Langerhans cells articles from across Nature Portfolio

Langerhans cells (LC) can prime tolerogenic as well as immunogenic responses in the skin. Here the authors show, by transcriptomic, epigenetic and CRISPR editing analyses, that during LC migration and maturation the transcription factor IRF4 regulates expression of antigen presentation and co-stimulatory gene modules while attenuating inflammatory response genes.

Langerhans cells (LC) and langerin-expressing conventional dendritic cells are made from distinct progenitors and enriched in the distinct microenvironments of the skin. Here the authors show that these immune cells are regulated by retinoic acid receptor alpha (RARα) via simultaneous induction of LC-promoting Runx3 and repression of LC-inhibiting C/EBPβ.

Kaplan reviews the development of skin-resident Langerhans cells and their unique functional roles that distinguish these cells from other skin antigen-presenting cells.

Imiquimod exacerbates IL-23-induced skin inflammation and models psoriasis in mice. Here the authors show that this pathology is not dependent on resident dendritic cells, but on CCR6-induced immigration of monocyte-derived cells.

Florent Ginhoux reflects on a 2002 paper by Merad and colleagues that challenged the dogma that adult Langerhans cells arise from blood-circulating precursors.

CD1a on Langerhans cells in the epidermis is the lipid receptor for the plant-derived allergen urushiol and self lipids and is a key amplifier of inflammatory responses in urushiol-induced contact dermatitis as well as in psoriasis.

Paradoxically, radiotherapy can reinforce immunosuppressive pathways that undermine anticancer immunosurveillance and treatment efficacy. Irradiation induces Langerhans cells to migrate from the skin to lymph nodes, where they stimulate regulatory T cells.

LL-37 produced by HSV-2-infected keratinocytes increases the susceptibility of neighbouring Langerhans cells to HIV infection.

Most myeloid cells express the growth-factor receptor CSF1R. Recognition of interleukin 34 by CSF1R is required for the development of tissue-resident Langerhans cells and microglia, which explains the independence of their growth from CSF1.