FOXP3+ and CD39+ regulatory T cells in subtypes of cutaneous lupus erythematosus

2015 ◽  
Vol 29 (10) ◽  
pp. 1972-1977 ◽  
Author(s):  
T. Gambichler ◽  
J. Pätzholz ◽  
L. Schmitz ◽  
N. Lahner ◽  
A. Kreuter
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Lupus Erythematosus ◽  
Cutaneous Lupus Erythematosus ◽  
Cutaneous Lupus

scholarly journals Low number of regulatory T cells in skin lesions of patients with cutaneous lupus erythematosus

2007 ◽  
Vol 56 (6) ◽  
pp. 1910-1920 ◽  
Author(s):  
B. Franz ◽  
B. Fritzsching ◽  
A. Riehl ◽  
N. Oberle ◽  
C.-D. Klemke ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Lupus Erythematosus ◽  
Cutaneous Lupus Erythematosus ◽  
Skin Lesions ◽  
Cutaneous Lupus

scholarly journals Inflammatory and T Helper 17/ Regulatory T Cells Related Cytokines Balance in Cutaneous Lupus Erythematosus (CLE)

2020 ◽  
Author(s):  
Mohammad-Reza Yazdani ◽  
Elham Aflaki ◽  
Nasser Gholijani
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Lupus Erythematosus ◽  
Transforming Growth Factor ◽  
Cutaneous Lupus Erythematosus ◽  
Enzyme Linked Immunosorbent Assay ◽  
Healthy Controls ◽  
T Helper ◽  
Malar Rash ◽  
Cutaneous Lupus

The cutaneous lupus erythematosus (CLE) is a common manifestation among systemic lupus erythematosus (SLE) patients. Malar rash and discoid lupus (DLE) are in the category of acute and chronic CLE, respectively. The pathogenesis of CLE is multifactorial, and cytokine imbalances contribute to immune dysfunction and the induction of organ damage. Many aspects of cytokine dysregulation are still unclear in SLE and in particular CLE. Therefore, we concurrently measured the inflammatory [Tumor necrosis factor-alpha (TNF-α) and Interleukin (IL)-6)], T helper (Th)-17 (IL-17 and IL-23) and regulatory T cells [Transforming growth factor-beta (TGFβ) and IL-10)]-related cytokines in patients with CLE (patients with malar rash and/or DLE) and compared them with SLE patients and healthy individuals (n=25 in each group, a total of 75 patients). The serum levels of cytokines were assessed by Enzyme-Linked Immunosorbent Assay (ELISA) method. IL-6 cytokine was significantly higher in SLE, DLE, and malar rash patients compared to those in healthy controls (p=0.025) and in patients with arthralgia (p=0.038), and gastrointestinal involvement (p=0.048). IL-17 was significantly higher in malar rash patients compared to normal individuals (p=0.023), SLE (p=0.008) and DLE patients (p=0.019) and in patients with oropharyngeal ulcer (p=0.05) but, IL-23 was significantly higher only in DLE patients than healthy controls (p=0.019). In conclusion, inflammatory cytokines such as IL-6 involved in inflammation and differentiation of Th17 cells are probably responsible in part for Th17 activity in CLE. IL-17, IL-23, and IL-6/IL-6R (IL-6 receptor) inhibitors may be good treatments for CLE patients. So targeting these cytokines activity pathways can improve the CLE treatment strategy and may open a novel guideline for SLE and CLE treatment.

scholarly journals Regulatory T cells in inflammatory skin disease: from mice to humans

2019 ◽  
Vol 31 (7) ◽  
pp. 457-463 ◽  
Author(s):  
Lokesh A Kalekar ◽  
Michael D Rosenblum
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Lupus Erythematosus ◽  
Immune Cell ◽  
Critical Role ◽  
Cutaneous Lupus Erythematosus ◽  
The Body ◽  
Immune Cell Subsets ◽  
Organ Repair ◽  
And Function

Abstract The skin is the largest organ in the body and one of the primary barriers to the environment. In order to optimally protect the host, the skin is home to numerous immune cell subsets that interact with each other and other non-immune cells to maintain organ integrity and function. Regulatory T cells (Tregs) are one of the largest immune cell subsets in skin. They play a critical role in regulating inflammation and facilitating organ repair. In doing so, they adopt unique and specialized tissue-specific functions. In this review, we compare and contrast the role of Tregs in cutaneous immune disorders from mice and humans, with a specific focus on scleroderma, alopecia areata, atopic dermatitis, cutaneous lupus erythematosus and psoriasis.

Selective Expansions of T cells Expressing Vβ38 and Vβ13 in Skin Lesions of Patients with Chronic Cutaneous Lupus Erythematosus

1996 ◽  
Vol 23 (10) ◽  
pp. 670-676 ◽  
Author(s):  
Fukumi Furukawa ◽  
Yoshiki Tokura ◽  
Kayo Matsushita ◽  
Kayoko Iwasaki-Inuzuka ◽  
Kazue Onagi-Suzuki ◽  
...  
Keyword(s):  
T Cells ◽  
Lupus Erythematosus ◽  
Cutaneous Lupus Erythematosus ◽  
Skin Lesions ◽  
Cutaneous Lupus

Expression pattern of tissue-resident memory T cells in cutaneous lupus erythematosus

Lupus ◽  
2021 ◽  
pp. 096120332110172
Author(s):  
Hyeon-Jung Gu ◽  
Shinyoung Song ◽  
Joo Young Roh ◽  
YunJae Jung ◽  
Hee Joo Kim
Keyword(s):  
T Cells ◽  
Lupus Erythematosus ◽  
Memory T Cells ◽  
Cutaneous Lupus Erythematosus ◽  
Discoid Lupus Erythematosus ◽  
Type I ◽  
Systemic Lupus ◽  
Peripheral Tissues ◽  
Resident Memory T Cells ◽  
Cutaneous Lupus

Background Tissue resident memory T cells (TRMs) persist long-term in peripheral tissues without recirculation, triggering an immediate protective inflammatory state upon the re-recognition of the antigen. Despite evidence incriminating the dysregulation of TRMs in autoimmune diseases, few studies have examined their expression in cutaneous lupus erythematosus (CLE). Objectives We aimed to examine whether there are differences among TRM populations in CLE depending on different clinical conditions, such as the CLE subtype or association with systemic lupus erythematosus, and to determine the effect of type I interferon (IFN) on the development of TRMs in CLE. Methods CLE disease activity was evaluated using the Cutaneous Lupus Erythematosus Disease Area and Severity Index. The expression of the TRM markers CD69 and CD103 in CLE lesions was evaluated by immunofluorescence. Flow cytometry was performed on peripheral blood mononuclear cells after IFNα treatment. Results The number of TRMs expressing either CD69 or CD103 was significantly higher in CLE lesions than in control skin; however, it was not significantly different between discoid lupus erythematosus and subacute CLE, or dependent on the presence of concomitant systemic lupus. Lesional severity was not correlated with an increase in TRMs in CLE. IFNα treatment induced a conspicuous increase in CD69 expression in skin-homing T cells, more profoundly in CD4+ T cells than in CD8+ T cells. Conclusions Skin TRMs, either CD69 or CD103-positive cells, showed increased levels in the lesional skin of CLE, and IFNα increased the expression of CD69 in T cells.

PD-1H (VISTA)–mediated suppression of autoimmunity in systemic and cutaneous lupus erythematosus

2019 ◽  
Vol 11 (522) ◽  
pp. eaax1159 ◽  
Author(s):  
Xue Han ◽  
Matthew D. Vesely ◽  
Wendy Yang ◽  
Miguel F. Sanmamed ◽  
Ti Badri ◽  
...  
Keyword(s):  
T Cells ◽  
Autoimmune Diseases ◽  
Lupus Erythematosus ◽  
Immune Cell ◽  
Cutaneous Lupus Erythematosus ◽  
Myeloid Cells ◽  
Discoid Lupus Erythematosus ◽  
Critical Element ◽  
Inhibitory Receptor ◽  
Cutaneous Lupus

Systemic lupus erythematosus (SLE) and discoid lupus erythematosus (DLE) of the skin are autoimmune diseases characterized by inappropriate immune responses against self-proteins; the key elements that determine disease pathogenesis and progression are largely unknown. Here, we show that mice lacking immune inhibitory receptor VISTA or programmed death-1 homolog (PD-1H KO) on a BALB/c background spontaneously develop cutaneous and systemic autoimmune diseases resembling human lupus. Cutaneous lupus lesions of PD-1H KO mice have clustering of plasmacytoid dendritic cells (pDCs) similar to human DLE. Using mass cytometry, we identified proinflammatory neutrophils as critical early immune infiltrating cells within cutaneous lupus lesions of PD-1H KO mice. We also found that PD-1H is highly expressed on immune cells in human SLE, DLE lesions, and cutaneous lesions of MRL/lpr mice. A PD-1H agonistic monoclonal antibody in MRL/lpr mice reduces cutaneous disease, autoantibodies, inflammatory cytokines, chemokines, and immune cell expansion. Furthermore, PD-1H on both T cells and myeloid cells including neutrophils and pDCs could transmit inhibitory signals, resulting in reduced activation and function, establishing PD-1H as an inhibitory receptor on T cells and myeloid cells. On the basis of these findings, we propose that PD-1H is a critical element in the pathogenesis and progression of lupus, and PD-1H activation could be effective for treatment of systemic and cutaneous lupus.

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