AG Dr. C. Schwartz

Obesity-associated inflammation and Type 2 immune responses

The AG Schwartz at the Institute of Clinical Microbiology, Immunology and Hygiene investigates how obesity shapes immune responses at barrier tissues. Our research focuses on understanding the mechanisms through which metabolic dysfunction influences Type 2 immunity during allergic inflammation, parasitic infections, and tissue homeostasis.

Obesity has become a major public health challenge, affecting more than half of adults in Germany and one in six children. Beyond its well-known association with cardiovascular disease and type 2 diabetes, obesity profoundly impacts immune function and barrier tissue integrity, contributing to:

• Development and exacerbation of allergic diseases, particularly atopic dermatitis

• Impaired wound healing and tissue regeneration

• Increased susceptibility to bacterial infections

• Altered asthma pathogenesis

Our research integrates three interconnected areas:

1. Innate regulation of T cell responses

Innate immune cells - including dendritic cells, macrophages, and innate lymphoid cells (ILCs) - orchestrate adaptive immunity by providing critical signals to T cells. We investigate how costimulatory molecules, particularly the immune checkpoint protein PD-L1 (CD274), regulate T helper cell responses in different inflammatory contexts. Our work has revealed context-dependent functions of PD-L1: during infection with the helminth Nippostrongylus brasiliensis, PD-L1 on pulmonary ILC2s promotes Th2 responses and parasite expulsion (Schwartz, 2017). In contrast, in obesity, PD-L1 expression on dendritic cells limits Th1-biased adipose tissue inflammation and ameliorates diet-induced weight gain and metabolic syndrome (Schwartz, 2022). These findings establish PD-L1 as a critical checkpoint regulating immune homeostasis in metabolic disease and have implications for immune-related adverse events during checkpoint inhibitor therapy.

2. Skin barrier dysfunction in obesity

We recently demonstrated that obesity impairs skin barrier function and facilitates allergic sensitization (Martinek, 2025). Diet-induced obesity compromises barrier integrity through downregulation of tight junctions and desmosomes, leading to increased transepidermal water loss and enhanced allergen penetration. This work establishes obesity-induced barrier dysfunction as a targetable mechanism in allergic skin disease.

3. Microbiome-immune interactions in obesity

The microbiota plays a crucial role in immune education and barrier tissue homeostasis (Schwartz, 2019). We investigate how the composition of microbial communities and their metabolites regulate costimulatory molecule expression on innate cells, thereby influencing local and systemic immune responses. This work connects metabolic changes in obesity to altered microbiome-immune crosstalk.

Translational approach:

Our research combines mechanistic studies in preclinical mouse models with analysis of human patient samples, aiming to identify therapeutic targets for obesity-associated inflammatory diseases. We employ advanced techniques including single-cell RNA sequencing, spectral flow cytometry, metabolic profiling, and in vivo models of obesity, infections and allergic