Author

J. Ruland

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· 2 Cancer Biology· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Assay:bulk RNA-seq· 2 Research Focus:host-pathogen & immune response· 2 Organism:mouse· 2 Research Focus:cancer & tumor microenvironment· 1 Research Focus:cell signaling & trafficking· 1 Research Focus:cell type annotation· 1 Assay:flow cytometry· 1

Frequent Co-Authors

A. Al Jawazneh· 1 shared A. Buck· 1 shared A. Goerlach· 1 shared A. Petry· 1 shared A. Schlitzer· 1 shared A. Sipol· 1 shared B. Blissenbach· 1 shared B. Xue· 1 shared

Activity by Year

2020-2022 · peak 2/yr

Co-Author Collaboration Network

10 top collaborators · 14 mutual co-author links

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1 shared paperImmunology

A. Al Jawazneh

Mutual co-authors in cluster

Author profile →

3 papers

Recent·Most cited

Apolipoprotein E controls Dectin-1-dependent development of monocyte-derived alveolar macrophages upon pulmonary β-glucan-induced inflammatory adaptation

H. Theobald, D. Bejarano, N. Katzmarski, J. Haub, J. Schulte-Schrepping, J. Yu, K. Bassler, C. Osei-Sarpong, F. Piattini, L. Vornholz, X. Xu, S. Sheoran, A. Al Jawazneh, S. Chakarov, K. Haendler, , A. Schlitzer

This study identifies Apolipoprotein E's role in Dectin-1-dependent development of monocyte-derived alveolar macrophages during pulmonary β-glucan-induced inflammation.

bioRxiv · Sep 15, 2022Immunology

B/T cell crosstalk and aberrant inflammatory IgG exacerbate autoimmune intestinal inflammation

I. Gadjalova, J. M. Heinze, M. C. Goess, J. Hofmann, J. J. Albers, R. Spallek, B. Blissenbach, A. Buck, M.-C. Weber, E. Scherer, M. Kampick, R. Oellinger, O. Krut, R. Rad, K. Steiger, , S. J. Keppler

This study identifies B cell-driven inflammatory mechanisms, including aberrant IgG production and CD86-mediated T cell activation, as contributors to exacerbated intestinal inflammation in IBD.

bioRxiv · Sep 12, 2022 · PreprintImmunology

MondoA Drives Malignancy in cALL through Enhanced Adaptation to Metabolic Stress

A. Sipol, E. Hameister, B. Xue, A. Petry, C. Prexler, M. Barenboim, R. A. Rubio, M. C. Baldauf, D. G. Franchina, J. Schmaeh, G. Richter, G. Cario, T. G. P. Gruenewald, A. Goerlach, D. Brenner, , S. E. G. Burdach

This study shows MondoA promotes malignancy in pediatric cALL by enhancing metabolic stress adaptation, with potential therapeutic implications.

bioRxiv · Nov 1, 2020Cancer Biology