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S Masli, B Turpie, JW Streilein; Thrombospondin (TSP) Is the Primary Molecular Mediator of ACAID-Inducing Properties of TGFß2-Treated Antigen Presenting Cells (APC) . Invest. Ophthalmol. Vis. Sci. 2002;43(13):2958.
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Purpose:Exposure of APCs to TGFß2 up-regulates several immunomodulatory genes: TGFß, thrombospondin, IFNα/ß. We wished to determine if one of these gene products serves as the major molecular mediator of the ACAID-promoting effects of TGFß2. Methods:Macrophage hybridoma #59 cells were pulsed with ovalbumin (OVA) and cultured in the presence of TGFß2, TSP, or IFNß. The treated cells were examined (a) in vitro by RT-PCR, for expression of genes known to be up-regulated by TGFß2 treatment: TSP, MIP-2, TGFß, IFNα, IFNß, IFNα/ßReceptor and flow cytometry for TSP receptors (CD47, CD36); and (b) in vivo for their capacity to suppress OVA-specific delayed hypersensitivity (DH) when injected into naïve mice immunized subsequently with OVA plus complete Freunds' adjuvant. Results:APCs treated with TSP or TGFß2, but not with IFNß, impaired DH responses in vivo. TSP-treated APCs displayed enhanced expression of MIP-2, TGFß similar to TGFß2-treatment, whereas IFNß-treated APCs displayed suppressed expression of these same genes that are known to be important in ACAID induction. Conclusion:TSP acts as a surrogate for TGFß2 in conferring ACAID-inducing properties on APCs. Since it is a very early response gene after TGFß2 treatment, TSP appears to be the major mediator of the ACAID-promoting activities of TGFß2.
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