Purpose: The inflammatory response in acute anterior uveitis (AU) is believed to be primarily mediated by autoreactive Tcells. We wanted to evaluate whether t he T-cell activation marker CD40 ligand is involved in the AU immunopathogenesi s. Methods: We evaluated the expression of the CD40 ligand on CD4+T-cells, CD8 +T-cells and CD19+B-cells on peripheral blood mononuclear cells using flow c ytometry in six patients with unilateralAU, six patientswith monosymptomatic opt ic neuritis (ON) as inflammatory controls, and in six healthy controls. The ex v ivo induction of the CD40 ligand on T-cells in patients and controls was also s tudied. Results: A significantly higher expression of the CD40 ligand on both CD 4+(p< 0.05)-and CD8+(p< 0.05) T-cells in patients with AU compared to ON pat ients and healthy controls was found. There was a significantly higher induction of the CD40 ligand on CD8+T-cells in AU patients compared to ON patients and healthy controls (p < 0.01). No differences in the B-cell population were obser ved between the three groups. Conclusion: Patients with AU had increased express ion of the CD40 ligand on T-cells in the blood and expressed higher levels of t he CD40 ligand when stimulated, compared to ophthalmological inflammatory contro ls and healthy controls. The data suggest that the CD40 ligand is involved in th e development of AU. Purpose: The inflammatory response in acute anterior uveitis (AU) is believed to be primarily mediated by autoreactive T cells. We wanted to evaluate whether t T-cell activation marker CD40 ligand is involved in the immunopathogenes s. Methods: We evaluated the expression of the CD40 ligand on CD4 + T-cells, CD8 + T-cells and CD19 + B-cells on peripheral blood mononuclear cells using flow c ytometry in six patients with unilateral AU, six patients with monosymptomatic opt ic neuritis (ON) as inflammatory controls, and in six healthy controls. The ex v ivo induction of the CD40 ligand on T-cells in patients and controls was also tudied. Results: A significantly higher expression of the CD40 ligand on both CD 4+ (p <0.05) -and CD8 + (p <0.05) T-cells in patients with AU compared to ON patients and healthy controls was found. There was a significantly higher induction of the CD40 ligand on CD8 + T-cells in AU patients compared to ON patients and healthy controls (p <0.01). No differences in the B-cell population were observed ved between the three groups. Conclusion: Patients with AU had increased express ion of the CD40 ligand on T-cells in the blood and expressed higher levels of t he CD40 ligand when stimulated, compared to ophthalmological inflammatory contro ls and healthy controls. The data suggest that the CD40 ligand is involved in th e development of AU.