Rheumatology and immunology research最新文献

Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) encompasses a group of potentially life-threatening disorders characterized by necrotizing small vessel vasculitis with positive serum ANCA. To date, the pathogenesis of AAV has not been fully elucidated, but remarkable progress has been achieved in the past few decades. In this review, we summarize the mechanism of AAV. The pathogenesis of AAV involves various factors. ANCA, neutrophils, and the complement system play key roles in disease initiation and progression, forming a feedback amplification loop leading to vasculitic injury. Neutrophils activated by ANCA undergo respiratory burst and degranulation, as well as releasing neutrophils extracellular traps (NETs), thus causing damage to vascular endothelial cells. Activated neutrophils could further activate the alternative complement pathway, leading to the generation of complement 5a (C5a), which amplifies the inflammatory response by priming neutrophils for ANCA-mediated overactivation. Neutrophils stimulated with C5a and ANCA could also activate the coagulation system, generate thrombin, and subsequently cause platelet activation. These events in turn augment complement alternative pathway activation. Moreover, disturbed B-cell and T-cell immune homeostasis is also involved in disease development. In-depth investigation in pathogenesis of AAV might help to offer more effective targeted therapies.

Relapsing polychondritis (RP) is a rare autoimmune disease in which recurrent and progressive chondritis occurs throughout the body. We report a case of a 56-year-old female subject presented as intermittent fever and cough, who was found obvious luminal stenosis and intense ¹⁸F-fluorodeoxyglucose (FDG) uptake in her larynx and trachea via bronchoscopy and FDG positron emission tomography/computed tomography (PET/CT). The auricular cartilage biopsy demonstrated chondritis. At first she was diagnosed as RP and treated by glucocorticoid and methotrexate, leading to completely response. Fever and cough recurred after 18 months, and FDG PET/CT were performed again and targeted a newfound nasopharyngeal lesion, where the biopsy proved to be an extranodal natural killer (NK)/T-cell lymphoma, nasal type.

Objectives: Risk stratification and prognosis prediction are critical for appropriate management of anti-neutrophil cytoplasmic antibody (ANCA) associated vasculitis (AAV). Herein, we aim to develop and internally validate a prediction model specifically for long-term survival of patients with AAV.

Methods: We thoroughly reviewed the medical charts of patients with AAV admitted to Peking Union Medical College Hospital from January 1999 to July 2019. The Least Absolute Shrinkage and Selection Operator method and the COX proportional hazard regression was used to develop the prediction model. The Harrell's concordance index (C-index), calibration curves and Brier scores were calculated to evaluate the model performance. The model was internally validated by bootstrap resampling methods.

Results: A total of 653 patients were included in the study, including 303 patients with microscopic polyangiitis, 245 patients with granulomatosis with polyangiitis and 105 patients with eosinophilic granulomatosis with polyangiitis, respectively. During a median follow-up of 33 months (interquartile range 15-60 months), 120 deaths occurred. Age at admission, chest and cardiovascular involvement, serum creatinine grade, hemoglobin levels at baseline and AAV sub-types were selected as predictive parameters in the final model. The optimism-corrected C-index and integrated Brier score of our prediction model were 0.728 and 0.109. The calibration plots showed fine agreement between observed and predicted probability of all-cause death. The decision curve analysis (DCA) showed that in a wide range of threshold probabilities, our prediction model had higher net benefits compared with the revised five factor score (rFFSand) and the birmingham vasculitis activity score (BVAS) system.

Conclusion: Our model performs well in predicting outcomes of AAV patients. Patients with moderate-to-high probability of death should be followed closely and personalized monitoring plan should be scheduled.

Our understanding of the pathogenesis of large vessel vasculitis (LVV) are mainly achieved by studying the arteries taken from temporal artery biopsy in giant cell arteries (GCA) or surgical or autopsy specimens in Takayasu arteritis (TAK). These artery specimens provide invaluable information about pathological changes in these conditions that GCA and TAK are similar but are distinctly different in immune cell infiltrate and distribution of inflammatory cells in anatomical locations. However, these specimens of established arteritis do not provide information of the arteritis initiation and early events which are impossible to obtain in human artery specimens. Animal models for LVV are needed but not available. Here, several approaches are proposed for experimentation to generate animal models to aid in delineating the interaction of immune reaction with arterial wall components.

Objectives: Topical administration of Tacrolimus (TAC) is efective in the treatment of psoriasis in human patients and in mouse models. Previously, we showed that, though promoting the proliferative expansion of CD4⁺Foxp3⁺ regulatory T cells (Tregs), TNFR2 was protective in mouse psoriasis model. We thus examined the role of TNFR2 signal in the efect of TAC in the treatment of mouse psoriasis.

Methods: To this end, psoriasis was induced in WT, or TNFR1 KO, or TNFR2 KO mice, and the psoriatic mice were treated with or without IMQ.

Results: The results showed that TAC treatment potently inhibited the development of psoriasis in WT and TNFR1 KO mice, but not in TNFR2 KO mice. However, the treatment of TAC failed to induce the expansion of Tregs in psoriatic mice. In addition to playing a decisive role in the activation of Tregs, TNFR2 stimulates the generation and activation of myeloid-derived suppressor cells (MDSCs). This led us to found that the topical treatment with TAC markedly increased the number of MDSCs in the spleen of WT and TNFR1 KO mice, but not in TNFR2 KO mice. Consequently, TAC potently decreased serum levels of IL-17A, INF-γ, and TNF and their mRNA levels in the inflamed skin lesion.

Conclusion: Therefore, our study for the first time found that the therapeutic efect of TAC in psoriasis is associated with the expansion of MDSCs in a TNFR2-dependent manner.

Social media broadly refers to an internet-based platform that allows for the online publication of content that is shared across a virtual community or network. Over recent years, there has been growing utilization of social media in the medical community. The field of rheumatology is no different. Social media allows for the sharing of information among rheumatologists, which can be useful in online education, disseminating research findings, forming new networks of collaborators, and discussing the latest advances in the field. However, there are several challenges facing clinicians using social media. As such, regulatory bodies have produced advisory codes of conduct to ensure better awareness concerning the appropriate use of social media among clinicians. In addition, clinicians (even those who do not use social media) need to be mindful of the fact that many patients will use these online platforms to find information, and with this comes the risk of false information. In this review, we highlight the benefits and challenges facing rheumatologists in relation to the world of social media.

The use of social media has heralded a new era of communication and social interaction, presenting important and often untapped potential and opportunity for professional organizations to thrive. In this article, we discuss the use of social media by rheumatology societies, focusing on strategy and marketing development. We share first-hand insights and tips for using social media in a way that can help rheumatology societies and professional organizations overall to thrive.