Possibility of inducing anterior chamber-associated immune deviation by TGF-β2 treatment of monocytes isolated from Behcet's patients

• Published in: Experimental Eye Research Vol. 83; no. 4; pp. 981 - 988
• Main Authors: Takeuchi, Masaru, Keino, Hiroshi, Suzuki, Jun, Usui, Yoshihiko, Hattori, Takaaki, Takeuchi, Aya, Oh-I, Keiko, Okunuki, Yoko, Kezuka, Takeshi, Usui, Masahiko
• Format: Journal Article
• Language: English; Japanese
• Published: Elsevier Ltd 01.10.2006; Elsevier BV
• Subjects: Adult; Aged; Anterior Chamber; anterior chamber-associated immune deviation (ACAID); Behcet Syndrome; CD4-Positive T-Lymphocytes; CD40 Antigens; Cell Adhesion; Cell Proliferation; Cells, Cultured; Female; Humans; immune privilege; immune regulation; Immune Tolerance; Interferon-gamma; Interleukin-12; Lymphocyte Activation; Lymphocyte Culture Test, Mixed; Male; Middle Aged; Monocytes; Transforming Growth Factor beta; Transforming Growth Factor beta2; anterior chamber-associated immune deviation (ACAID); immune privilege; immune regulation
• ISSN: 0014-4835; 1096-0007
• DOI: 10.1016/j.exer.2006.05.005

Murine macrophages treated with TGF-β2 are capable of inducing anterior chamber-associated immune deviation (ACAID), and these macrophages are characterized by impaired IL-12 production and CD40 expression, consequently failing to promote Th1 cell differentiation. In this study, we investigated whether human monocytes can also acquire the specific functions by TGF-β2 treatment, even when the monocytes are isolated from patients with Behcet's disease (BD). Adherent monocytes isolated from peripheral blood mononuclear cells (PBMC) of 16 BD patients and 16 healthy controls, were cultured overnight with or without 5 ng/ml of TGF-β2. Then, TGF-β2-treated or untreated adherent cells were co-cultured with allogeneic CD4 + T cells obtained from healthy subjects. TGF-β2 treatment inhibited the abilities of adherent monocytes obtained from BD patients to stimulate the proliferation and IFN-γ production of allogeneic CD4 + T cells. The reduced IFN-γ production was also confirmed by IFN-γ mRNA expression in the co-cultured T cells. IL-12 production and CD40 molecule expression by adherent monocytes obtained from BD patients were strikingly reduced by TGF-β2 treatment. These results suggest a possibility that adherent monocytes isolated from BD patients may acquire a property to induce ACAID by treatment with TGF-β2.