T Cells Involved in Psoriasis Vulgaris Belong to the Th1 Subset

Schlaak, J. F.; Buslau, Michael; Jochum, Wolfram; Hermann, E.; Girndt, Matthias; Gallati, H.; Büschenfelde, Karl‐Hermann Meyer zum; Fleischer, Bernhard

doi:10.1111/1523-1747.ep12371752

Cited by 420 publications

(320 citation statements)

References 35 publications

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“…This hypothesis fits well with the expression of PML in psoriasis 3 since in this disease, Th1 cells producing IFN␥ have been recently demonstrated. 16 Despite the expression of PML in the skin lesions of chronic GVHD, our patients do not display anti-PML antibodies in contrast with what is found in PBC and other auto-immune diseases. 5 This absence is rather curious since features of chronic GVHD are close to those of PBC (including the presence of antimitochondrial antibodies) 17 and since antinuclear 18 and antinucleolar 19 antibodies are frequently detected in chronic GVHD sera.…”

Section: Patient's Sera Do Not Display Anti-pml Antibodiescontrasting

confidence: 60%

PML is expressed in chronic graft-versus-host disease lesions

Aractingi

Thé

Gluckman

et al. 1997

Bone Marrow Transplant

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Summary:sera of patients with primary biliary cirrhosis (PBC) has been demonstrated, 5 raising the hypothesis that this antigen may therefore represent an autoantigenic trigger. In the The PML (for 'ProMyelocytic Leukemia') gene product is a nuclear zinc finger protein, identified when the same way, 70% of patients with other autoimmune diseases and antibodies against Sp100 (another nuclear dot antigen) chromosomal translocation fusing this gene to the retinoic acid receptor was found in acute promyelocytic leualso also had circulating anti-PML antibodies. 5 Chronic graft-versus-host disease (GVHD) is a frequent kemia. Recently, a frequent occurrence of autoantibodies against the PML protein was detected in primary and disabling complication of bone marrow transplantation whose pathogenesis is still not well understood. In contrast biliary cirrhosis (PBC) sera, suggesting that this protein could represent an autoantigenic trigger in PBC.with acute GVHD where donor anti-host T cells have been shown to be solely involved, 6,7 the pathogenesis of chronic Chronic GVHD features are close to those of PBC and in addition, antinuclear and antinucleolar antibodies GVHD seems to rely on a complex interaction between alloimmune and autoimmune mechanisms. 8,9 Liver chronic are frequently detected in patients' sera. In order to determine if an abnormal expression of PML, followed GVHD is very close to PBC. In view of this similarity and in order to determine if an abnormal expression of PML by the development of anti-PML antibodies, can be implicated in chronic GVHD pathogenesis, we studied followed by the development of anti-PML antibodies can be implicated in chronic GVHD pathogenesis, we studied the expression of PML in the skin of seven patients with chronic GVHD as well as the presence of circulating the expression of PML in the skin and the presence of circulating anti-PML antibodies. anti-PML antibodies. PML was highly expressed by the lesional skin keratinocytes, but circulating antibodies were never detected. PML is induced by interferon (IFN)␥. The expression of PML by GVHD epidermis is likely secondary to the IFN␥ produced by infiltrating Patients and methods lymphocytes. Since PML display growth suppressor properties, the role of this protein in tissue lesions is disPatients cussed. Keywords: GVHD; PML; skin Seven patients with chronic GVHD included in this study are summarized in Table 1. All had cutaneous lesions and four also had liver GVHD. Cutaneous biopsies were done The non-random chromosomal translocation t(15;17) on the lesions and when possible on non-lesional skin also. characteristic of the acute promyelocytic leukemia (APL) Positive controls were obtained from patients with psoriasis has led to the identification of a fusion between the PML (a disease already shown to be associated with PML gene (for 'ProMyelocytic Leukemia') present on chromoexpression in keratinocytes). Negative controls were done some 15 and the retinoic acid receptor (RAR␣) on chromoon normal skin specimens obtained from breast ...

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Section: Patient's Sera Do Not Display Anti-pml Antibodiescontrasting

confidence: 60%

PML is expressed in chronic graft-versus-host disease lesions

Aractingi

Thé

Gluckman

et al. 1997

Bone Marrow Transplant

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“…Infiltrating CD4 ϩ T cells in psoriatic skin have thus far been characterized as displaying an inflammatory Th1 phenotype due to elevated levels of IFN-␥, TNF-␣, and IL-12. (3,4). Consistent with this hypothesis, an Ab anti-blocking the p40 subunit of IL-12, a cytokine essential for Th1 development, has demonstrated early clinical efficacy in the treatment of psoriasis (5).…”

mentioning

confidence: 77%

The Effects of IL-20 Subfamily Cytokines on Reconstituted Human Epidermis Suggest Potential Roles in Cutaneous Innate Defense and Pathogenic Adaptive Immunity in Psoriasis

Susan

Valdez²,

Wu³

et al. 2007

The Journal of Immunology

447

256

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IL-19, IL-20, IL-22, IL-24, and IL-26 are members of the IL-10 family of cytokines that have been shown to be up-regulated in psoriatic skin. Contrary to IL-10, these cytokines signal using receptor complex R1 subunits that are preferentially expressed on cells of epithelial origin; thus, we henceforth refer to them as the IL-20 subfamily cytokines. In this study, we show that primary human keratinocytes (KCs) express receptors for these cytokines and that IL-19, IL-20, IL-22, and IL-24 induce acanthosis in reconstituted human epidermis (RHE) in a dose-dependent manner. These cytokines also induce expression of the psoriasisassociated protein S100A7 and keratin 16 in RHE and cause persistent activation of Stat3 with nuclear localization. IL-22 had the most pronounced effects on KC proliferation and on the differentiation of KCs in RHE, inducing a decrease in the granular cell layer (hypogranulosis). Furthermore, gene expression analysis performed on cultured RHE treated with these cytokines showed that IL-19, IL-20, IL-22, and IL-24 regulate many of these same genes to variable degrees, inducing a gene expression profile consistent with inflammatory responses, wound healing re-epithelialization, and altered differentiation. Many of these genes have also been found to be up-regulated in psoriatic skin, including several chemokines, ␤-defensins, S100 family proteins, and kallikreins. These results confirm that IL-20 subfamily cytokines are important regulators of epidermal KC biology with potentially pivotal roles in the immunopathology of psoriasis.

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“…Such T-cell clones could be generated from both dermis and epidermis. According to a high level production of IL-2 and IFN-g they were considered as TH1-cells [12,13]. A more broadened analysis of their lymphokine profile, however, identified a variety of other mediators including TNF-b, IL-3 and IL-5, thus suggesting a hitherto unrecognized regulatory T-cell subset [14].…”

Section: Lesional Psoriatic T Lymphocytes -A Particular Regulalatory mentioning

confidence: 99%

Psoriasis Vulgaris, Streptococci and the Immune System: A Riddle to be Solved Soon?

Prinz

1997

Scand J Immunol

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T Cells Involved in Psoriasis Vulgaris Belong to the Th1 Subset

Cited by 420 publications

References 35 publications

PML is expressed in chronic graft-versus-host disease lesions

PML is expressed in chronic graft-versus-host disease lesions

The Effects of IL-20 Subfamily Cytokines on Reconstituted Human Epidermis Suggest Potential Roles in Cutaneous Innate Defense and Pathogenic Adaptive Immunity in Psoriasis

Psoriasis Vulgaris, Streptococci and the Immune System: A Riddle to be Solved Soon?

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