Autoimmunity

Type 1 diabetes susceptibility arises from a complex interplay between genetic and environmental factors, traditionally linked to adaptive immunity (i.e., T and B cells). However, growing evidence highlights the significant role of innate inflammation in disease onset (i.e., neutrophils and NK cells). Our research focuses on unraveling the complex interactions among immune cells—including T cells, B cells, NK cells, and neutrophils—that contribute to beta-cell destruction and drive type 1 diabetes progression.

Overview of all projects

©Volker Brinkmann / Max Planck Institute for Infection Biology

T cells

Neutrophils

While traditionally associated with acute inflammation, neutrophils are emerging as key contributors to the early inflammatory signals in type 1 diabetes. By creating an environment conducive to T cell activation and autoimmunity, these cells may play a pivotal role in the onset of immune dysregulation. Although their precise function in the disease remains under investigation, growing evidence points to their involvement in initiating immune activation.

©National Institute of Allergy and Infections diseases (NIAID)

T cells

NK cells

NK cells, key components of the innate immune system, do not directly target beta cells. However, they can amplify inflammation and contribute to tissue damage within the pancreas, thereby intensifying autoimmune responses.

©Steve Gschmeissner / Science Photo Library

T cells

B cells

B-cells play a dual role in type 1 diabetes. They produce autoantibodies against beta-cell antigens, serving as key biomarkers of autoimmunity. Additionally, B-cells function as antigen-presenting cells, activating T-cells and amplifying the immune response.

©Steve Gschmeissner / Science Photo Library

T cells

T cells

Autoreactive T cells, particularly CD8+ cytotoxic T cells, are key drivers of the autoimmune response in type 1 diabetes, directly recognizing and destroying beta cells. CD4+ T cells intensify this assault by secreting pro-inflammatory cytokines. Compounding the problem, a disruption or imbalance in T regulatory (Treg) cell subsets, which typically suppress pathogenic T cells, may further promote disease development.

Autoimmunity

Together, these immune cells drive beta-cell destruction, leading to disease progression in type 1 diabetes.

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