Systemic lupus erythematosus (SLE) disproportionately affects those with low socioeconomic status. Evidence from the past 2 decades has revealed clearer distinctions on the mechanisms of poverty that affect long-term outcomes in SLE. Poverty exacerbates direct, indirect, and humanistic costs and is associated with worse SLE disease damage, greater mortality, and poorer quality of life. Ongoing commitments from medicine and society are required to reduce disparities, improve access to care, and bolster resilience in persons with SLE who live in poverty.Assessment of quality of care for people with systemic lupus erythematosus (SLE) provides opportunities to identify gaps in health care and address disparities. Poor access to specialty care has been shown to negatively impact care in SLE and is associated with poor disease outcomes. Racial/ethnic minorities and those with low socioeconomic status are at higher risk for poor access and lower quality of care. Quality measures evaluating processes of care have shown significant deficiencies in care of SLE patients across studies. High SLE patient volume correlates with better quality of care for providers in hospital and ambulatory settings.Limitations in the ability to assemble large cohorts of patients with lupus from previously underrepresented groups have inhibited better understanding of many unanswered questions. The Georgians Organized Against Lupus (GOAL) Research Cohort is designed to overcome many of these limitations and is a rich and diverse repository of clinical, biological, sociodemographic, psychosocial, and health services data, and biologic material. Studies with the GOAL cohort will improve the understanding of how various factors interact and may lead to interventions on an individual and systems and societal level and help to mitigate the significant disparities that continue to exist in lupus.According to critical race theory (CRT), racism is ubiquitous in society. In the field of medicine, systems of racism are subtly interwoven with patient care, medical education, and medical research. https://www.selleckchem.com/products/rcm-1.html Public health critical race praxis (PHCRP) is a tool that allows researchers to apply CRT to research. This article discusses the application of CRT and PHCRP to 3 race-related misconceptions in rheumatology (1) giant cell arteritis is rare in non-White populations; (2) Black patients are less likely to undergo knee replacement because of patient preference; and (3) HLA-B*5801 screening should only be performed for patients of Asian descent.Class switch recombination (CSR) plays an important role in humoral immunity by generating antibodies with different effector functions. CSR to a particular antibody isotype is induced by external stimuli, and occurs between highly repetitive switch (S) sequences. CSR requires transcription across S regions, which generates long non-coding RNAs and secondary structures that promote accessibility of S sequences to activation-induced cytidine deaminase (AID). AID initiates DNA double-strand breaks (DSBs) intermediates that are repaired by general DNA repair pathways. Switch transcription is controlled by various regulatory elements, including enhancers and insulators. The current paradigm posits that transcriptional control of CSR involves long-range chromatin interactions between regulatory elements and chromatin loops-stabilizing factors, which promote alignment of partner S regions in a CSR centre (CSRC) and initiation of CSR. In this review, we focus on the role of IgH transcriptional control elements in CSR and the chromatin-based mechanisms underlying this control.Natural killer (NK) cells are innate immune cells critically involved in the control of cancer. Their important role in cancer immunity reflects the ability of NK cells to recognize malignant cells through an array of germline-encoded receptors expressed on their surface, enabling NK cells to detect and rapidly kill tumor cells through targeted cytotoxicity. In addition to their cytotoxic activity, NK cells fulfill a fundamental and often underappreciated role in the local orchestration of cancer immunity through their ability to communicate with innate and adaptive immune cells within the tumor microenvironment (TME), which is achieved through the secretion of multiple chemokines, cytokines, and growth factors. Within tumor tissue, NK cells regulate the recruitment, survival and functional activity of various immune cells including monocytes, granulocytes, dendritic cells and T cells, thereby shaping intratumoral immune cell composition and functionality. Emerging evidence further suggest a role of NK cells in the regulation of stromal cells within the TME. Here, we discuss key aspects of NK cell communication with other intratumoral cell types and its role for cancer immunity. Strategies aimed at boosting anti-cancer immunity by enhancing NK cell communication and functionality within tumor tissue provide attractive new ways for treatment of cancer patients.Reversible lysine acetylation of histones is a key epigenetic regulatory process controlling gene expression. Reversible histone acetylation is mediated by two opposing enzyme families histone acetyltransferases (HATs) and histone deacetylases (HDACs). Moreover, many non-histone targets of HATs and HDACs are known, suggesting a crucial role for lysine acetylation as a posttranslational modification on the cellular proteome and protein function far beyond chromatin-mediated gene regulation. The HDAC family consists of 18 members and pan-HDAC inhibitors (HDACi) are clinically used for the treatment of certain types of cancer. HDACi or individual HDAC member-deficient (cell lineage-specific) mice have also been tested in a large number of preclinical mouse models for several autoimmune and autoinflammatory diseases and in most cases HDACi treatment results in an attenuation of clinical disease severity. A reduction of disease severity has also been observed in mice lacking certain HDAC members. This indicates a high therapeutic potential of isoform-selective HDACi for immune-mediated diseases. Isoform-selective HDACi and thus targeted inactivation of HDAC isoforms might also overcome the adverse effects of current clinically approved pan-HDACi. This review provides a brief overview about the fundamental function of HDACs as epigenetic regulators, highlights the roles of HDACs beyond chromatin-mediated control of gene expression and summarizes the studies showing the impact of HDAC inhibitors and genetic deficiencies of HDAC members for the outcome of autoimmune and autoinflammatory diseases with a focus on rheumatoid arthritis, inflammatory bowel disease and experimental autoimmune encephalomyelitis (EAE) as an animal model of multiple sclerosis.