Publications by authors named "B L Kelsall"

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiological agent of the coronavirus disease 2019 (COVID-19) pandemic, remains endemic worldwide ~5 years since the first documented case. Severe COVID-19 is widely considered to be caused by a dysregulated immune response to SARS-CoV-2 within the respiratory tract. Circulating levels of the chemokine CXCL10 are strongly positively associated with poor outcome; however, its precise role in pathogenesis and its suitability as a therapeutic target have remained undefined.

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Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the etiological agent of the coronavirus disease 2019 (COVID-19) pandemic, remains endemic worldwide. Circulating levels of the chemokine CXCL10 are strongly positively associated with poor outcome; however, its precise role in SARS-CoV-2 pathogenesis and its suitability as a therapeutic target have remained undefined. Here, we challenged mice genetically deficient in Cxcl10 with a mouse-adapted strain of SARS-CoV-2.

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Introduction: TAM receptor-mediated efferocytosis plays an important function in immune regulation and may contribute to antigen tolerance in the lungs, a site with continuous cellular turnover and generation of apoptotic cells. Some studies have identified failures in efferocytosis as a common driver of inflammation and tissue destruction in lung diseases. Our study is the first to characterize the function of the TAM receptors, Axl and MerTk, in the innate immune cell compartment, cytokine and chemokine production, as well as the alveolar macrophage (AM) phenotype in different settings in the airways and lung parenchyma.

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Tissue-resident macrophages are critical for tissue homeostasis and repair. We previously showed that dermis-resident macrophages produce CCL24 which mediates their interaction with IL-4 eosinophils, required to maintain their M2-like properties in the T1 environment of the Leishmania major infected skin. Here, we show that thymic stromal lymphopoietin (TSLP) and IL-5 type 2 innate lymphoid cells are also required to maintain dermis-resident macrophages and promote infection.

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Article Synopsis
  • Tissue-resident macrophages (TRMs) are essential for maintaining skin health and repair, interacting with eosinophils through CCL24 to sustain their numbers and functions in infected skin.
  • The study reveals that TRMs also produce TSLP, a signaling molecule that further supports their own maintenance and promotes infection by working with innate lymphoid cells (ILC2s).
  • Single-cell RNA sequencing shows that TRMs are the only source of both TSLP and CCL24, and removing TSLP from TRMs leads to a decrease in their numbers and improvement in disease outcomes, highlighting their role in a type 2 immune response.
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