Back

T cell-intrinsic lymphoproliferation as a key driver of intestinal autoimmunity in acquired generalized lipodystrophy

Letizia, M.; Omar, T.; Weidner, P.; Jakob, M. O.; Freise, I.; Krug, S. M.; Löscher, B.-S.; Rosati, E.; Obermayer, B.; Gamez-Belmonte, M. d. l. R.; Hecker, J.; Ziegler, J.-F.; Weixler, B.; Asbach, P.; Kunkel, D.; Stumvoll, M.; Miehle, K.; Becker, C.; Klose, C. S. N.; Glauben, R.; Beule, D.; Kühl, A.; Franke, A.; Sanders, A.; Siegmund, B.; Weidinger, C.

2025-02-24 endocrinology
10.1101/2025.02.19.25322160 medRxiv
Show abstract

Acquired generalized lipodystrophy (AGL) is a rare metabolic disorder frequently associated with autoimmunity. Its etiology is incompletely understood and the impact of adipose tissue loss on autoimmunity and intestinal inflammation in AGL remains unclear. Using mass cytometry and single-cell RNA sequencing, we observed an oligoclonal expansion of T cells in the periphery and inflamed intestine in a patient with AGL and Crohns disease (AGLCD). To explore if loss of adipose tissue triggers lymphoproliferation, we studied lipodystrophic mice as a model for AGL. Unexpectedly, lipodystrophic mice did not show T-cell expansion, were protected from colitis and displayed a defect in the development of pro-inflammatory T cells, which could be reversed by allogeneic fat transplantations, indicating that clonal T-cell expansion is not primarily caused by lipodystrophy. Instead, gene sequencing revealed a T cell-intrinsic de-novo NRAS mutation, pointing towards somatic mosaicism as a driver of clonal T-cell expansion and systemic autoimmunity in AGLCD.

Matching journals

The top 6 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.