title: Possibility of inducing anterior chamber-associated immune deviation by TGF-beta2 treatment of monocytes isolated from Behcet's patients.
abstract: Murine macrophages treated with TGF-beta2 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-beta2 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-beta2. Then, TGF-beta2-treated or untreated adherent cells were co-cultured with allogeneic CD4(+) T cells obtained from healthy subjects. TGF-beta2 treatment inhibited the abilities of adherent monocytes obtained from BD patients to stimulate the proliferation and IFN-gamma production of allogeneic CD4(+) T cells. The reduced IFN-gamma production was also confirmed by IFN-gamma 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-beta2 treatment. These results suggest a possibility that adherent monocytes isolated from BD patients may acquire a property to induce ACAID by treatment with TGF-beta2.
authors.affiliation: Department of Ophthalmology, Tokyo Medical University, 6-7-1 Nishishinjuku, Tokyo 160-0023, Japan. takeuchi@tokyo-med.ac.jp
authors.forename: Masaru
authors.initials: M
authors.lastname: Takeuchi
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Keino
authors.forename: Jun
authors.initials: J
authors.lastname: Suzuki
authors.forename: Yoshihiko
authors.initials: Y
authors.lastname: Usui
authors.forename: Takaaki
authors.initials: T
authors.lastname: Hattori
authors.forename: Aya
authors.initials: A
authors.lastname: Takeuchi
authors.forename: Keiko
authors.initials: K
authors.lastname: Oh-I
authors.forename: Yoko
authors.initials: Y
authors.lastname: Okunuki
authors.forename: Takeshi
authors.initials: T
authors.lastname: Kezuka
authors.forename: Masahiko
authors.initials: M
authors.lastname: Usui
mesh_terms: D000328:Adult; D000368:Aged; D000867:Anterior Chamber / Q000276:immunology*; D001528:Behcet Syndrome / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D019013:CD40 Antigens / Q000378:metabolism; D002448:Cell Adhesion / Q000276:immunology; D049109:Cell Proliferation; D002478:Cells, Cultured; D005260:Female; D006801:Humans; D007108:Immune Tolerance; D007371:Interferon-gamma / Q000096:biosynthesis; D018664:Interleukin-12 / Q000096:biosynthesis; D008213:Lymphocyte Activation / Q000276:immunology; D007959:Lymphocyte Culture Test, Mixed; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology*; D016212:Transforming Growth Factor beta / Q000276:immunology*; D053781:Transforming Growth Factor beta2
chemical_list: D019013:CD40 Antigens; C509041:TGFB2 protein, human; D016212:Transforming Growth Factor beta; D053781:Transforming Growth Factor beta2; D018664:Interleukin-12; D007371:Interferon-gamma