Psoriasis and systemic lupus erythematosus (SLE) are complex immune-mediated diseases with burdens to patients and society. Recently, there has been considerable progress in understanding of autoimmunity, revealing critical roles for cytokine-mediated pathways that are common to both SLE and psoriasis. Ongoing pharmacogenomic and signaling studies coupled with clinical trials hold promise to better delineate overlaps and divergence in pathogenesis and lead to definition of biomarkers that can predict disease subsets, disease states, organ involvement and responsiveness to treatment. This review will compare SLE and psoriasis with regard to mutually relevant immune pathways and examine their significance as an influx of new biologic treatments comes into use.
NestleF.O., KaplanD.H., BarkerJ.Psoriasis. N Engl J Med.2009; 361: 496–509.
2.
TsokosG.C.Mechanisms of Disease: Systemic Lupus Erythematosus. N Engl J Med.2011; Dec 1;365(22): 2110–21.
3.
VolinM.V., ShahraraS.Role of TH-17 cells in rheumatic and other autoimmune diseases. Rheumatology (Sunnyvale).2011; Oct 20;1(104).
4.
BettelliE., CarrierY., GaoW.Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells. Nature.2006; 441: 235–8.
5.
WeaverC.T., HattonR.D., ManganP.R., HarringtonL.E.IL-17 family cytokines and the expanding diversity of effector T cell lineages. Annu Rev Immunol.2007; 25: 821–52.
6.
KagamiS., RizzoH.L., LeeJ.J., KoguchiY., BlauveltA.Circulating Th17, Th22, and Th1 cells are increased in psoriasis. J Invest Dermatol.2009; 130: 1373–1383.
7.
LinA.M., RubinC.J., KhandpurR.Mast cells and neutrophils release IL-17 through extracellular trap formation in psoriasis. J Immunol.2011; 187: 490–500.
8.
AlbanesiC., CavaniA., GirolomoniG.IL-17 is produced by nickel-specific T lymphocytes and regulates ICAM-1 expression and chemokine production in human keratinocytes: Synergistic or antagonist effects with IFN-gamma and TNF-alpha. J Immunol.1999; 162: 494–502.
9.
ZhangZ., KyttarisV.C., TsokosG.C.The role of IL-23/IL-17 axis in lupus nephritis. J Immunol.2009; 183: 3160–69.
10.
TeunissenM.B., KoomenC.W., de Waal MalefytR., WierengaE.A., BosJ.D.Interleukin-17 and interferon-gamma synergize in the enhancement of proinflammatory cytokine production by human keratinocytes. J Invest Dermatol.1998; 111: 645–9.
11.
WilsonN.J., BonifaceK., ChanJ.R., McKenzieB.S., BlumenscheinW.M.Development, cytokine profile and function of human interleukin 17-producing helper T cells. Nat Immunol.2007; 8: 950–57.
12.
PantelyushinS., HaakS., IngoldB., KuligP.Rorγt+innate lymphocytes and γδ T cells initiate psoriasiform plaque formation in mice. J Clin Invest.2012 June 1; 122(6): 2252–2256.
13.
CaiY., ShenX., DingC.Pivotal role of dermal IL-17-producing γδ T cells in skin inflammation. Immunity.2011; 35: 596–610.
14.
PiskinG., TursenU., Sylva-SteenlandR.M., BosJ.D., TeunissenM.B.Clinical improvement in chronic plaque-type psoriasis lesions after narrow-band UVB therapy is accompanied by a decrease in the expression of IFN-γ inducers – IL-12, IL-18 and IL-23. Exp Dermatol.2004. 13: 764–72.
15.
GottliebA.B., ChamianF., MasudS., CardinaleI., AbelloM.V.TNF inhibition rapidly down regulates multiple proinflammatory pathways in psoriasis plaques. J Immunol.2005. 175: 2721–29.
16.
ZhengY., DanilenkoD.M., ValdezP.Interleukin-22, a T(H)17 cytokine, mediates IL-23-induced dermal inflammation and acanthosis. Nature.2007; 445: 648.
17.
ChanJ.R., BlumenscheinW., MurphyE.IL-23 stimulates epidermal hyperplasia via TNF and IL-20R2-dependent mechanisms with implications for psoriasis pathogenesis. J Exp Med.2006; 203: 2577.
18.
RizzoH.L., KagamiS., PhillipsK.G.IL-23-mediated psoriasis-like epidermal hyperplasia is dependent on IL-17A. J Immunol.2011; 186: 1495.
19.
CrispinJ.C., OukkaM., BaylissG.Expanded double negative T cells in patients with systemic lupus erythematosus produce IL-17 and infiltrate the kidneys. J Immunol.2008; 181: 8761–6.
20.
WongC.K., LitL.C., TamL.S., LiE.K., WongP.T., LamC.W.Hyperproduction of IL-23 and IL-17 in patients with systemic lupus erythematosus: Implications for Th17-mediated inflammation in auto-immunity. Clin Immunol.2008; 127: 385–93.
21.
KruegerG.G., LangleyR.G., LeonardiC.A human interleukin-12/23 monoclonal antibody for the treatment of psoriasis. N Engl J Med.2007; 356: 580.
22.
PappK.A., GriffithsC.E., GordonK., LebwohlM.Long-term safety of ustekinumab in patients with moderate-to-severe psoriasis: final results from 5 years of follow-up. Br J Dermatol.2013 Apr; 168(4): 844–54.
23.
LoM.S., TsokosG.C.Treatment of systemic lupus erythematosus: new advances in targeted therapy. Ann NY Acad Sci.2012 Jan; 1247: 138–52.
24.
DahlC., JohansenC., KragballeK., OlesenA.B.Ustekinumab in the treatment of refractory chronic cutaneous lupus erythematosus: a case report. Acta Derm Venereol.2013. May; 93(3): 368–9.
25.
WinchesterD., DuffinK.C., HansenC.Response to ustekinumab in a patient with both severe psoriasis and hypertrophic cutaneous lupus. Lupus.2012 Aug; 21(9): 1007–10.
26.
De SouzaA., Ali-ShawT., StroberB.E., FranksAGJr.Successful treatment of subacute lupus erythematosus with ustekinumab. Arch Dermatol.2011 Aug; 147(8): 896–8.
27.
AsarchA., BarakO., LooD.S., GottliebA.B.Th17 cells: a new therapeutic target in inflammatory dermatoses. J Dermatolog Treat.2008; 19(6): 318–26.
28.
PappK.A., LeonardiC., MenterA.Brodalumab, an anti-interleukin-17-receptor antibody for psoriasis. N Engl J Med.2012; 366(13): 1181–9.
29.
LeonardiC., MathesonR., ZachariaeC.Anti-interleukin-17 monoclonal antibody ixekizumab in chronic plaque psoriasis. N Engl J Med.2012; 366(13): 1190–9.
30.
HueberW., PatelD.D., DryjaT.Effects of AIN457, a fully human antibody to interleukin-17A, on psoriasis, rheumatoid arthritis, and uveitis. Sci Transl Med.2010; 2(52): 52ra72.
31.
KruegerJ.G., FretzinS., Suárez-FariñasM.IL-17A is essential for cell activation and inflammatory gene circuits in subjects with psoriasis. J Allergy Clin Immunol.2012; 130(1): 145–54.
WollenbergA., WagnerM., GüntherS.Plasmacytoid dendritic cells: a new cutaneous dendritic cell subset with distinct role in inflammatory skin diseases. J Invest Dermatol.2002; 119(5): 1096.
34.
SchmidP., ItinP., CoxD., McMasterG.K., HorisbergerM.A.The type I interferon system is locally activated in psoriatic lesions. J Interferon Res.1994; Oct; 14(5): 229–34.
35.
LandeR., GregorioJ., FacchinettiV.Plasmacytoid dendritic cells sense self-DNA coupled with antimicrobial peptide. Nature.2007; 449: 564–9.
36.
ArakuraF., HidaS., IchikawaE.Genetic control directed toward spontaneous IFN-alpha/IFN-beta responses and downstream IFN-gamma expression influences the pathogenesis of a murine psoriasis-like skin disease. J Immunol.2007 Sep 1; 179(5): 3249–57.
37.
BaechlerE.C., BatliwallaF.M., KarypisG.Interferon-inducible gene expression signature in peripheral blood cells of patients with severe lupus. Proc Natl Acad Sci USA.2003; 100: 2610–5.
38.
Garcia-RomoG.S., CaielliS., VegaB.Netting Neutrophils Are Major Inducers of Type I IFN Production in Pediatric Systemic Lupus Erythematosus. Sci Transl Med.2011 Mar 9; 3(73): 73ra20.
39.
LövgrenT., ElorantaM.L., BaveU., AlmG.V., RonnblomL.Induction of interferon-alpha production in plasmacytoid dendritic cells by immune complexes containing nucleic acid released by necrotic or late apoptotic cells and lupus IgG. Arthritis Rheum.2004; 50: 1861–1872.
40.
LövgrenT., ElorantaM.L., KastnerB.Induction of interferon-alpha by immune complexes or liposomes containing systemic lupus erythematosus autoantigen and Sjögren's syndrome autoantigen associated RNA. Arthritis Rheum.2006; 54: 1917–1927.
41.
WenzelJ., BauerR., BieberT., BoehmI.Presence of antinuclear antibodies in patients with lupus erythematosus is correlated with diminished T-helper cells. Br J Dermatol.2000; 143: 1100–1101.
WenzelJ., WorenkamperE., FreutelS.Enhanced type I interferon signalling promotes Th1-biased inflammation in cutaneous lupus erythematosus. J Pathol.2005; 205: 435–442.
44.
RonnblomL., ElorantaM.L., AlmG.V.The type I interferon system in systemic lupus erythematosus. Arthritis Rheum.2006; 54: 408–420.
45.
KetikoglouI., KaratapanisS., ElefsiniotisI.Extensive psoriasis induced by pegylated interferon alpha-2b treatment for chronic hepatitis B. Eur J Dermatol.2005; 15: 107.
46.
Van der FitsL., MouritsS., VoermanJ.S.Imiquimod-induced psoriasis-like skin inflammation in mice is mediated via the IL-23/IL-17 axis. J Immunol.2009; 182: 5836.
47.
PatelU., MarkN.M., MachlerB.C., LevineV.J.Imiquimod 5% cream induced psoriasis: a case report, summary of the literature and mechanism. Br J Dermatol.2011; 164: 670.
48.
CrowsonA.N., MagroC.The cutaneous pathology of lupus erythematosus: a review. J CutanPathol.2001; 28: 1–23.
49.
RonnblomL., ElorantaM.L., AlmG.V.The type I interferon system in systemic lupus erythematosus. Arthritis Rheum.2006; 54: 408–420.
50.
MerrillJ.T., WallaceD.J., PetriM.Safety profile and clinical activity of sifalimumab, a fully human anti-interferon alpha monoclonal antibody, in systemic lupus erythematosus: a phase I, multicentre, double-blind randomised study. Ann Rheum Dis.70 (2011); 1905–1913.
51.
YaoY., RichmanL., HiggsB.W.Neutralization of interferon-alpha/beta-inducible genes and downstream effect in a phase I trial of an anti-interferon-alpha monoclonal antibody in systemic lupus erythematosus. Arthritis Rheum.60 (2009); 1785–1796.
52.
AricanO., AralM., SasmazS., CiragilP.Serum levels of TNF-alpha, IFN-gamma, IL-6, IL-8, IL-12, IL-17, and IL-18 in patients with active psoriasis and correlation with disease severity. Mediators Inflamm.2005 Oct 24; 2005(5): 273–9.
53.
TeunissenM.B., KoomenC.W., de Waal MalefytR., WierengaE.A., BosJ.D.Interleukin-17 and interferon-γ synergize in the enhancement of proinflammatory cytokine production by human keratinocytes. J Investig Dermatol.1998; 111: 645–49.
54.
Linker-IsraeliM.Elevated levels of endogenous IL-6 in systemic lupus erythematosus: a putative role in pathogenesis. J Immunol.1991; 147: 117–123.
55.
JeonJ.Y.Interleukin 6 gene polymorphisms are associated with systemic lupus erythematosus in Koreans. J Rheumatol.2010; 37: 2251–2258.
56.
SantosM.J.Interleukin-6 promoter polymorphism–174 G/C is associated with nephritis in Portuguese Caucasian systemic lupus erythematosus patients. Clin Rheumatol.2011; 30: 409–413.
57.
CashH., RelleM., MenkeJ., BrochhausenC.Interleukin 6 (IL-6) deficiency delays lupus nephritis in MRL-Faslpr mice: the IL-6 pathway as a new therapeutic target in treatment of autoimmune kidney disease in systemic lupus erythematosus. J Rheumatol.2010 Jan; 37(1): 60–70.
58.
ShirotaY., YarboroC., FischerR.Impact of anti-interleukin-6 receptor blockade on circulating T and B cell subsets in patients with systemic lupus erythematosus. Ann Rheum Dis.2013 Jan; 72(1): 118–28.
GraslandA., MahéE., RaynaudE., MahéI.Psoriasis onset with tocilizumab. Joint Bone Spine.2013 Oct; 80(5): 541–2.
63.
WendlingD., Letho-GyselinckH., GuillotX., PratiC.Psoriasis onset with tocilizumab treatment for rheumatoid arthritis. J Rheumatol.2012 Mar; 39(3): 657.
64.
ChiricozziA., Guttman-YasskyE., Suárez-FariñasM.Integrative Responses to IL-17 and TNF-α in Human Keratinocytes Account for Key Inflammatory Pathogenic Circuits in Psoriasis. J Invest Dermatol.2011; 131, 677–687.
65.
UyemuraK., YamamuraM., FivensonD.F.The cytokine network in lesional and lesion-free psoriatic skin is characterized by a T-helper type 1 cell-mediated response. J Invest Dermatol.1993; 101: 701
66.
HaiderA.S., LowesM.A., Suarez-FarinasM.Cellular genomic maps help dissect pathology in human skin disease. J Invest Dermatol.2008; 128: 606–15.
67.
SonkolyE., WeiT., JansonP.C.MicroRNAs: novel regulators involved in the pathogenesis of psoriasis?PLoS One.2007; 2(7): e610.
68.
ReichK., NestleF.O., PappK.Infliximab induction and maintenance therapy for moderate-to-severe psoriasis: a phase III, multicentre, double-blind trial. Lancet.2005; 366: 1367.
69.
MenterA., TyringS.K., GordonK.Adalimumab therapy for moderate to severe psoriasis: A randomized, controlled phase III trial. J Am Acad Dermatol.2008; 58: 106.
70.
PappK.A., TyringS., LahfaM.A global phase III randomized controlled trial of etanercept in psoriasis: safety, efficacy, and effect of dose reduction. Br J Dermatol.2005; 152: 1304.
71.
ZabaL.C., CardinaleI., GilleaudeauP.Amelioration of epidermal hyperplasia by TNF inhibition is associated with reduced Th17 responses. J Exp Med.2007; 204: 3183–3194.
72.
CaproniM., AntigaE., MelaniL.Serum levels of IL-17 and IL-22 are reduced by etanercept, but not by acitretin, in patients with psoriasis: a randomized- controlled trial. J Clin Immunol.2009; 29: 210–214.
73.
LowesM.A., KikuchiT., Fuentes-DuculanPsoriasis vulgaris lesions contain discrete populations of Th1 and Th17 T cells. J Invest Dermatol.2008; 128: 1207–1211.
74.
KontoyiannisD., KolliasG.Accelerated autoimmunity and lupus nephritis in NZB mice with an engineered heterozygous deficiency in tumor necrosis factor. Eur J Immunol.2000; 30: 2038–47.
75.
ZabaL.C., Suarez-FarinasM., Fuentes-DuculanJ.Effective treatment of psoriasis with etanercept is linked to suppression of IL-17 signaling, not immediate response TNF genes. J Allergy Clin Immunol.2009; 124: 1010–1022.
76.
BrennanD.C., YuiM.A., WuthrichR.P., KelleyV.E.Tumor necrosis factor and IL-1 in New Zealand Black/White mice. Enhanced gene expression and acceleration of renal injury. J Immunol.1989; 143: 3470–75.
77.
ZhuL.J., Landolt-MarticorenaC., LiT.Altered expression of TNF-α signaling pathway proteins in systemic lupus erythematosus. J Rheumatol.2010, 37: 1658–1666.
78.
GomezD., CorreaP.A., GomezL.M., CadenaJ., MolinaJ.F., AnayaJ.M.Th1/Th2 cytokines in patients with systemic lupus erythematosus: is tumor necrosis factor alpha protective?Semin Arthritis Rheum.2004, 33: 404–413.
79.
LópezP., GómezJ., PradoC.Influence of functional interleukin 10/tumor necrosis factor-alpha polymorphisms on interferon-alpha, IL-10, and regulatory T cell population in patients with systemic lupus erythematosus receiving antimalarial treatment. J Rheumatol.2008; 35: 1559.
80.
PopovicK., EkM., EspinosaA.Increased expression of the novel proinflammatory cytokine high mobility group box chromosomal protein 1 in skin lesions of patients with lupus erythematosus. Arthritis Rheum.2005; 52: 3639–45.
81.
ValesiniG., IannuccelliC., MarocchiE., PascoliL., ScalziV., Di FrancoM.Biological and clinical effects of anti-TNF alpha treatment. Autoimmun Rev.2007; 7: 35e41.
82.
MackayI.R., LeskovsekN.V., RoseN.R.Cell damage and autoimmunity: a critical appraisal. J Autoimmun.2008; 30: 5e11.
83.
AringerM., SmolenJ.S.The role of tumor necrosis factor-alpha in systemic lupus erythematosus. Arthritis Res Ther.2008; 10: 202.
84.
CharlesP.J., SmeenkR.J., De JongJ., FeldmannM., MainiR.N.Assessment of antibodies to double-stranded DNA induced in rheumatoid arthritis patients following treatment with infliximab, a monoclonal antibody to tumor necrosis factor alpha: findings in open-label and randomized placebo-controlled trials. Arthritis Rheum.2000; 43: 2383–90.
85.
De BandtM., SibiliaJ., Le LoetX.Systemic lupus erythematosus induced by anti-tumour necrosis factor alpha therapy: a French national survey. Arthritis Res Ther.2005; 7(3): R545–51.
86.
ObermoserG., SontheimerR.D., ZelgerB.Overview of common, rare and atypical manifestations of cutaneous lupus erythematosus and histopathological correlates. Lupus.2010; 19: 1050.
87.
AringerM., GraningerW.B., SteinerG., SmolenJ.S.Safety and efficacy of tumor necrosis factor alpha blockade in systemic lupus erythematosus: an open-label study. Arthritis Rheum.2004; 50: 3161–9.
88.
AringerM., HoussiauF., GordonC.Adverse events and efficacy of TNF-α blockade with infliximab in patients with systemic lupus erythematosus (SLE). Long-term follow-up of thirteen patients. Rheumatology (Oxford).2009; Nov;48(11): 1451–4.
89.
PowellJ.D., PollizziK.N., HeikampE.B., HortonM.R.Regulation of Immune Responses by mTOR. Annu Rev. Immunol.2012; 30: 39–68.
90.
KangJ., HuddlestonS.J., FraserJ.M., KhorutsA.De novo induction of antigen-specific CD4+CD25+Foxp3+ regulatory T cells in vivo following systemic antigen administration accompanied by blockade of mTOR. J Leukoc Biol.2008; 83: 1230–39.
91.
KopfH., de la RosaG.M., HowardO.M., ChenX.Rapamycin inhibits differentiation of Th17 cells and promotes generation of FoxP3+ T regulatory cells. Int Immunopharmacol.2007; 7: 1819–24.
92.
DelgoffeG.M., KoleT.P., ZhengY.The mTOR kinase differentially regulates effector and regulatory T cell lineage commitment. Immunity.2009; 30: 832–44.
93.
PowellJ.D., LernerC.G., SchwartzR.H.Inhibition of cell cycle progression by rapamycin induces T cell clonal anergy even in the presence of costimulation. J Immunol.1999; 162: 2775–84.
94.
FernandezD., BonillaE., MirzaN., PerlA.Rapamycin reduces disease activity and normalizes T-cell activation-induced calcium fluxing in patients with systemic lupus erythematosus. Arth Rheum.2006; 54: 2983–2988.
95.
LaiZ., BorsukR., ShadakshariA., YuJ.mTOR activation triggers IL-4 production and necrotic death of double-negative T cells in patients with systemic lupus erythematosus. J. Immunol. In press. 2013; http://www.jimmunol.org/content/191/5/2236.abstract.
96.
FernandezD., TelaricoT., BonillaE.Activation of mTOR controls the loss of TCR in lupus T cells through HRES-1/Rab4-regulated lysosomal degradation. J. Immunol.2009; 182: 2063–2073.
97.
GergelyPJr., NilandB, GonchoroffN, PullmannRJr., PhillipsPE, PerlA.Persistent mitochondrial hyperpolarization, increased reactive oxygen intermediate production, and cytoplasmic alkalinization characterize altered IL-10 signaling in patients with systemic lupus erythematosus. J Immunol.2002; 169: 1092–1101.
98.
SielingP.A., PorcelliS.A., DuongB.T., SpadaF.Human Double-Negative T Cells in Systemic Lupus Erythematosus Provide Help for IgG and Are Restricted by CD1c. J Immunol.2000; 165: 5338–5344.
99.
WarnerL.M., AdamsL.M., SehgalS.N.Rapamycin prolongs survival and arrests pathophysiologic changes in murine systemic lupus erythematosus. Arthritis Rheum.1994 Feb; 37(2): 289–97.
100.
JavierA.F., Bata-CsorgoZ., EllisC.N.Rapamycin (sirolimus) inhibits proliferating cell nuclear antigen expression and blocks cell cycle in the G1 phase in human keratinocyte stem cells. J Clin Invest.1997 May 1; 99(9): 2094–9.
101.
BuergerC., MalisiewiczB., EiserA., HardtK., BoehnckeW.H.Mammalian target of rapamycin and its downstream signalling components are activated in psoriatic skin. Br J Dermatol.2013; 169(1), pp. 156–159.
102.
HaidingerM., PoglitschM., GeyereggerR., KasturiS., ZeydaM.A versatile role of mammalian target of rapamycin in human dendritic cell function and differentiation. J Immunol.2010; 185: 3919–31.
103.
CaoW., ManicassamyS., TangH., KasturiS.P.Toll-like receptor-mediated induction of type I interferon in plasmacytoid dendritic cells requires the rapamycin-sensitive PI(3)K-mTORp70S6K pathway. Nat Immunol.2008; 9: 1157–64.
104.
ColinaR., Costa-MattioliM., DowlingR.J., JaramilloM.Translational control of the innate immune response through IRF-7. Nature.2008; 452: 323–28.
105.
ReitamoS., SpulsP., SassolasB., LahfaM., ClaudyA., GriffithsC.E.Efficacy of sirolimus (rapamycin) administered concomitantly with a subtherapeutic dose of cyclosporin in the treatment of severe psoriasis: a randomized controlled trial. Br J Dermatol.2001 Sep; 145(3): 438–45.
106.
JacobC.O., FronekZ., LewisG.D.Heritable major histocompatibility complex class II-associated differences in production of tumor necrosis factor alpha: relevance to genetic predisposition to systemic lupus erythematosus. Proc Natl Acad Sci USA.1990 Feb; 87(3): 1233–7.
107.
AustinL.M., OzawaM., KikuchiT.The majority of epidermal T cells in Psoriasis vulgaris lesions can produce type 1 cytokines, interferon-gamma, interleukin-2, and tumor necrosis factor-alpha, defining TC1 (cytotoxic T lymphocyte) and TH1 effector populations: A type 1 differentiation bias is also measured in circulating blood T cells in psoriatic patients. J Invest Dermatol.1999; 113, 752–759.
108.
TsokosG.C.Deficient gamma-interferon production in patients with systemic lupus erythematosus. Arthritis Rheum.1986; 29, 1210–1215.
109.
PereraG.K., Di MeglioP., NestleF.O.Psoriasis. Annu Rev Pathol.2012; 7: 385–422.
110.
BalatoA., SchiattarellaM., LemboS.Interleukin-1 family members are enhanced in psoriasis and suppressed by vitamin D and retinoic acid. Arch Dermatol Res.2013 Apr; 305(3): 255–62.
111.
YapD.Y., LaiK.N.The role of cytokines in the pathogenesis of systemic lupus erythematosus – from bench to bedside. Nephrology.2013 Apr; 18(4): 243–55.
112.
WongC.K., HoC.Y., LiE.K., TamL.S., LamC.W.Elevated production of interleukin-18 is associated with renal disease in patients with systemic lupus erythematosus. Clin Exp Immunol.2002; 130: 345–51.
113.
AustinL.M., OzawaM., KikuchiT.The majority of epidermal T cells in psoriasis vulgaris lesions can produce type 1 cytokines, interferon-γ, interleukin-2, and tumor necrosis factor α, defining TC1 (cytotoxic T lymphocyte) and Th1 effector populations: A type 1 differentiation bias is also measured in circulating blood T cells in psoriatic patients. J Investig Dermatol.1999; 113: 752–59.
114.
JuangY.T.Systemic lupus erythematosus serum IgG increases CREM binding to the IL-2 promoter and suppresses IL-2 production through CaMKIV. J Clin Invest.2005 Apr; 115(4): 996–1005.
115.
Alcocer-VarelaJ., Alarcon-SegoviaD.Decreased production of and response to interleukin-2 by cultured lymphocytes from patients with systemic lupus erythematosus. J Clin Invest.1982; 69, 1388–1392.
116.
GhoreschiK., ThomasP., BreitS.Interleukin-4 therapy of psoriasis induces Th2 responses and improves human autoimmune disease. Nat Med.2003 Jan; 9(1): 40–6.
117.
CharlesN., HardwickD., DaugasE.Basophils and the T helper 2 environment can promote the development of lupus nephritis. Nat Med.2010; Jun; 16(6): 701–7.
118.
ReichK.Response of psoriasis to interleukin-10 is associated with suppression of cutaneous type 1 inflammation, downregulation of the epidermal interleukin-8/CXCR2 pathway and normalization of keratinocyte maturation. J. Invest Dermatol.2001; 116, 319–329.
119.
AsadullahK., SabatR., FriedrichM., VolkH.D., SterryW.Interleukin-10: an important immunoregulatory cytokine with major impact on psoriasis. Curr Drug Targets Inflamm Allergy.2004; 3: 185–92.
120.
ElkonK.Autoantibodies in systemic lupus erythematosus. Curr Opin Rheumatol.1995; 7: 384.
121.
NardelliB., BelvedereO., RoschkeV.Synthesis and release of B-lymphocyte stimulator from myeloid cells. Blood.2001; 97: 198–204.
122.
ZhengY., DanilenkoD.M., ValdezP.Interleukin-22, a T(H)17 cytokine, mediates IL-23-induced dermal inflammation and acanthosis. Nature.2007; 445: 648–51.
123.
ChengF., GuoZ., XuH.Decreased plasma IL22 levels, but not increased IL17 and IL23 levels, correlate with disease activity in patients with systemic lupus erythematosus. Ann Rheum Dis.2009; 68, 604–606.
124.
PanH.F., LiX.P., ZhengS.G., YeD.Q.Emerging role of interleukin-22 in autoimmune diseases. Cytokine Growth Factor Rev.2013 Feb; 24(1): 51–7.
125.
HanG., WilliamsC.A., SalterK.A role for TGF beta signaling in the pathogenesis of psoriasis. J Invest Dermatol.2010 Feb; 130(2): 371–7.
126.
OhtsukaK., GrayJ.D., StimmlerM.M., ToroB., HorwitzD.A.Decreased production of TGF-beta by lymphocytes from patients with systemic lupus erythematosus. J Immunol.1998 Mar 1; 160(5): 2539–45.
127.
GerlV., LischkaA., PanneD.Blood dendritic cells in systemic lupus erythematosus exhibit altered activation state and chemokine receptor function. Ann Rheum Dis.2010; 69: 1370.
