S. J. Jenkins

Mucins shed from the laminated layer in cystic echinococcosis are captured by Kupffer cells via the lectin receptor Clec4F

The paper shows that mucins from the laminated layer of E. granulosus are captured by Kupffer cells via Clec4F, highlighting a mechanism for host clearance of parasite-derived materials.

Hypoxia shapes the immune landscape in lung injury promoting inflammation persistence

This study shows hypoxia suppresses type I interferon signaling in ALI, leading to monocytopenia and unchecked inflammation, which can be mitigated by CSF1 administration.

Systemic influences of mammary cancer on monocytes in mice

This study shows that mammary cancer in mice increases circulating and splenic monocytes without altering their ratios or half-lives, but changes their transcriptome, particularly in the bone marrow and blood, with differences from human breast cancer.

Classical macrophage polarisation is limited by human β-defensin 3 via an autocrine IL-4 dependent process.

This paper shows HBD3 limits macrophage classical activation and promotes alternative activation via IL-4R, enabling a repair-conducive state.

The transcription factor EGR2 is indispensable for tissue-specific imprinting of alveolar macrophages in health and tissue repair

This study identifies EGR2 as essential for the identity and function of alveolar macrophages in health and tissue repair.

Recruited macrophages that colonise the post-inflammatory peritoneal niche convert into functionally divergent resident cells

This study shows inflammation-elicited macrophages in the peritoneal cavity can adopt a resident-like identity but are functionally divergent due to environmental influences and time of residency.

Macrophages can inhibit and enhance endometriosis depending on their origin

This study shows that macrophages in endometriosis lesions can either promote or suppress disease depending on their origin, with eutopic endometrial macrophages being pro-endometriosis and recruited monocyte-derived macrophages being anti-endometriosis.

Origin and microenvironment contribute to the sexually dimorphic phenotype and function of peritoneal macrophages.

This study shows that sex and age influence peritoneal macrophage behavior through bone marrow replenishment and microenvironment signals, affecting disease resistance.