p38 mitogen-activated protein kinase (p38 MAPK)-mediated autoimmunity: Lessons to learn from ANCA vasculitis and pemphigus vulgaris

Mavropoulos, Αthanasios; Orfanidou, Timoklia; Liaskos, Christos; Smyk, Daniel S.; Billinis, Charalambos; Blank, Miri; Rigopoulou, Eirini I.; Bogdanos, Dimitrios P.

doi:10.1016/j.autrev.2012.10.019

Cited by 45 publications

(43 citation statements)

References 179 publications

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“…Drugs probably act as triggers by either modifying the immune response or altering the antigenic properties of the epidermal basement membrane [81]. However etiopathology of BP is still partially unknown, and possible mechanisms might be discovered in the near future as it is happening for pemphigus [134] The diagnosis of DIBP can be very difficult because of the heterogeneous clinical manifestations but the histologic, and immunopathologic features are identical or closely similar to those of the idiopathic disease. It should be noted that an accurate drug history of patients must be taken.…”

Section: Atypical Presentations Of Bullous Pemphigoidmentioning

confidence: 96%

Atypical presentations of bullous pemphigoid: Clinical and immunopathological aspects

Cozzani

Gasparini

Burlando

et al. 2015

Autoimmunity Reviews

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Section: Atypical Presentations Of Bullous Pemphigoidmentioning

confidence: 96%

Atypical presentations of bullous pemphigoid: Clinical and immunopathological aspects

Cozzani

Gasparini

Burlando

et al. 2015

Autoimmunity Reviews

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“…Other pathologies that involve the dysregulation of JNKs include insulin resistance [109] and some cases of inflammation [113]. The p38s are involved primarily in the induction of pathological and/or chronic inflammation, and as such, they are currently considered as key therapeutic targets for inflammation-related pathologies and diseases of the immune system [114] including autoimmune disorders [115]. The dysregulation of the p38 cascade was also shown to be involved in cardiovascular diseases [116] and neurodegenerative diseases [117].…”

Section: Mapk Cascades In Diseasementioning

confidence: 99%

The Nuclear Translocation of Mitogen-Activated Protein Kinases: Molecular Mechanisms and Use as Novel Therapeutic Target

et al. 2018

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The mitogen-activated protein kinase (MAPK) cascades are central signaling pathways that play a central role in the regulation of most stimulated cellular processes including proliferation, differentiation, stress response and apoptosis. Currently 4 such cascades are known, each termed by its downstream MAPK components: the extracellular signal-regulated kinase 1/2 (ERK1/2), cJun-N-terminal kinase (JNK), p38 and ERK5. One of the hallmarks of these cascades is the stimulated nuclear translocation of their MAPK components using distinct mechanisms. ERK1/2 are shuttled into the nucleus by importin7, JNK and p38 by a dimer of importin3 with either importin9 or importin7, and ERK5 by importin-α/β. Dysregulation of these cascades often results in diseases, including cancer and inflammation, as well as developmental and neurological disorders. Much effort has been invested over the years in developing inhibitors to the MAPK cascades to combat these diseases. Although some inhibitors are already in clinical use or clinical trials, their effects are hampered by development of resistance or adverse side-effects. Recently, our group developed 2 myristoylated peptides: EPE peptide, which inhibits the interaction of ERK1/2 with importin7, and PERY peptide, which prevents JNK/p38 interaction with either importin7 or importin9. These peptides block the nuclear translocation of their corresponding kinases, resulting in prevention of several cancers, while the PERY peptide also inhibits inflammation-induced diseases. These peptides provide a proof of concept for the use of the nuclear translocation of MAPKs as therapeutic targets for cancer and/or inflammation.

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“…The uveitogenic peptide used for B6 was IRBP1-20 (amino acids [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20] of human IRBP, 150 μg/ mouse) and that for B10RIII mice was IRBP161-180 (amino acids 161-180 of human IRBP, 75 μg/mouse). The peptides were emulsified in either complete Freund's adjuvant (CFA), incomplete Freund's adjuvant (IFA) or IFA containing TLR-2 ligand PGN.…”

Section: Induction Of Eau and Adoptive Transfermentioning

confidence: 99%

“…MAPKs are composed of three major subgroups: extracellular signalrelated kinase1/2 (ERK1/2), p38 and c-Jun N-terminal kinase (JNK). Among them, the p38 MAPK pathway has been demonstrated to play an important role in the development of autoimmunity [17]. Excessive activation of the p38 MAPK is associated with autoimmune diseases, and inhibitors of this pathway have been considered as new therapeutic strategies [18].…”

Section: Introductionmentioning

confidence: 99%

Engagement of Toll-like receptor 2 enhances interleukin (IL)-17+ autoreactive T cell responses via p38 mitogen-activated protein kinase signalling in dendritic cells

Wei

Dong

Xiao

et al. 2014

Clinical and Experimental Immunology

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SummaryFunctional analysis of single Toll-like receptors (TLRs) in vivo is necessary to understand how they shape the ocular inflammation involved in uveitis. In this study we explored the role and mechanisms of TLR-2 agonists on the autoreactive T helper type 17 (Th17) response in experimental autoimmune uveitis (EAU). Treatment by peptidoglycan (PGN), a specific TLR-2 agonist, remarkably increased mRNA levels of Th17-lineage genes interleukin (

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p38 mitogen-activated protein kinase (p38 MAPK)-mediated autoimmunity: Lessons to learn from ANCA vasculitis and pemphigus vulgaris

Cited by 45 publications

References 179 publications

Atypical presentations of bullous pemphigoid: Clinical and immunopathological aspects

Atypical presentations of bullous pemphigoid: Clinical and immunopathological aspects

The Nuclear Translocation of Mitogen-Activated Protein Kinases: Molecular Mechanisms and Use as Novel Therapeutic Target

Engagement of Toll-like receptor 2 enhances interleukin (IL)-17+ autoreactive T cell responses via p38 mitogen-activated protein kinase signalling in dendritic cells

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