Epithelial surfaces such as gut, skin and eye are commonly affected in spondyloarthritis (SpA), a

chronic immune-mediated inflammatory disease which leads to inflammation in the spine and joints.

A unifying cell type residing in these tissues are γδ T cells, a specialized immune cell with features of

innate and adaptive immunity. We hypothesize that functional changes in these cells are at the basis

of differential responses to treatment depending on the affected organ and stage of the disease. We

speculate that especially in early stages of SpA, γδ T cells retain much more functional plasticity than

in established disease, which could account for the ability to reverse these changes to a healthy

phenotype. In this project, we will therefore conduct a deep functional- and immunophenotyping in

gut, joint and blood of new onset SpA patients and assess changes in phenotype plasticity in relation

to the ability to induce drug-free remission in early SpA. Moreover, using experimental animal models

of SpA, we will track gut immune cells using transgenic mice to monitor their ability to home to

joints. Thus, we will unravel how resident immune cells shift from tissue protective status to a

disease promoting status in SpA and how this can be reverted.