THE ROLE OF T-CELLS IN POLYETHYLENE PARTICULATE INDUCED INFLAMMATION

Objective. To investigate the role of T lymphocytes in ultra-high mole cular weight polyethylene (UHMWPE) induced inflammation in joint arthr oplasty. Method. We address the role of T cells in wear induced inflam mation by injecting the knee joints of both immune competent rats and mice and severe combined immunodeficient (SCID) mice with UHMWPE, Hist ological and immunohistochemical analysis of the synovial tissues was compared. Interaction between human T cells and UHMWPE particles was e xamined in vitro using T cell activation assays. Results. Histological and immunohistochemical analysis of the knees of the immune competent animals showed significant UHMWPE induced inflammation. In contrast, the tissue in the SCID mice knee joints showed very little inflammator y response to UHMWPE despite phagocytosis of the particulate. Since th e SCID mice have no functional T or B lymphocytes, it is highly likely that the lack of inflammation in knee joints may be due to the absenc e of mouse T cells, as the infiltration of T cells into the joint tiss ue may enhance the inflammatory response to UHMWPE particles. T cell a ctivation assays showed that T cells were not directly activated by UH MWPE particles and the nature of the interaction was not revealed from these experiments, Conclusions. Although T cells are not directly inv olved in UHMWPE particle induced inflammation, as shown by the T cell activation assays, the histological data from the mice studies clearly show differences in the amplitude of inflammation from animals with a nd without functional T cells. Our studies suggest that the T cells ma y enhance the inflammatory response due to a bystander effect. Since t he macrophages upon ingestion of UHMWPE particles release several cyto kines including tumor necrosis factor-alpha, interleukin 1, and IL-6, it is possible that T cells in the vicinity of these macrophages may b ecome attracted to the knee joint and activated due to cytokine releas e.