NK cells participate in the control of infection and cell transformation but, on the other hand, they are involved in the pathology of different inflammatory disorders. Recent evidences suggest that inflammation is an important regulator of osteoarthritis, but the mechanism and cells responsible of inflammation maintenance are not well defined.

To understand the role of NK cells in osteoarthritis, we have performed a preliminary study to compare the phenotype and function of peripheral blood with synovial fluid NK cells from 49 patients with osteoarthritis undergoing total knee arthroplasty. A phenotype analysis of NK cells were carried out by flow cytometry using lineage surface marker. For the first time, the expression of granzyme A, granzyme B and perforin was also performed. Finally, cytotoxicity assays were carried out using previously isolated NK cells co-cultured with their natural target K562 cells.

The majority of NK cells from the synovial fluid were CD56brightCD16negative cells. Moreover, CD56brightCD16negative cells present in synovial fluid showed higher expression of granzyme A and low expression of granzyme B and perforin. In addition, and in contrast to NK cells isolated from the peripheral blood, synovial NK cells were not able to kill K562 cells.

Our results indicate that NK cells from the synovium of patients with osteoarthritis, which present an immunoregulatory non-cytotoxic phenotype, show a different to phenotype of NK cells from peripheral blood, preferably expressing granzyme A, a pro-inflammatory molecule which may contribute to the establishment of chronic articular inflammation in this type of patients.