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Deinzer, A.

Publications and source records attributed to Deinzer, A..

2 recordsLinked to original sources
bioRxiv2026

Preserved Type 2 Immune Cell Plasticity in Human Obesity and Differential Immune Reconstitution After Bariatric Surgery

BackgroundObesity disrupts type 2 immune cell populations in white adipose tissue, replacing the homeostatic network of group 2 innate lymphoid cells (ILC2s), eosinophils, T helper 2 (Th2) cells, and alternatively activated macrophages (AAMs) with pro-inflammatory type 1 populations. Whether this remodelling reflects permanent immune impairment or a reversible shift in cellular equilibrium, and to what extent bariatric surgery restores type 2 immunity, remain incompletely understood. MethodsWe performed comprehensive immunophenotyping of visceral white adipose tissue (WAT) and peripheral blood from persons with severe obesity (people with obesity, PWO) scheduled for or having undergone bariatric surgery (sleeve gastrectomy, gastric bypass), combined with lean controls. Using flow cytometry, quantitative PCR, and in vitro polarization assays, we assessed immune cell frequencies, transcription factor expression, cytokine profiles, and functional polarization capacity across lean, pre-operative, and post-operative states. ResultsObesity was associated with decreased eosinophil and CD8+ T cells frequencies in WAT, accompanied by an increase in CD4+ frequency and a shift from Th2 toward Th1 predominance, as well as elevated PD-1 expression on T cell subsets. Bariatric surgery partially normalised peripheral immune cell composition, reducing CD8+ T cell frequencies while increasing CD4+ T cells. Macrophage polarization capacity, dampened in pre-operative PWO, recovered after surgery. Conversely, Th2 polarization capacity and IL-13 production were reduced in post-operative T cells despite preserved function pre-operatively, indicating divergent trajectories of innate and adaptive immune reconstitution. ConclusionType 2 immune cells retain functional plasticity in human obesity despite reduced frequency. Bariatric surgery differentially reconstitutes immune function, restoring macrophage plasticity while paradoxically reducing Th2 polarization capacity, arguing against uniform immune normalisation after weight loss. FundingGerman Federal Ministry of Research, Technology and Space (BMFTR, FKZ 01KI2109), Interdisciplinary Center for Clinical Research (IZKF, Faculty of Medicine, Friedrich-Alexander Universitat (FAU) Erlangen-Nurnberg).

immunology↗
bioRxiv2026

Obesity selectively disrupts long-lasting type 2 immune cell depots in white adipose tissue

White adipose tissue (WAT) has emerged as a tissue-resident niche for immunological memory, but whether this depot function extends to type 2 immune memory and how it is modulated by metabolic disease remains incompletely understood. Here, we show that Nippostrongylus brasiliensis infection, in which the parasite transits and damages the lung, establishes a long-lasting immune cell depot in distal abdominal WAT comprising eosinophils, group 2 innate lymphoid cells (ILC2s), and memory T cells that persists after parasite clearance. Intranasal papain administration recapitulates this depot phenotype, demonstrating that depot formation is a general feature of pulmonary type 2 inflammation rather than a response restricted to live infection. Adoptive transfer of OT-II T cells together with ovalbumin-coated N. brasiliensis larvae confirms that WAT accumulates bona fide antigen-experienced T cells. Diet-induced obesity selectively disrupts depot establishment, while leaving acute lung-stage immune cell recruitment, parasite clearance, and the intrinsic competence of cells that do accumulate largely intact. Despite preserved early lung recruitment, obese mice show exacerbated peri-alveolar tissue damage, consistent with an uncoupling of immune cell infiltration from productive type 2-dependent wound repair. Together, these findings establish WAT as a broadly competent type 2 immunological memory niche, identify obesity as a selective disruptor of depot formation rather than effector function, and provide a cellular framework for the impaired vaccine and infection responses associated with obesity.

immunology↗