Psoriasis

Nestle, Frank O.; Kaplan, Daniel H.; Barker, Jonathan

doi:10.1056/nejmra0804595

Cited by 2,642 publications

(2,537 citation statements)

References 98 publications

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“…We also used in vivo and in vitro experiments to confirm the cytotoxic effect of TPA treatment. Some factors released from keratinocytes may facilitate the initial progression of skin inflammation (4)(5)(6). It is speculated that, similar to the immune modulation of damage-associated molecular patterns, a proinflammatory role of MIF prompts the early activation of the targeted cells, which express MIF receptors at high levels, to produce inflammatory mediators and undergo chemotaxis during skin inflammation.…”

Section: Discussionmentioning

confidence: 99%

“…The effects of MIF inhibition on skin inflammation have not been investigated in vivo using an animal model of psoriasis. The pathological changes in psoriatic inflammatory lesions include a thickening of the epidermis, parakeratosis, elongated rete ridges, and the infiltration of several cell types, including T cells, dendritic cells, neutrophils, and other immune cells (4,5,29). To our knowledge, this study provides the first evidence that pharmacological inhibition of MIF with the MIF antagonist ISO-1 effectively retards TPA-induced ear edema, the infiltration of multiple immune cell types (IFN-g-producing cells and granulocytes), epidermal keratinocyte proliferation, and angiogenesis.…”

Section: Discussionmentioning

confidence: 99%

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Macrophage Migration Inhibitory Factor Triggers Chemotaxis of CD74+CXCR2+ NKT Cells in Chemically Induced IFN-γ–Mediated Skin Inflammation

Hsieh

Chen

Lin

et al. 2014

The Journal of Immunology

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IFN-γ mediates chemically induced skin inflammation; however, the mechanism by which IFN-γ–producing cells are recruited to the sites of inflammation remains undefined. Secretion of macrophage migration inhibitory factor (MIF), a proinflammatory cytokine, from damaged cells may promote immune cell recruitment. We hypothesized that MIF triggers an initial step in the chemotaxis of IFN-γ–producing cells in chemically induced skin inflammation. Using acute and chronic models of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced skin inflammation in mouse ears, MIF expression was examined, and its role in this process was investigated pharmacologically. The cell populations targeted by MIF, their receptor expression patterns, and the effects of MIF on cell migration were examined. TPA directly caused cytotoxicity accompanied by MIF release in mouse ear epidermal keratinocytes, as well as in human keratinocytic HaCaT cells. Treatment with the MIF antagonist (S,R)-3-(4-hydroxyphenyl)-4,5-dihydro-5-isoxazole acetic acid methyl ester considerably attenuated TPA-induced ear swelling, leukocyte infiltration, epidermal cell proliferation, and dermal angiogenesis. Inhibition of MIF greatly diminished the dermal infiltration of IFN-γ+ NKT cells, whereas the addition of exogenous TPA and MIF to NKT cells promoted their IFN-γ production and migration, respectively. MIF specifically triggered the chemotaxis of NKT cells via CD74 and CXCR2, and the resulting depletion of NKT cells abolished TPA-induced skin inflammation. In TPA-induced skin inflammation, MIF is released from damaged keratinocytes and then triggers the chemotaxis of CD74+CXCR2+ NKT cells for IFN-γ production.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Macrophage Migration Inhibitory Factor Triggers Chemotaxis of CD74+CXCR2+ NKT Cells in Chemically Induced IFN-γ–Mediated Skin Inflammation

Hsieh

Chen

Lin

et al. 2014

The Journal of Immunology

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“…Although anti-TNF are considered firstline drugs for certain cases -given their cost-benefit, their use has been limited due to the risk of reactivating latent tuberculosis infection (LTBI) in patients previously treated. 6 The initial warning was given by a study of 70 patients who were treated for rheumatoid arthritis with infliximab and had their tuberculosis reactivated. Out of these patients, 56% had the extrapulmonary form of the disease and 24% had the disseminated form.…”

Section: Biological Therapiesmentioning

confidence: 99%

“…6,7,8 To associate these findings, Gottlieb, Chao and Dann (2008) proposed a model of interrelations between psoriasis and other diseases of a chronic inflammatory nature (Figure 1).…”

mentioning

confidence: 99%

Investigação de infecção tuberculosa latente em pacientes com psoríase candidatos ao uso de drogas imunobiológicas

Lima

Duarte

et al. 2011

An. Bras. Dermatol.

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The use of tumor necrosis factor inhibitors for the treatment of patients with psoriasis has been related to a higher incidence of tuberculosis, specially the disseminated and extrapulmonary forms. Despite their efficacy, these drugs increase the risk of reactivating latent tuberculosis infection, thus requiring diagnosis of the condition before their administration. Investigation of latent tuberculosis infection with tuberculin skin test is ineffective due to its low specificity and the dubious results that it generates in patients with psoriasis. Assays based on the detection of synthesis of gamma interferon in vitro by peripheral monoclonal cells, stimulated by specific antigens (ESAT-6 and CFP-10), seem to offer better accuracy when compared to the Mantoux test in identifying latent tuberculosis infection. This diagnosis tool has demonstrated higher specificity, since it has no correlation with indirect forms of exposure to M. tuberculosis such as BCG vaccination or with infections by other mycobacteria. Keywords: Psoriasis; Tuberculosis; Tumor necrosis factor-alpha Resumo: O uso dos ini bi do res do fator de necro se tumo ral no tra ta men to de pacien tes com pso ría se vem sendo rela cio na do a uma maior inci dên cia de tuber cu lo se, par ti cu lar men te, nas suas for mas extrapul mo nar e dis se mi na da. Apesar de sua indis cu tí vel efi cá cia, essas dro gas ele vam o risco da rea ti va ção de infec ção tuber cu lo sa laten te (ITBL), tor nan do obri ga tó rio o diag nós ti co da refe ri da con di ção antes da sua admi nis tra ção. A inves ti ga ção da infec ção tuber cu lo sa laten te pelo teste cutâ neo da tuber cu li na é falha, dada sua baixa espe ci fi ci da de, além de apre sen tar resul ta dos duvi do sos em pacien tes com psoría se. Ensaios basea dos na detec ção da pro du ção de inter fe ron-gama in vitro por célu las mono clo nais peri fé ri cas, esti mu la das por antí ge nos espe cí fi cos (Esat-6 e CFP-10), pare cem ofe re cer maior acu rá cia quan do com pa ra dos ao teste de Mantoux na iden ti fi ca ção de infec ção tuber cu lo sa laten te. Essa fer ramen ta diag nós ti ca tem ofe re ci do maior espe ci fi ci da de, já que não apre sen ta cor re la ção com medi das indi re tas de expo si ção ao M. tuber cu lo sis, como a vaci na ção por BCG, e com infec ções por outras micobac té rias. Palavras-chave: Fator de necro se tumo ral alfa; Tuberculose; Psoríase

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“…Expression levels of antimicrobial peptides are highly upregulated in (non)lesional psoriatic skin, and they are considered to play a role in the induction of psoriasis via immune-modulation such as recruitment of leukocytes (5,6). The activated epidermis is characterized by a high keratin 17 (K17) and a low GATA3 expression, high levels of antimicrobial peptides such as psoriasin (S100A7) and b-defensin-2 (hBD2), growth factors including nerve growth factor (NGF), and the proinflammatory cytokines IL-1b and IL-6 (2,(7)(8)(9). These molecules activate IL-23 producing dendritic cells (DC), resulting in the induction of skin T cells that produce cytokines such as TNF-a, IFN-g, IL-17, and IL-22.…”

mentioning

confidence: 99%

IL-4 Downregulates IL-1β and IL-6 and Induces GATA3 in Psoriatic Epidermal Cells: Route of Action of a Th2 Cytokine

Onderdijk

Baerveldt

Kurek

et al. 2015

The Journal of Immunology

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Clinical improvement of psoriasis induced by IL-4 treatment has been ascribed to changes in dermal inflammatory cells, such as activation of Th2 cells and tolerization of dendritic cells by suppressing IL-23 production. The pathologic epidermal alterations in psoriatic lesional skin include increased epidermal expression of IL-1β, IL-6, S100A7, and human β-defensin 2 (hBD2) and a downregulated expression of the epidermal transcription factor GATA3. Effects of IL-4 on the epidermal compartment of psoriasis lesions were not previously investigated. Therefore, we investigated whether IL-4 directly affects abovementioned psoriatic markers in the epidermal compartment. We cultured freshly isolated psoriatic epidermal cells, whole psoriatic and healthy skin biopsies, human keratinocytes and Langerhans cells with IL-4. The secretion of IL-1β and IL-6 by psoriatic epidermal cells was inhibited by IL-4 via transcriptional and posttranscriptional mechanisms, respectively. In normal skin, IL-4 inhibited IL-1β- and IL-17A–induced hBD2 expression in vitro. In addition, IL-4 reduced the protein expression of hBD2 in psoriatic skin biopsies and induced phospho-STAT6 protein. Epidermal GATA3 mRNA and protein were significantly upregulated by IL-4 in epidermal cells and keratinocytes. Our data argue that IL-4 improves psoriasis not only via modification/induction of Th2 cells and type II dendritic cells, but also via direct inhibition of inflammatory cytokines in resident IL-4R–expressing epidermal cells and thereby alters the psoriatic skin phenotype toward a healthy skin phenotype.

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Psoriasis

Cited by 2,642 publications

References 98 publications

Macrophage Migration Inhibitory Factor Triggers Chemotaxis of CD74+CXCR2+ NKT Cells in Chemically Induced IFN-γ–Mediated Skin Inflammation

Macrophage Migration Inhibitory Factor Triggers Chemotaxis of CD74+CXCR2+ NKT Cells in Chemically Induced IFN-γ–Mediated Skin Inflammation

Investigação de infecção tuberculosa latente em pacientes com psoríase candidatos ao uso de drogas imunobiológicas

IL-4 Downregulates IL-1β and IL-6 and Induces GATA3 in Psoriatic Epidermal Cells: Route of Action of a Th2 Cytokine

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