SignificanceTLS, which are clusters of lymphocytes and stromal cells observed at sites of chronic inflammation, play a key role in sustaining disease progression in autoimmune conditions. While the role of lymphocytes in these structures has been studied extensively, the role of fibroblasts, nonhematopoietic stromal cells, in the formation and maintenance of TLS has not been demonstrated. Here, we establish that, at sites of TLS establishment, resident fibroblasts expand and acquire immunological features in a process that is dependent on IL13 and IL22. Interference with this process or depletion of immunofibroblasts leads to involution of TLS, resulting in decreased immune-cell activation and resolution of tissue pathology, thus supporting the use of fibroblast-targeting strategies to treat TLS-associated autoimmune diseases.