppalapati S.R.
        • Sanmiguel J.C.
        • Zou W.
        • Jensen L.E.
        Interleukin-36β provides protection against HSV-1 infection, but does not modulate initiation of adaptive immune responses.
        Sci Rep. 2017; 7: 5799
        • Uribe-Herranz M.
        • Lian L.H.
        • Hooper K.M.
        • Milora K.A.
        • Jensen L.E.
        IL-1R1 signaling facilitates Munro’s microabscess formation in psoriasiform imiquimod-induced skin inflammation.
        J Invest Dermatol. 2013; 133: 1541-1549
        • Zaladonis A.
        • Zhang X.
        • Manupipatpong K.K.
        • Kalaiselvan S.
        • Alvarez P.
        • Jensen L.E.
        Interleukin-36 (IL-36) system in the 1-fluoro-2,4-dinitrobenzene (DNFB) mouse model of allergic contact dermatitis.
        Allergy. 2020; 75: 2078-2081