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Sepsis — which is caused by a dysregulated host response to infection — is a life-threatening organ dysfunction. This Review describes the recent advances in our understanding of sepsis pathogenesis and discusses strategies for the development of successful therapies.
In this Review, the authors propose that disease-associated genetic variants modulate signalling downstream of B cell receptors, Toll-like receptors and cytokine receptors in B cells to drive autoimmune responses. This altered signalling favours a naive B cell repertoire that is skewed towards self-reactivity and promotes the peripheral activation of autoreactive B cell clones.
The transcriptional repressors BTB and CNC homology 1 (BACH1) and BACH2 compete with transcriptional activators of the basic region leucine zipper (bZIP) family to control widespread functions of the innate and adaptive immune systems.
In this Opinion article, the authors discuss the limitations of categorizing tissue-resident macrophages based on their ontogeny. Instead, they propose that competition for a limited number of tissue niches may serve as a better framework for understanding the origins and functions of tissue macrophages.