Contribution of pathogenic T helper 1 and 17 cells to bursitis and tenosynovitis in polymyalgia rheumatica.

BACKGROUND

Although polymyalgia rheumatica (PMR) is a very common rheumatic inflammatory disease, current insight into the pathobiology of PMR is limited and largely based on studies in blood. We investigated T helper 1 (T) and T helper 17 (T) cell responses in blood, synovial fluid and bursa tissue of patients with PMR.

MATERIALS AND METHODS

Blood samples were collected from 18 patients with new-onset PMR and 32 healthy controls. Synovial fluid was aspirated from the inflamed shoulder bursae or biceps tendon sheath of 13 patients. Ultrasound-guided biopsies of the subacromial-subdeltoid (SASD) bursa were obtained from 11 patients. T cells were examined by flow cytometry, immunohistochemistry and immunofluorescence staining.

RESULTS

Besides an increase of T (CD4IL-17IFN-γ) cells and T cytotoxic 17 (T; CD8IL-17IFN-γ) cells, no other major changes were noted in the circulating T cell compartment of patients with PMR. Absolute numbers of CD4 and CD8 T cells were similar in blood and synovial fluid of patients with PMR. Synovial fluid T cells showed an effector-memory (CD45ROCCR7) phenotype. Percentages of T (CD4IFN-γIL-17) cells and T/T (CD4IFN-γIL-17) cells, but not T or T cells, were increased in the synovial fluid. Bursa tissue biopsies contained a small number of T cells, which were mostly CD8 negative. The majority of bursa tissue T cells produced IFN-γ but not IL-17. For comparison, B cells were scarcely detected in the bursa tissue.

CONCLUSION

Although the circulating T cell pool is expanded in patients with PMR, our findings indicate that T cells are involved in the inflammation of bursae and tendon sheaths in this condition. Our study points towards the T cell pathway as a potential target for therapy in PMR.