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Our immune system is an invaluable ally, protecting us from viruses and other foreign invaders that would do us harm. But sometimes this powerful defensive armoury turns against healthy tissues. Now, researchers are finding ways to bring the immune system back on side.
The COVID-19 pandemic led to unprecedented changes in rheumatology clinical practice. In this Viewpoint article, we asked five experts to describe their experiences of the COVID-19 pandemic, how their clinical practice has changed, and the opportunities and challenges that lie ahead.
In this Review, the authors discuss the roles of B cells in multiple sclerosis and consider the insights gained from the immunological effects of B cell-targeted therapies and autologous haematopoietic stem cell transplantation as well as the potential for these insights to improve our understanding.
This Review highlights the research advances, advantages and challenges in several different strategies for generating functional β-cells for therapeutic use in diabetes mellitus. In addition, scalable bioengineering processes are also discussed for the realization of the therapeutic potential of derived β-cells.
Therapies based on adoptive cellular transfer of regulatory T (Treg) cells are currently undergoing clinical trials for autoimmune diseases, graft-versus-host disease and the prevention of transplant rejection. This Review provides an overview of Treg cell biology and discusses the latest approaches to enhance Treg cells for therapeutic purposes.
This Review outlines several genetic and epigenetic mechanisms that could explain sex bias in rheumatic diseases, including X chromosome inactivation, sex chromosome aneuploidy and microchimerism, considering evidence from clinical and experimental studies.
Germ-free mice co-colonized with two bacterial strains from the small intestinal flora showed increased susceptibility to experimental autoimmune encephalomyelitis, implicating the synergistic effects of these microorganisms in this mouse model of multiple sclerosis.
An HLA- and gluten-dependent mouse model of coeliac disease with villous atrophy provides evidence for the cooperative role of IL-15 and gluten-specific CD4+ T cells in licensing the full activation of cytotoxic T cells that are necessary for inducing epithelial damage.