Who Is Caring for Health Care Workers' Families Amid COVID-19?

Amid the COVID-19 pandemic, women in medicine, including faculty, residents, medical students, and other health care workers (HCWs), are facing unparalleled challenges. The burdens of pandemic-associated increases in domestic and caregiving responsibilities, professional demands, health risks associated with contracting COVID-19, and the resulting psychosocial distress have exacerbated existing gender disparities at home, at work, and in academia. School and day care closures have created additional childcare needs, primarily for women, yet little support exists for parents and families. These increased childcare and domestic responsibilities have forced women HCWs, who make up the overwhelming majority of the workforce, to adapt their schedules and, in some cases, leave their jobs entirely. In this article, the authors detail how COVID-19 has exacerbated existing childcare accessibility and affordability issues as well as gender disparities. They argue that unless government and health care organization support for childcare increases, families, specifically women and children, will continue to suffer. Lack of access to affordable childcare can prevent HCWs from doing their jobs, including conducting and publishing academic scholarship. This poses incalculable risks to families, science, and society. COVID-19 should serve as a call to action to all sectors, including the government and health care organizations, to prioritize childcare provision and increase support for women HCWs, both now during the pandemic and going forward.

Adenosine 2a Receptor Signal Blockade of Murine Autoimmune Arthritis via Inhibition of Pathogenic Germinal Center-Follicular Helper T Cells.

OBJECTIVE: CD4 germinal center (GC)-follicular helper T (Tfh) cells are important in the pathogenesis of autoimmune arthritis. Previous studies have shown that adenosine 2a receptor (A2aR; Adora2a) signaling can divert CD4 T cells away from the GC-Tfh cell lineage during the primary response to foreign antigens. This study was undertaken to examine the effects of A2aR signaling on CD4 T cells during the recognition of self antigen in a murine model of autoimmune arthritis. METHODS: Wild-type and Adora2a-deficient mouse KRN T cell receptor-transgenic CD4 T cells specific for glucose-6-phosphate isomerase (GPI)/I-Ag7 were transferred into immunodeficient Tcra-/- I-Ag7 -expressing mice to induce arthritis. Recipients were then treated with either the selective A2aR agonist CGS-21680 (CGS) or phosphate buffered saline alone. Severity of disease, autoantibody titers, KRN T cell numbers and phenotype, and GPI-specific isotype class-switched plasmablasts were tracked. RESULTS: CGS treatment inhibited the development of arthritis and differentiation of KRN GC-Tfh cells, blocked the appearance of high-affinity GPI-specific and IgG1 isotype class-switched polyclonal plasmablasts, and led to a reduction in serum titers of anti-GPI IgG1. In addition, therapeutic administration of CGS after the onset of arthritis blocked further disease progression in association with reductions in the number of KRN GC-Tfh cells and anti-GPI IgG1 serum titers. CONCLUSION: Strong A2aR signaling diverts autoreactive CD4 T cell differentiation away from the GC-Tfh cell lineage, thus reducing help for the differentiation of dangerous autoreactive B cells that promote arthritis. These data in a mouse model of autoimmune arthritis suggest that A2aR and its downstream signaling pathways in CD4 T cells may be promising therapeutic targets for interfering with potentially dangerous autoreactive GC-Tfh cell differentiation.