Author

L. Arike

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Immunology· 1 Microbiology· 1 Physiology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Research Focus:host-pathogen & immune response· 2 Organism:mouse· 2 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Research Focus:development & morphogenesis· 1 Organism:human· 1 Assay:proteomics· 1

Frequent Co-Authors

T. Pelaseyed· 3 shared B. Dolan· 2 shared E. Layunta· 2 shared A. Johansson· 1 shared A. Rajan· 1 shared A. S. Luis· 1 shared A. Wullaert· 1 shared B. A. Vallance· 1 shared

Activity by Year

2024-2024 · peak 3/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

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3 shared papersImmunology

T. Pelaseyed

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Neonatal microbiota colonization drives maturation of primary and secondary goblet cell mediated protection in the pre-weaning colon

A. Johansson, M. Venkita Subramani, B. Yilmaz, E. Nystrom, E. Layunta, L. Arike, F. Sommer, P. Rosenstiel, L. Vereecke, L. Manneras Holm, A. Wullaert, T. Pelaseyed, M. E. V. Johansson, G. M. H. Birchenough

This study shows that neonatal microbiota colonization sequentially programs primary and secondary goblet cell functions in the colon, with MyD88 and Duox2 playing key roles in mucus barrier and sentinel cell development.

bioRxiv · Jul 3, 2024 · PreprintImmunology

BPP43_05035 is a Brachyspira pilosicoli cell surface adhesin that weakens the integrity of the epithelial barrier during infection

A. Rajan, P. Gallego, B. Dolan, P. Patel, C. Dwibedi, A. S. Luis, S. Trillo-Muyo, L. Arike, S. van der Post, M. Simren, T. Pelaseyed

This study identifies BPP43_05035 as a Brachyspira pilosicoli adhesin that disrupts epithelial tight junctions, increasing barrier permeability during infection.

bioRxiv · Apr 6, 2024 · PreprintMicrobiology

MUC17 is an essential small intestinal glycocalyx component that is disrupted in Crohn's disease

E. Layunta, S. Javerfelt, F. C. van de Koolwijk, M. Sivertsson, B. Dolan, L. Arike, S. Thulin, B. A. Vallance, T. Pelaseyed

The paper identifies MUC17 as a critical component of the small intestinal glycocalyx that is disrupted in Crohn's disease, leading to bacterial contact and epithelial defects.

bioRxiv · Feb 8, 2024Physiology