Rheumatologie und Klinische Immunologie

The Innate Immune System in Large Vessel Vasculitis and Inflammatory Rheumatic Diseases 

Inflammatory rheumatic diseases encompass a heterogeneous group of disorders characterized by dysregulated immune responses, ultimately leading to tissue damage and organ dysfunction. The innate immune system, comprising cells such as monocytes, macrophages, dendritic cells, and neutrophils, represents the body’s first line of immunological defense and is characterized by its rapid responsiveness, potent cytokine production, and its capacity to drive tissue inflammation and destruction, thereby playing a central role in disease initiation, propagation, and chronicity. 

Our research group focuses on the contribution of innate immune mechanisms to the pathogenesis of large vessel vasculitides like giant cell arteritis (GCA). These conditions primarily affect medium- and large-sized arteries and are associated with significant morbidity due to vascular inflammation, remodeling, and ischemic complications.

Innate immune cells play a pivotal role in orchestrating vascular inflammation. In GCA, vascular dendritic cells located in the adventitia act as tissue-resident sentinels that sense danger signals and initiate immune activation. Monocytes are actively recruited from the circulation and infiltrate the vessel wall. Their capacity to penetrate inflamed vascular tissue and to produce high levels of pro-inflammatory mediators positions them as key drivers of both vascular inflammation and subsequent tissue remodeling. 

A central aim of our work is to dissect the cellular and molecular basis of innate immune activation in chronic inflammatory diseases. Using high-dimensional approaches—including single-cell transcriptomics, spatial tissue profiling, and functional immunological assays—we seek to define pathogenic cell states and regulatory networks that shape innate immune–driven pathology in rheumatic diseases.