Publications by authors named "Heather C West"

Article Synopsis
  • T cell pathology in the skin causes an influx of monocytes, but we lack knowledge about how these recruited cells behave over time and affect immune balance in the skin.
  • Research combining a mouse model of acute graft-versus-host disease (aGVHD) and patient samples reveals that disease leads to the differentiation of macrophages specifically in the skin's dermis and results in a dominance of these macrophages, reducing the presence of resting MHCII cells.
  • After the disease resolves, exposing the altered skin to certain substances can cause overactivation of regulatory T cells (Tregs), leading to a loss of immune tolerance and an enduring impact on immune regulation, referred to as an "immunological scar."
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A dense population of embryo-derived Langerhans cells (eLCs) is maintained within the sealed epidermis without contribution from circulating cells. When this network is perturbed by transient exposure to ultraviolet light, short-term LCs are temporarily reconstituted from an initial wave of monocytes but thought to be superseded by more permanent repopulation with undefined LC precursors. However, the extent to which this process is relevant to immunopathological processes that damage LC population integrity is not known.

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Langerhans cells (LC) are a unique population of tissue-resident macrophages that form a network of cells across the epidermis of the skin, but which have the ability to migrate from the epidermis to draining lymph nodes (LN). Their location at the skin barrier suggests a key role as immune sentinels. However, despite decades of research, the role of LC in skin immunity is unclear; ablation of LC results in neither fatal susceptibility to skin infection nor overt autoimmunity due to lack of immune regulation.

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