Research team Martin Stradner

We focus on the earliest stages of Sjögren’s disease—a condition that is frequently missed for years—so we can intervene sooner and improve long‑term outcomes. While most knowledge about Sjögren’s comes from patients with established, chronic disease, our lab studies the onset of autoimmunity before irreversible glandular damage occurs. By shifting the spotlight to early biology, we aim to transform diagnosis and open the door to timely, effective care.

Our team leads the Pre‑Sjögren Disease Targeted Immunology Evaluation (preSStige) cohort in collaboration with partners in Europe. This longitudinal study follows individuals at risk of Sjögren’s over time. To date, we have enrolled more than one hundred Ro/SSA‑antibody–positive participants, with 23% developing Sjögren’s within six years. Leveraging clinical research, biobanked samples, and cutting‑edge multi‑omics, we map the earliest molecular events that precede disease. We integrate these data with AI‑powered deep learning to predict diagnosis and uncover robust biomarkers.

Contact

Martin Stradner

T: +43 316 385 81794

E: martin.stradner(at)medunigraz.at

Research profile

What we aim to deliver

Biomarkers and data to enable novel classification criteria for early Sjögren’s diagnosis
Clinical “red flags” to guide earlier referral and treatment
Tools and insights that enable future clinical trials in early disease
Outreach that raises awareness among physicians and the public

By combining longitudinal human cohorts with advanced analytics, the Stradner Lab is building the evidence and tools needed to detect Sjögren’s disease early—when treatment can make the greatest difference.

Our projects

Pre-Sjögren Disease Targeted Immunology Evaluation

The overarching goal of the project is to discern whether identified immune system changes are root causes of pSD or mere consequences of persistent inflammation. Structured as a longitudinal cohort study, the project identifies individuals at risk for pSD (pre-Sjogren patients) and follows their progression until the development of pSD or other systemic autoimmune diseases. Instead of relying on data from long-term patients with established immune system dysregulation, this research ventures into uncharted territory, studying changes in individuals as they develop the autoimmune disease. The methodology blends clinical research with cutting-edge laboratory techniques to validate and comprehend the findings. Employing advanced tools like single-cell RNA sequencing, the study conducts in-depth profiling of the involved immune cells.

The Association of Immune Aging and PI3K Signaling in Common Variable Immunodeficiency

Premature ageing of immune cells, also known as immunosenescence, is a commonly observed phenomenon in various conditions like chronic infections, autoimmune diseases and immunodeficiency disorders, like Common variable immunodeficiency (CVID). The underlying mechanisms that lead to this phenomenon are multifaceted and might be overlapping to various degrees in these entities. However, there are diseases that have a well-defined underlying mechanism for this phenomenon, like Activated phosphoinositide 3 kinase (PI3K) -delta syndrome (APDS). In APDS, mutations in the PI3K cause an overactivation of the downstream signaling pathway and consequently lead to premature ageing of immune cells. However, if immunosenescence in patients with autoimmunity is linked to altered PI3K signaling is unclear.
Here, we will investigate whether immunosenescent phenotypes are associated with altered PI3K signaling, regardless of the disease entity. Despite multifaceted underlying mechanisms of immune ageing, there might be an overarching functional alteration that could serve as a therapeutic target.