scholarly journals Psoriasis and Antimicrobial Peptides

2020 ◽  
Vol 21 (18) ◽  
pp. 6791 ◽  
Author(s):  
Toshiya Takahashi ◽  
Kenshi Yamasaki
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Antimicrobial Peptides ◽  
Psoriatic Skin ◽  
Myeloid Dendritic Cells ◽  
Dna And Rna ◽  
Systemic Inflammatory Disease ◽  
Th1 Cytokines ◽  
Molecular Patterns ◽  
Damage Associated Molecular Patterns

Psoriasis is a systemic inflammatory disease caused by crosstalk between various cells such as T cells, neutrophils, dendritic cells, and keratinocytes. Antimicrobial peptides (AMPs) such as β-defensin, S100, and cathelicidin are secreted from these cells and activate the innate immune system through various mechanisms to induce inflammation, thus participating in the pathogenesis of psoriasis. In particular, these antimicrobial peptides enhance the binding of damage-associated molecular patterns such as self-DNA and self-RNA to their receptors and promote the secretion of interferon from activated plasmacytoid dendritic cells and keratinocytes to promote inflammation in psoriasis. Neutrophil extracellular traps (NETs), complexes of self-DNA and proteins including LL-37 released from neutrophils in psoriatic skin, induce Th17. Activated myeloid dendritic cells secrete a mass of inflammatory cytokines such as IL-12 and IL-23 in psoriasis, which is indispensable for the proliferation and survival of T cells that produce IL-17. AMPs enhance the production of some of Th17 and Th1 cytokines and modulate receptors and cellular signaling in psoriasis. Inflammation induced by DAMPs, including self-DNA and RNA released due to microinjuries or scratches, and the enhanced recognition of DAMPs by AMPs, may be involved in the mechanism underlying the Köbner phenomenon in psoriasis.

scholarly journals Recent Advances in Psoriasis Research; the Clue to Mysterious Relation to Gut Microbiome

2020 ◽  
Vol 21 (7) ◽  
pp. 2582 ◽  
Author(s):  
Mayumi Komine
Keyword(s):  
Diabetes Mellitus ◽  
T Cells ◽  
Dendritic Cells ◽  
Cardiovascular Diseases ◽  
Regulatory T Cells ◽  
Gut Microbiota ◽  
Psoriatic Skin ◽  
Myeloid Dendritic Cells ◽  
Inflammatory Status ◽  
Recent Advances

Psoriasis is a chronic inflammatory cutaneous disease, characterized by activated plasmacytoid dendritic cells, myeloid dendritic cells, Th17 cells, and hyperproliferating keratinocytes. Recent studies revealed skin-resident cells have pivotal roles in developing psoriatic skin lesions. The balance in effector T cells and regulatory T cells is disturbed, leading Foxp3-positive regulatory T cells to produce proinflammatory IL-17. Not only acquired but also innate immunity is important in psoriasis pathogenesis, especially in triggering the disease. Group 3 innate lymphoid cell are considered one of IL-17-producing cells in psoriasis. Short chain fatty acids produced by gut microbiota stabilize expression of Foxp3 in regulatory T cells, thereby stabilizing their function. The composition of gut microbiota influences the systemic inflammatory status, and associations been shown with diabetes mellitus, cardiovascular diseases, psychomotor diseases, and other systemic inflammatory disorders. Psoriasis has been shown to frequently comorbid with diabetes mellitus, cardiovascular diseases, psychomotor disease and obesity, and recent report suggested the similar abnormality in gut microbiota as the above comorbid diseases. However, the precise mechanism and relation between psoriasis pathogenesis and gut microbiota needs further investigation. This review introduces the recent advances in psoriasis research and tries to provide clues to solve the mysterious relation of psoriasis and gut microbiota.

scholarly journals CD1d on Myeloid Dendritic Cells Stimulates Cytokine Secretion from and Cytolytic Activity of Vα24JαQ T Cells: A Feedback Mechanism for Immune Regulation

2000 ◽  
Vol 165 (7) ◽  
pp. 3756-3762 ◽  
Author(s):  
Otto O. Yang ◽  
Frederick K. Racke ◽  
Phuong Thi Nguyen ◽  
Rudolf Gausling ◽  
Michael E. Severino ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Immune Regulation ◽  
Feedback Mechanism ◽  
Cytolytic Activity ◽  
Cytokine Secretion ◽  
Myeloid Dendritic Cells

scholarly journals Murine Myeloid Dendritic Cells That Phagocytose Apoptotic T Cells Inhibit the Immune Response via NO

PLoS ONE ◽  
2012 ◽  
Vol 7 (11) ◽  
pp. e49378 ◽  
Author(s):  
Kaili Zhong ◽  
Wengang Song ◽  
Qian Wang ◽  
Chao Wang ◽  
Xi Liu ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Dendritic Cells ◽  
Myeloid Dendritic Cells

scholarly journals Immunopathogenesis of Acute Kidney Injury

2018 ◽  
Vol 46 (8) ◽  
pp. 930-943 ◽  
Author(s):  
Zaher A. Radi
Keyword(s):  
Acute Kidney Injury ◽  
T Cells ◽  
Kidney Tissue ◽  
Kidney Injury ◽  
Drug Induced ◽  
Inflammatory Damage ◽  
Anti Inflammatory ◽  
Renal Tubular ◽  
Molecular Patterns ◽  
Damage Associated Molecular Patterns

Pathophysiologically, the classification of acute kidney injury (AKI) can be divided into three categories: (1) prerenal, (2) intrinsic, and (3) postrenal. Emerging evidence supports the involvement of renal tubular epithelial cells and the innate and adaptive arms of the immune system in the pathogenesis of intrinsic AKI. Pro-inflammatory damage-associated molecular patterns, pathogen-associated molecular patterns, hypoxia inducible factors, toll-like receptors, complement system, oxidative stress, adhesion molecules, cell death, resident renal dendritic cells, neutrophils, T and B lymphocytes, macrophages, natural killer T cells, cytokines, and secreted chemokines contribute to the immunopathogenesis of AKI. However, other immune cells and pathways such as M2 macrophages, regulatory T cells, progranulin, and autophagy exhibit anti-inflammatory properties and facilitate kidney tissue repair after AKI. Thus, therapies for AKI include agents such as anti-inflammatory (e.g., recombinant alkaline phosphatase), antioxidants (iron chelators), and apoptosis inhibitors. In preclinical toxicity studies, drug-induced kidney injury can be seen after exposure to a nephrotoxicant test article due to immune mechanisms and dysregulation of innate, and/or adaptive cellular immunity. The focus of this review will be on intrinsic AKI, as it relates to the immune and renal systems cross talks focusing on the cellular and pathophysiologic mechanisms of AKI.

scholarly journals Regulatory T Cells and Human Myeloid Dendritic Cells Promote Tolerance via Programmed Death Ligand-1

PLoS Biology ◽  
2010 ◽  
Vol 8 (2) ◽  
pp. e1000302 ◽  
Author(s):  
Shoba Amarnath ◽  
Carliann M. Costanzo ◽  
Jacopo Mariotti ◽  
Jessica L. Ullman ◽  
William G. Telford ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Regulatory T Cells ◽  
Myeloid Dendritic Cells ◽  
Programmed Death Ligand 1 ◽  
Programmed Death

Pathogenic CCR6+ dendritic cells in the skin lesions of discoid lupus patients: a role for damage-associated molecular patterns

2013 ◽  
Vol 23 (2) ◽  
pp. 169-182 ◽  
Author(s):  
Aniela Méndez-Reguera ◽  
Gibrán Pérez-Montesinos ◽  
Marcela Alcántara-Hernández ◽  
Virginia Martínez-Estrada ◽  
Jorge Rafael Cazarin-Barrientos ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Skin Lesions ◽  
Molecular Patterns ◽  
Damage Associated Molecular Patterns

scholarly journals Interaction of Rotavirus with Human Myeloid Dendritic Cells

2005 ◽  
Vol 79 (23) ◽  
pp. 14526-14535 ◽  
Author(s):  
Carlos F. Narváez ◽  
Juana Angel ◽  
Manuel A. Franco
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Transforming Growth Factor Beta ◽  
Mononuclear Cells ◽  
Transforming Growth Factor ◽  
Myeloid Dendritic Cells ◽  
Peripheral Blood Mononuclear ◽  
Necrosis Factor Alpha ◽  
Stimulation Of

ABSTRACT We have previously shown that very few rotavirus (RV)-specific T cells that secrete gamma interferon circulate in recently infected and seropositive adults and children. Here, we have studied the interaction of RV with myeloid immature (IDC) and mature dendritic cells (MDC) in vitro. RV did not induce cell death of IDC or MDC and induced maturation of between 12 and 48% of IDC. Nonetheless, RV did not inhibit the maturation of IDC or change the expression of maturation markers on MDC. After treatment with RV, few IDC expressed the nonstructural viral protein NSP4. In contrast, a discrete productive viral infection was shown in MDC of a subset of volunteers, and between 3 and 46% of these cells expressed NSP4. RV-treated IDC secreted interleukin 6 (IL-6) (but not IL-1β, IL-8, IL-10, IL-12, tumor necrosis factor alpha, or transforming growth factor beta), and MDC released IL-6 and small amounts of IL-10 and IL-12p70. The patterns of cytokines secreted by T cells stimulated by staphylococcal enterotoxin B presented by MDC infected with RV or uninfected were comparable. The frequencies and patterns of cytokines secreted by memory RV-specific T cells evidenced after stimulation of peripheral blood mononuclear cells (PBMC) with RV were similar to those evidenced after stimulation of PBMC with RV-infected MDC. Finally, IDC treated with RV strongly stimulated naive allogeneic CD4+ T cells to secrete Th1 cytokines. Thus, although RV does not seem to be a strong maturing stimulus for DC, it promotes their capacity to prime Th1 cells.

scholarly journals Monomethyl fumarate treatment impairs maturation of human myeloid dendritic cells and their ability to activate T cells

2017 ◽  
Vol 25 (1) ◽  
pp. 63-71 ◽  
Author(s):  
Maria Antonietta Mazzola ◽  
Radhika Raheja ◽  
Keren Regev ◽  
Vanessa Beynon ◽  
Felipe von Glehn ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
Dimethyl Fumarate ◽  
Nuclear Factor Κb ◽  
Interleukin 17 ◽  
Myeloid Dendritic Cells ◽  
Gm Csf ◽  
Monomethyl Fumarate ◽  
And Function

Background: Dimethyl fumarate (DMF) and its active metabolite monomethyl fumarate (MMF) effectively lead to reduction in disease relapses and active magnetic resonance imaging (MRI) lesions. DMF and MMF are known to be effective in modulating T- and B-cell responses; however, their effect on the phenotype and function of human myeloid dendritic cells (mDCs) is not fully understood. Objective: To investigate the role of MMF on human mDCs maturation and function. Methods: mDCs from healthy controls were isolated and cultured in vitro with MMF. The effect of MMF on mDC gene expression was determined by polymerase chain reaction (PCR) array after in vitro MMF treatment. The ability of mDCs to activate T cells was assessed by in vitro co-culture system. mDCs from DMF-treated multiple sclerosis (MS) patients were analyzed by flow cytometry and PCR. Results: MMF treatment induced a less mature phenotype of mDCs with reduced expression of major histocompatibility complex class II (MHC-II), co-stimulatory molecules CD86, CD40, CD83, and expression of nuclear factor κB (NF-κB) subunits RELA and RELB. mDCs from DMF-treated MS patients also showed the same immature phenotype. T cells co-cultured with MMF-treated mDCs showed reduced proliferation with decreased production of interferon gamma (IFN-γ), interleukin-17 (IL-17), and granulocyte-macrophage colony-stimulating factor (GM-CSF) compared to untreated cells. Conclusion: We report that MMF can modulate immune response by affecting human mDC function.

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