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ID PMID Title PublicationDate abstract
29802846 Synthetic analogues of the parasitic worm product ES-62 reduce disease development in in v 2018 Sep Parasitic worms are receiving much attention as a potential new therapeutic approach to treating autoimmune and allergic conditions but concerns remain regarding their safety. As an alternative strategy, we have focused on the use of defined parasitic worm products and recently taken this one step further by designing drug-like small molecule analogues of one such product, ES-62, which is anti-inflammatory by virtue of covalently attached phosphorylcholine moieties. Previously, we have shown that ES-62 mimics are efficacious in protecting against disease in mouse models of rheumatoid arthritis, systemic lupus erythematosus and skin and lung allergy. Given the potential role of chronic inflammation in fibrosis, in the present study we have focused our attention on lung fibrosis, a debilitating condition for which there is no cure and which in spite of treatment slowly gets worse over time. Two mouse models of fibrosis - bleomycin-induced and LPS-induced - in which roles for inflammation have been implicated were adopted. Four ES-62 analogues were tested - 11a and 12b, previously shown to be active in mouse models of allergic and autoimmune disease and 16b and AIK-29/62 both of which are structurally related to 11a. All four compounds were found to significantly reduce disease development in both fibrosis models, as shown by histopathological analysis of lung tissue, indicating their potential as treatments for this condition.
29718222 Genetic Variation Affects C-Reactive Protein Elevations in Crohn's Disease. 2018 Aug 16 BACKGROUND: C-reactive protein (CRP) is a serum marker that is used to measure disease activity in Crohn's disease (CD). However, a subset of CD patients have normal CRP during flares. In rheumatoid arthritis and lupus, genetic variants can restrict CRP elevations during flares. This study sought to determine if common CRP genetic variants affect CRP values during active CD. METHODS: Subjects with CD who participated in the Partners HealthCare BioBank were genotyped for 5 common CRP genetic variants (rs2794520, rs3122012, rs3093077, rs2808635, and rs1800947). Medical records were reviewed to determine disease activity and the highest CRP value during active CD. CRP values during active infection or malignancy at the time of the test were excluded. CRP values were compared by genotype using the Mann-Whitney test. RESULTS: The study included 199 subjects with active CD (21 to 86 years of age). Subjects with the rs2794520 TT genotype had a lower CRP than subjects with the CC genotype (58.3 mg/L vs 28.4 mg/L, P = 0.008). Subjects with the rs1800947 CG genotype had a lower CRP than those with the CC genotype (54.3 mg/L vs 22.4 mg/L, P < 0.0001); 41.6% of TT subjects had a normal CRP compared with 24.1% of CT subjects and 16.5% of CC subjects (P = 0.041). CONCLUSIONS: This study demonstrates that rs2794520 and rs1800947 are associated with a restriction of CRP elevations during active CD. While CRP is typically a reliable biomarker in CD, there is a subset of CD patients with a genetically determined restriction of CRP in whom other disease markers should be utilized.
29699911 Novel amidrazone derivatives: Design, synthesis and activity evaluation. 2018 Jul 23 A series of new 6-styryl-naphthalene-2-amidrazone derivatives were synthesized and evaluated as potential ASIC1a inhibitors. Among them, compound 5e showed the most activity to inhibit [Ca(2+)](i). elevation in acid-induced articular chondrocytes. Together with the important role of ASIC1a in the pathogenesis of tissue acidification diseases including rheumatoid arthritis, these results might provide a meaningful hint or inspiration in developing drugs targeting at tissue acidification diseases.
29624481 Craniofacial Manifestations of Systemic Disorders: CT and MR Imaging Findings and Imaging 2018 May Many systemic diseases or conditions can affect the maxillofacial bones; however, they are often overlooked or incidentally found at routine brain or head and neck imaging performed for other reasons. Early identification of some conditions may significantly affect patient care and alter outcomes. Early recognition of nonneoplastic hematologic disorders, such as thalassemia and sickle cell disease, may help initiate earlier treatment and prevent serious complications. The management of neoplastic diseases such as lymphoma, leukemia, or Langerhans cell histiocytosis may be different if diagnosed early, and metastases to the maxillofacial bones may be the first manifestation of an otherwise occult neoplasm. Endocrinologic and metabolic disorders also may manifest with maxillofacial conditions. Earlier recognition of osteoporosis may alter treatment and prevent complications such as insufficiency fractures, and identification of acromegaly may lead to surgical treatment if there is an underlying growth hormone-producing adenoma. Bone dysplasias sometimes are associated with skull base foraminal narrowing and subsequent involvement of the cranial nerves. Inflammatory processes such as rheumatoid arthritis and sarcoidosis may affect the maxillofacial bones, skull base, and temporomandibular joints. Radiologists should be familiar with the maxillofacial computed tomographic and magnetic resonance imaging findings of common systemic disorders because these may be the first manifestations of an otherwise unrevealed systemic process with potential for serious complications. Online supplemental material is available for this article. (©)RSNA, 2018.
28687059 Exploring the interplay between autoimmunity and cancer to find the target therapeutic hot 2018 Jun Autoimmunity arises when highly active immune responses are developed against the tissues or substances of one's own body. It is one of the most prevalent disorders among the old-age population with prospects increasing with age. The major cause of autoimmunity and associated diseases is the dysregulation of host immune surveillance. Impaired repairment of immune system and apoptosis regulation can be seen as major landmarks in autoimmune disorders such as the mutation of p53 gene which results in rheumatoid arthritis, bowel disease which consequently lead to tissue destruction, inflammation and dysfunctioning of body organs. Cytokines mediated apoptosis and proliferation of cells plays a regulatory role in cell cycle and further in cancer development. Anti-TNF therapy, Treg therapy and stem cell therapy have been used for autoimmune diseases, however, with the increase in the use of immunomodulatory therapies and their development for autoimmune diseases and cancer, the understanding of human immune system tends to become an increasing requirement. Hence, the findings associated with the relationship between autoimmune diseases and cancer may prove to be beneficial for the improvement in the health of suffering patients. Here in, we are eliciting the underlying mechanisms which result in autoimmune disorders causing the onset of cancer, exploration of interactome to find the pathways which are mutual to both, and recognition of hotspots which might play important role in autoimmunity mediated therapeutics with different therapies such as anti-TNF therapy, Treg therapy and stem cell therapy.
31308818 Impact of NR1I2, adenosine triphosphate-binding cassette transporters genetic polymorphism 2019 Jul BACKGROUND: Ginsenoside compound K (CK) is a promising drug candidate for rheumatoid arthritis. This study examined the impact of polymorphisms in NR1I2, adenosine triphosphate-binding cassette (ABC) transporter genes on the pharmacokinetics of CK in healthy Chinese individuals. METHODS: Forty-two targeted variants in seven genes were genotyped in 54 participants using Sequenom MassARRAY system to investigate their association with major pharmacokinetic parameters of CK and its metabolite 20(S)-protopanaxadiol (PPD). Subsequently, molecular docking was simulated using the AutoDock Vina program. RESULTS: ABCC4 rs1751034 TT and rs1189437 TT were associated with increased exposure of CK and decreased exposure of 20(S)-PPD, whereas CFTR rs4148688 heterozygous carriers had the lowest maximum concentration (C(max)) of CK. The area under the curve from zero to the time of the last quantifiable concentration (AUC(last)) of CK was decreased in NR1I2 rs1464602 and rs2472682 homozygous carriers, while C(max) was significantly reduced only in rs2472682. ABCC4 rs1151471 and CFTR rs2283054 influenced the pharmacokinetics of 20(S)-PPD. In addition, several variations in ABCC2, ABCC4, CFTR, and NR1I2 had minor effects on the pharmacokinetics of CK. Quality of the best homology model of multidrug resistance protein 4 (MRP4) was assessed, and the ligand interaction plot showed the mode of interaction of CK with different MRP4 residues. CONLUSION: ABCC4 rs1751034 and rs1189437 affected the pharmacokinetics of both CK and 20(S)-PPD. NR1I2 rs1464602 and rs2472682 were only associated with the pharmacokinetics of CK. Thus, these hereditary variances could partly explain the interindividual differences in the pharmacokinetics of CK.
35111494 Efficacy and risks of fondaparinux 7.5 mg for deep vein thrombosis after total knee arthr 2019 OBJECTIVES: High-dose fondaparinux therapy at 7.5 mg/day (FPX 7.5 mg) for deep vein thrombosis (DVT) may increase the risk of hemorrhage. We investigated the efficacy and safety of FPX 7.5 mg to treat DVT after total knee arthroplasty. METHODS: This study included 101 patients (91 with osteoarthritis, 10 with rheumatoid arthritis; mean age at total knee arthroplasty: 72.9 years) with asymptomatic postoperative DVT. Medical prophylaxis for DVT was started on postoperative day 1. Vascular ultrasound was conducted within 2 days postoperatively; patients were switched to FPX 7.5 mg after DVT diagnosis. Ultrasound was repeated to monitor DVT resolution. Adverse reactions were assessed. RESULTS: DVT resolved in 72 patients (71.3%) receiving FPX 7.5 mg. There were no significant differences between patients with versus without DVT resolution in the timing of FPX 7.5 mg therapy, treatment period, age, body mass index, or D-dimer or hemoglobin levels. There was no significant difference in DVT outcome between patients starting FPX 7.5 mg within 4 days postoperatively versus on day 5 or later, or between patients treated for ≤7 versus ≥8 days. Hemoglobin decreased to ≤7 g/dL in three patients (2.9%). CONCLUSIONS: FPX 7.5 mg can be expected to resolve DVT in 71.3% of patients; however, the risk of associated hemorrhagic complications may be higher than the risk of pulmonary embolism. To treat DVT with FPX 7.5 mg without compromising safety, patients should be selected carefully and the timing of treatment should be adjusted appropriately.
30408584 The characteristics and pivotal roles of triggering receptor expressed on myeloid cells-1 2019 Jan Triggering receptor expressed on myeloid cells-1 (TREM-1) engagement can directly trigger inflammation or amplify an inflammatory response by synergizing with TLRs or NLRs. Autoimmune diseases are a family of chronic systemic inflammatory disorders. The pivotal role of TREM-1 in inflammation makes it important to explore its immunological effects in autoimmune diseases. In this review, we summarize the structural and functional characteristics of TREM-1. Particularly, we discuss recent findings on TREM-1 pathway regulation in various autoimmune diseases, including rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), inflammatory bowel disease (IBD), type 1 diabetes (T1D), and psoriasis. This receptor may potentially be manipulated to alter the inflammatory response to chronic inflammation and possible therapies are explored in this review.
30362576 Dielectrophoretic characterization and separation of monocytes and macrophages using 3D ca 2019 Jan Monocyte heterogeneity and its prevalence are revealed as indicator of several human diseases ranking from cardiovascular diseases to rheumatoid arthritis, chronic kidney diseases, autoimmune multiple sclerosis, and stroke injuries. When monocytes and macrophages are characterized and isolated with preserved genetic, phenotypic and functional properties, they can be used as label-free biomarkers for precise diagnostics and treatment of various diseases. Here, the dielectrophoretic responses of the monocytes and macrophages were examined. We present 3D carbon-electrode dielectrophoresis (carbon-DEP) as a separation tool for U937 monocytes and U937 monocyte-differentiated macrophages. The carbon-electrodes advanced the usability and throughput of DEP separation, presented wider electrochemical stability. Using the 3D carbon-DEP chip, we first identified the selective positive and negative DEP responses and specific crossover frequencies of monocytes and macrophages as their signatures for separation. The crossover frequency of monocytes and macrophages was 17 and 30 kHz, respectively. Next, we separated monocyte and macrophage subpopulations using their specific dielectrophoretic responses. Afterward, we used a fluorescence-activated cell sorter to confirm our results. Finally, we enriched 70% of monocyte cells from the mixed cell population, in other words, concentration of monocyte cells to macrophage cells was five times increased, using the 30-kHz, 10-Vpp electric field and 1 μL/min flow rate.
30306455 Upregulation of HRD1 promotes cell migration and invasion in colon cancer. 2019 Apr 3-Hydroxy-3-methylglutaryl reductase degradation (HRD1) is an E3 ubiquitin ligase that functions by promoting degradation of misfolded proteins in processes such as embryogenesis and rheumatoid arthritis. However, little is known about the role of HRD1 in cancer. The aim of the present study was to investigate the expression pattern and functions of HRD1 in human colon cancer (CC). We found that HRD1 expression was increased significantly in human CC tissues, and its overexpression was associated with TNM stage, tumor differentiation, tumor invasive depth, and distant metastasis. Knockdown of HRD1 using small hairpin (sh) RNA plasmid significantly inhibited CC cell migration and invasion. Furthermore, the silencing of HRD1 decreased the expression of MMP-2 and MMP-9, which is critical for CC cell migration and invasion. Taken together, these results revealed that HRD1 is overexpressed in CC and promotes migration and invasion of CC cells. Inhibition of HRD1 may be considered as an effective anti-CC strategy.
29971515 Intraoperative diagnosis with abnormal branching of the left A8 pulmonary artery from the 2018 Jul 3 BACKGROUND: Safety is of vital importance for lung resection. The dissection of pulmonary vessels is associated with vascular injury and bleeding, and identification of the vessels is necessary. The most common abnormal branching pattern of the left pulmonary artery is the mediastinal lingular artery. However, a mediastinal basal pulmonary artery is very rare. A case of abnormal branching from the left pulmonary artery to S8 which was diagnosed intraoperatively, and, thus, its dissection was avoided, is reported. CASE PRESENTATION: A 76-year-old woman with rheumatoid arthritis was diagnosed with left upper lung adenocarcinoma and visited our hospital. Contrast CT was not performed due to renal dysfunction, and abnormal branching of the left pulmonary artery was not identified. Video-assisted thoracoscopic left upper lobectomy and lymphadenectomy were performed. After the upper pulmonary vein was dissected and tissue around it was detached carefully, a pulmonary mediastinal branch from the left main pulmonary artery was identified descending between the upper pulmonary vein and upper bronchus. It was possible to separate the interlobar fissure safely and preserve A8. On retrospective examination, non-contrast CT showed A8. CONCLUSIONS: Although preoperative identification of left pulmonary mediastinal branches was difficult by non-contrast CT, a careful surgical procedure preserved the left pulmonary mediastinal A8.
29881387 A Decade of Th9 Cells: Role of Th9 Cells in Inflammatory Bowel Disease. 2018 T helper cell subsets play a critical role in providing protection against offending pathogens by secreting specific cytokines. However, unrestrained T helper cell responses can promote chronic inflammation-mediated inflammatory diseases. Dysregulated T helper cell responses have been suggested to be involved in the pathogenesis of multiple inflammatory diseases, including allergic airway inflammation, rheumatoid arthritis, and inflammatory bowel disease (IBD) among others. Aberrant pro-inflammatory responses induced by Th1, Th2, and Th17 subsets are known to trigger IBD. IBD is a chronic inflammatory disease characterized by weight loss, diarrhea, pain, fever, and rectal bleeding. It poses a major health burden worldwide owing to the increased risk of colorectal cancer development. Despite numerous therapeutic advancements, IBD still remains a major health burden due to the inefficiency of the conventional therapies. Recently, IL-9-secreting Th9 cells are known to be involved in the pathogenesis of IBD. However, the role of Th9 cells and their secretory cytokine IL-9 in IBD is unclear. The functional relevance of Th9 cells is also relatively understudied in IBD. Thus, investigating the actual role of various T helper cell subsets including Th9 cells in IBD is essential to develop novel therapies to treat IBD. Here, we highlight the role of Th9 cells in promoting IBD. We discuss the mechanisms that might be employed by Th9 cells and IL-9 in promoting IBD and thereby propose potential targets for the treatment of Th9 cell-mediated IBD.
29663380 Transglutaminase activity regulates differentiation, migration and fusion of osteoclasts v 2018 Sep Osteoclasts, bone resorbing cells, derive from monocyte/macrophage cell lineage. Increased osteoclast activity is responsible for bone destruction in diseases such as osteoporosis, periodontitis and rheumatoid arthritis. Transglutaminases (TGs), protein crosslinking enzymes, were recently found involved in osteoclastogenesis in vivo, however their mechanisms of action have remained unknown. In this study, we have investigated the role of TG activity in osteoclastogenesis in vitro using four TG inhibitors, NC9, Z006, T101, and monodansyl cadaverine. Our results showed that all TG inhibitors were capable of blocking the entire osteoclastogenesis process. The most potent of the inhibitors, NC9 when added to cultures at different phases of osteoclastogenesis, inhibited differentiation, migration, and fusion of pre-osteoclasts as well as resorption activity of mature osteoclasts. Further investigation into the mechanisms revealed that NC9 increased RhoA levels and blocked podosome belt formation suggesting that TG activity regulates actin dynamics in pre-osteoclasts. The inhibitory effect of NC9 on osteoclastogenesis as well as podosome belt formation was completely reversed with a Rho-family inhibitor Exoenzyme C3. Microtubule architecture, acetylation, and detyrosination of α-tubulin were not affected. Finally, we demonstrated that macrophages and osteoclasts expressed mRNA of three TGs:TG1, TG2, and Factor XIII-A which were all differentially regulated in these cells during differentiation. Immunofluoresence microscopic analysis showed that all three enzymes co-localized to podosomes in osteoclasts. Taken together, our data suggests that TG activity regulates differentiation, migration and fusion of osteoclasts via affecting actin dynamics and that this may involve contribution from all three TG enzymes.
29614819 Emerging Roles of Vascular Cell Adhesion Molecule-1 (VCAM-1) in Immunological Disorders an 2018 Apr 2 Tumor necrosis factor alpha (TNFα) is a pro-inflammatory cytokine that triggers the expression of inflammatory molecules, including other cytokines and cell adhesion molecules. TNFα induces the expression of intercellular cell adhesion molecule-1 and vascular cell adhesion molecule-1 (VCAM-1). VCAM-1 was originally identified as a cell adhesion molecule that helps regulate inflammation-associated vascular adhesion and the transendothelial migration of leukocytes, such as macrophages and T cells. Recent evidence suggests that VCAM-1 is closely associated with the progression of various immunological disorders, including rheumatoid arthritis, asthma, transplant rejection, and cancer. This review covers the role and relevance of VCAM-1 in inflammation, and also highlights the emerging potential of VCAM-1 as a novel therapeutic target in immunological disorders and cancer.
29610603 Myasthenia Gravis and Associated Diseases. 2018 Mar 15 BACKGROUND: Myasthenia gravis (MG) is an autoimmune disease caused by the action of specific antibodies to the postsynaptic membrane of the neuromuscular junction, leading to impaired neuromuscular transmission. Patients with MG have an increased incidence of other autoimmune diseases. AIM: to determine the presence of other associated diseases in patients with MG. METHOD: A group of 127 patients with MG followed in 10 years period, in which the presence of other associated diseases has been analysed. RESULTS: The sex ratio is in favour of the female sex, the average age of the initial manifestation of the disease is less than 50 years, 65.4% of the patients with MG have another disease. 15.0% patients have associated another autoimmune disease. Thyroid disease is the most common associated with MG, rarely rheumatoid arthritis (RA), systemic lupus erythematosus (SLE) and other autoimmune diseases. Other diseases include hypertension, heart disease, diabetes, respiratory diseases, dyslipidemia. 10.2% of the patients are diagnosed with extrathymic tumours of various origins. CONCLUSION: Associated diseases are common in patients with MG, drawing attention to the possible common basis for their coexistence, as well as their impact on the intensity and treatment of the disease.
29564307 Prevalence and Associated Risk Factors of Sarcopenia in Female Patients with Osteoporotic 2018 Feb BACKGROUND: We determined the prevalence of sarcopenia according to fracture site and evaluated the associated risk factors in female patients with osteoporotic fractures. METHODS: A total of 108 patients aged 50 years or older with an osteoporotic fracture (hip, spine, or wrist) were enrolled in this retrospective observational study. A diagnosis of sarcopenia was confirmed using whole-body densitometry for skeletal muscle mass measurement. Logistic regression analysis was used to analyze the risk factors for sarcopenia. RESULTS: Of 108 female patients treated for osteoporotic fractures between January 2016 and June 2017, sarcopenia was diagnosed in 39 (36.1%). Of these, 41.5% (17/41) had hip fractures, 35% (14/40) had spine fractures, and 29.6% (8/27) had distal radius fractures. Body mass index (BMI; P=0.036) and prevalence of chronic kidney disease (CKD; P=0.046) and rheumatoid arthritis (P=0.051) were significantly different between the groups. In multivariable analysis, BMI (odds ratio [OR], 0.76; 95% confidence interval [CI], 0.55-1.05, P=0.098) and CKD (OR 2.51; 95% CI, 0.38-16.2; P=0.233) were associated with an increased risk of sarcopenia; however, this was not statistically significant. CONCLUSIONS: This study evaluated the prevalence of sarcopenia according to the fracture site and identified associated risk factors in patients with osteoporotic fractures. A longterm, observational study with a larger population is needed to validate our results.
29559970 Interleukin-18 Amplifies Macrophage Polarization and Morphological Alteration, Leading to 2018 M2 macrophage (Mφ) promotes pathologic angiogenesis through a release of pro-angiogenic mediators or the direct cell-cell interaction with endothelium in the micromilieu of several chronic inflammatory diseases, including rheumatoid arthritis and cancer, where interleukin (IL)-18 also contributes to excessive angiogenesis. However, the detailed mechanism remains unclear. The aim of this study is to investigate the mechanism by which M2 Mφs in the micromilieu containing IL-18 induce excessive angiogenesis in the in vitro experimental model using mouse Mφ-like cell line, RAW264.7 cells, and mouse endothelial cell line, b.End5 cells. We discovered that IL-18 acts synergistically with IL-10 to amplify the production of Mφ-derived mediators like osteopontin (OPN) and thrombin, yielding thrombin-cleaved form of OPN generation, which acts through integrins α4/α9, thereby augmenting M2 polarization of Mφ with characteristics of increasing surface CD163 expression in association with morphological alteration. Furthermore, the results of visualizing temporal behavior and morphological alteration of Mφs during angiogenesis demonstrated that M2-like Mφs induced excessive angiogenesis through the direct cell-cell interaction with endothelial cells, possibly mediated by CD163.
29519321 Parthenolide reduces metastasis by inhibition of vimentin expression and induces apoptosis 2018 Mar 1 BACKGROUND: Use of pharmaceutical agent for breast cancer chemotherapy is an interesting method that induces cells death by different way, such as apoptosis. Parthenolide is the main compound in feverfew that has been used to cure migraine and rheumatoid arthritis for long time. Parthenolide has been predominately investigated as inducer of apoptosis in human cancer cells. PURPOSE: We examined the expression of vimentin and Elongation factor α - 1 as breast cancer biomarkers in MCF7 cells exposure to Parthenolide. METHOD: In this study, we investigated the antitumor mechanism of Parthenolide on the human breast cancer cell line MCF7, using SEM, flow cytometry and proteomics techniques. RESULT: Comparative proteome analyses are shown Elongation factor1-α and vimentin was suppressed in response to Parthenolide treatment.
29379508 Classic Ulcerative Pyoderma Gangrenosum Is a T Cell-Mediated Disease Targeting Follicular 2017 BACKGROUND: Pyoderma gangrenosum (PG) is a debilitating ulcerative skin disease that is one of the most common associated diseases seen in patients with inflammatory bowel disease and rheumatoid arthritis. Although PG is classified as a neutrophilic dermatosis, its pathophysiology is poorly understood. OBJECTIVE: Use data obtained from patient-reported histories, immunohistochemistry, and gene expression analysis to formulate a hypothesis on PG pathophysiology. METHODS: Ten PG patients participated and answered questions about new ulcer formation. Skin biopsies of healed prior ulcers and adjacent normal skin were obtained from four patients for immunohistochemistry. Scars from healthy patients and patients with discoid lupus were used as additional controls. New onset PG papules were analyzed using immunohistochemistry and gene expression analysis via quantitative real-time PCR. RESULTS: All PG patients reported that healed sites of previous ulceration are refractory to re-ulceration. Simultaneous biopsies of healed and uninvolved skin triggered ulceration only in the latter. On immunohistochemistry, healed PG scars showed complete loss of pilosebaceous units, which were present in normal skin, and to a lesser extent in control scars, and discoid scars. Early PG papules showed perivascular and peripilosebaceous T cell infiltrates, rather than neutrophils. These early inflammatory events were dominated by increased gene expression of CXCL9, CXCL10, CXCL11, IL-8, IL-17, IFNG, and IL-36G and transcription factors consistent with Th1 phenotype. LIMITATIONS: Small sample size was the main limitation. CONCLUSION: We put forth the hypothesis that PG is a T cell response resulting in the destruction of pilosebaceous units.
29279285 Ubiquitination-proteasome system: A new player in the pathogenesis of psoriasis and clinic 2018 Mar Ubiquitination is an important post-translational modification that regulates a myriad of biological processes such as inflammation, immune response, cell differentiation and proliferation. During the last decade, progress in proteomics contributed to the identification of new E3 ligases and their substrates. Hence, deregulated ubiquitination events are found to be involved in several inflammatory disorders, exemplifying by systemic lupus erythematosus (SLE), type 1 diabetes, rheumatoid arthritis (RA) and psoriasis. Psoriasis is a chronic inflammatory skin disease characterized by epidermal hyperproliferation and differentiation. Through regulation of key transcriptional factors or signaling members, ubiquitination is viewed as a key regulator in psoriasis. Thus, targeting ubiquitination pathway holds potential for the treatment of psoriasis. Herein, we summarize the current understanding of ubiquitination in psoriasis, and discuss the prospects for targeting ubiquitination in the treatment of psoriasis.