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frontiersin.org

Learn more about how Frontiers' open access agreements can benefit your institution by reading our frequently asked questions.

cell.com

publisher of over 50 scientific journals across the life, physical, earth, and health sciences, both independently and in partnership with scientific societies including cell, neuron, immunity, current biology, ajhg, and the trends journals.

biorxiv.org

biorxiv - the preprint server for biology, operated by cold spring harbor laboratory, a research and educational institution

europepmc.org

europe pmc is an archive of life sciences journal literature.

nature.com

Nature is the foremost international weekly scientific journal in the world and is the flagship journal for Nature Portfolio. It publishes the finest ...

scilit.com

Scilit is a comprehensive content aggregator platform for scholarly publications. It is developed and maintained by the open access publisher MDPI AG.

scienceopen.com

Background Human lung mast cells (HLMCs) infiltrate the airway epithelium and airway smooth muscle (ASM) in asthmatic airways. The mechanism of HLMC adhesion to both cell types is only partly defined, and adhesion is not inhibited by function-blocking anti-Kit and anti-stem cell factor (SCF) antibodies. Our aim was to identify adhesion molecules expressed by human mast cells that mediate adhesion to human ASM cells (HASMCs) and human airway epithelial cells. Methods We used phage-display to isolate single chain Fv (scFv) antibodies with adhesion-blocking properties from rabbits immunised with HLMC and HMC-1 membrane proteins. Results Post-immune rabbit serum labelled HLMCs in flow cytometry and inhibited their adhesion to human BEAS-2B epithelial cells. Mast cell-specific scFvs were identified which labelled mast cells but not Jurkat cells by flow cytometry. Of these, one scFv (A1) consistently inhibited mast cell adhesion to HASMCs and BEAS-2B epithelial cells by about 30 %. A1 immunoprecipitated Kit (CD117) from HMC-1 lysates and bound to a human Kit-expressing mouse mast cell line, but did not interfere with SCF-dependent Kit signalling. Conclusion Kit contributes to human mast cell adhesion to human airway epithelial cells and HASMCs, but may utilise a previously unidentified adhesion domain that lies outside the SCF binding site. Targeting this adhesion pathway might offer a novel approach for the inhibition of mast cell interactions with structural airway cells, without detrimental effects on Kit signalling in other tissues.

cabidigitallibrary.org

cabi digital library - research and learning in agriculture, the environment and the applied life sciences

elifesciences.org

eLife reviews research in areas including cell migration, proliferation and differentiation, and inductive and signaling interactions. Learn more about what we review and sign up for the latest research.