The expression of human leukocyte antigen‐DR and CD25 on circulating T cells in cutaneous lupus erythematosus and correlation with disease activity

Wenzel, Joerg; Henze, Stephanie; Brähler, Sabine; Bieber, Thomas; Tüting, Thomas

doi:10.1111/j.0906-6705.2005.00301.x

Cited by 39 publications

(29 citation statements)

References 25 publications

(42 reference statements)

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“…Deletion of Treg from healthy animals can break self-tolerance, leading to the development of autoimmune disease, whereas repopulation of these cells can re-establish self-tolerance and prevents autoimmune diseases [12][13][14]. This observation indicates that Treg play a critical role in the maintenance of self-tolerance and the prevention of organ-specific autoimmunity [15].…”

Section: Introductionmentioning

confidence: 99%

The histone deacetylase inhibitor trichostatin A upregulates regulatory T cells and modulates autoimmunity in NZB/W F1 mice

Reilly

Thomas

Gogal

et al. 2008

Journal of Autoimmunity

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Section: Introductionmentioning

confidence: 99%

The histone deacetylase inhibitor trichostatin A upregulates regulatory T cells and modulates autoimmunity in NZB/W F1 mice

Reilly

Thomas

Gogal

et al. 2008

Journal of Autoimmunity

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“…Treg cells regulate proliferation of the other immune cell subsets. Depletion of Treg cells caused healthy mice to develop autoimmune disease [Hayashi et al, 2005;Wahl and Chen, 2005;Wenzel et al, 2005;Liu et al, 2008]. Differentiation of CD4 + cells into Treg cells requires FOXP3 transcription factor.…”

Section: Drugs Targeting the Major Components Of The Epigenetic Mechamentioning

confidence: 99%

Aberrant Epigenetic Regulation in the Pathogenesis of Systemic Lupus Erythematosus and Its Implication in Precision Medicine

Zhan

Guo²,

Lu³

2016

Cytogenet Genome Res

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Great progress has been made in the last decades in understanding the complex immune dysregulation in systemic lupus erythematosus (SLE), yet the efforts to pursue an effective treatment of SLE proved to be futile. The pathoetiology of SLE involves extremely complicated and multifactorial interaction among various genetic and epigenetic factors. Multiple gene loci predispose to disease susceptibility, and the interaction with epigenetic modifications mediated through sex, hormones, and the hypothalamo-pituitary-adrenal axis complicates susceptibility and manifestations of this disease. Finally, certain environmental and psychological factors probably trigger the disease via epigenetic mechanisms. In this review, we summarize and discuss recent epigenetic studies of SLE and suggest a personalized approach to the dissection of disease onset and therapy or precision medicine. We speculate that in the future, precision medicine based on epigenetic and genetic information could help guide more effective targeted therapeutic intervention.

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“…[25][26][27] Wenzel suggested the following mechanism of the initiation of an inflammatory response: the Type 1 of the INF expression is caused by the absence of a stimulus which induces chemokines and the production of antiviral proteins, which, in turn, attracts T cells and dendritic cells to the skin. What is more, an ongoing inflammatory response [28][29][30] is fixed by the release of inflammatory cytokines from dendritic cells and accumulated apoptotic cells, together with the direct chemokine release from T cells.…”

Section: Etiology Of Cicatricial Alopeciamentioning

confidence: 99%

Cicatricial alopecia: What’s new in etiology?

2015

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Cicatricial alopecia is a rare, clinically diversified set of disorders causing permanent and irreversible hair loss, which often results in serious discomfort and patient’s mental problems. Clinically, this form of irreversible hair loss is characterized by visible loss of hair follicle openings in the bald spots. Histologically, it consists in destroying a hair follicle and replacing it with fibrocartilage. Such disorders are perceived as primary if a hair follicle itself is the target of the disease process and secondary if hair follicles are damaged incidentally in the context of more general tissue damage (e.g. deep skin infections, thermal burns, trauma or ionizing radiation). In this article we tried to summarize the knowledge on possible pathogenic mechanisms of cicatricial alopecia. The presented factors usually overlap and affect prognosis of particular patients. Their profound understanding may enable further research on the treatment methods of this challenging disease unit.

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The expression of human leukocyte antigen‐DR and CD25 on circulating T cells in cutaneous lupus erythematosus and correlation with disease activity

Cited by 39 publications

References 25 publications

The histone deacetylase inhibitor trichostatin A upregulates regulatory T cells and modulates autoimmunity in NZB/W F1 mice

The histone deacetylase inhibitor trichostatin A upregulates regulatory T cells and modulates autoimmunity in NZB/W F1 mice

Aberrant Epigenetic Regulation in the Pathogenesis of Systemic Lupus Erythematosus and Its Implication in Precision Medicine

Cicatricial alopecia: What’s new in etiology?

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