Grounded in intersubjective participatory action research, the people and dancefloors project has sought to produce a space for the co-creation of knowledge about dancefloors and drug taking, building a platform for developing insights from the positionality of current drug users. Through film, it provides hermeneutic insight while legitimising their voices. In this paper, we share some reflections as researchers/users/activists arising from our involvement in the project. To begin with, we reflect on the motivations for the project, and the epistemic suppositions that animated it. This is followed by conversational style interviews where we re-evaluate our position in light of the project, with a particular focus on the tensions that drug use introduces between professional, personal and political domains in our lives. These reflections are useful to people who use drugs and hold privilege by nature of their social and cultural position. While questioning the silencing of personal experiences in relation to drug use, we also react to some of the traditional tendencies of academia, including institutionalised individualism, which isolates researchers and discourages them from finding political collectivity, and the subjectivist/objectivist dichotomy, which supports a tendency to objectify research participants while removing the self from the equation. Despite the challenges that arise from disentangling our multiple experiences and identities, our intersubjective dialogue inspires deeper learning about ourselves and each other, encouraging us towards a more openly political stance.Th9 cells are a defined CD4+ helper T cell subgroup found to promote or suppress oncogenesis in a context-dependent manner. How microRNAs (miRNAs) shape Th9 cell functionality, however, remains to be studied. Herein, we determined that miR-143/145 is downregulated during Th9 differentiation. When these miRNAs were upregulated, this inhibited Th9 differentiation, proliferation, and IL-9 production. this website Overexpressing miR-143/145 in Th9 cells further suppressed NFATc1 expression at the protein and mRNA level, whereas the opposite phenotype was observed when miR-143/145 was downregulated in these cells. NFATc1 silencing markedly inhibited Th9 cell differentiation, whereas overexpressing this transcription factor was sufficient to reverse miR-143/145-associated phenotypes in these cells. These findings thus indicate that the ability of miR-143/145 to inhibit Th9 cell differentiation is attributable to their ability to target and suppress NFATc1 expression. Overall, our results highlight a novel mode of action whereby miR-143/145 controls Th9 differentiation, suggesting that this pathway may be amenable to therapeutic targeting in the context of anti-cancer treatment in the future.
Networks formed of numerous autoantibodies (aabs) directed against G-protein coupled receptors (GPCR) have been suggested to play important role in autoimmune disorders. In present study, we aimed to evaluate the association between anti-GPCR antibodies and primary Sjogren's syndrome (pSS) to determine the potential pathogenic factors.

By applying a cell membrane-based ELISA technique, which is capable of detecting aabs against conformational epitopes within GPCR, serum levels of fourteen GPCR were determined in well-characterized patients with pSS (n = 52) and gender-matched healthy controls (n = 54). Comparisons between groups were analyzed by two-tailed Mann-Whitney U test, Bonferroni correction was applied for multiple comparisons. Spearman`s rank correlation coefficients were calculated between variables and visualized by heat map.

Compared to healthy subjects, sera of patients with pSS showed significantly higher binding to β2AR and ETAR, but lower binding to C5aR1, C3aR1, CXCR3, and CXCR4. Autoantibodies against C5aR1, C3aR1, CXCR3, and CXCR4 were also decreased in patients with rheumatoid arthritis. In pSS patients, levels of anti-CXCR3 and anti-CXCR4 antibodies were negatively correlated with circulating lymphocyte counts. Furthermore, correlation signatures of anti-GPCR antibodies changed dramatically in the patients with pulmonary involvement.

This study demonstrates an association between pSS and autoantibodies recognizing GPCR, especially those functionally involved in immune cell migration and exocrine glandular secretion.
This study demonstrates an association between pSS and autoantibodies recognizing GPCR, especially those functionally involved in immune cell migration and exocrine glandular secretion.Emerging evidence has indicated that long noncoding RNAs (lncRNAs) are involved in various pathophysiological processes of disease, such as cancer occurrence, viral invasion, and inflammatory damage. The main inflammatory body component, nod-like receptor protein 3 (NLRP3), is the trigger point of inflammatory reactions and inflammation-related diseases and coordinates the body's response to inflammation. At present, increasing evidence shows that the interaction of lncRNAs and the NLRP3 inflammasome plays an important role in the inflammatory response and different diseases. This may be involved in the development and progression of various diseases by activating signalling pathways and a variety of molecular regulatory mechanisms-this article reviews progress in research on the relationship between lncRNAs and the NLRP3 inflammasome under different conditions.
Peripheral helper T (TPH) cells, a recently defined subset of Th cells, promote B cell differentiation and antibody production in inflamed tissues. This study investigated whether circulating TPH cells are associated with primary biliary cholangitis (PBC), a typical organ-specific autoimmune disease.

Twenty PBC patients and 20 age- and sex-matched healthy controls (HCs) were recruited. The circulating TPH cell subsets were analyzed by flow cytometry, and the associations of TPH cells with disease activity and plasma cells were determined. Functional analysis was performed using a TPH and B cell coculture experiment.

The frequencies of circulating TPH cells, ICOS
TPH cells, and CD28
TPH cells were increased in patients with PBC. Furthermore, the ICOS
TPH cell level was higher in PBC patients with or without cirrhosis than in HCs, and the level decreased after treatment. Moreover, ICOS
TPH cell levels correlated positively with specific clinical parameters (including anti-mitochondrial antibodies against M2 antigen (AMA-M2), IgM) and plasma cell levels, suggesting that the TPH cell activation status is associated with the severity of PBC.this website