title: Down-regulation of Listeria monocytogenes-specific Th1 cytokine response by treatment of mice with goat antibody to mouse IgD.
abstract: Injection of goat anti-mouse IgD antibody (G alpha M IgD) to mice has been shown to induce polyclonal IgG1 and IgE production by B cells and IL-4 production by goat Ig-specific T cells. Surface IgD crosslinking also activates function of B cells as antigen presenting cells. Although the G alpha M IgD treatment is a well established system for regulation of immune response against antigens that bind to B cell receptor, we found that the G alpha M IgD treatment also influences immune response against irrelevant bacterial antigen. The T cells from the G alpha M IgD-treated Listeria monocytogenes-infected mice showed increased IL-4 production and decreased IFN-gamma and IL-2 production against listerial antigen compared with those from control L. monocytogenes-infected mice. Interestingly, changes were also found in antigen presenting cells in the G alpha M IgD-treated mice. MHC class II expression of both B cells and macrophages decreased significantly in the G alpha M IgD-treated mice, suggesting cytokine induced by G alpha M IgD-treatment may suppress MHC class II expression and modulate APC function in the G alpha M IgD-treated mice. In accordance with the assumption, T cells from the G alpha M IgD-treated mice produced high amount of IL-4 and IL-10 in in vitro culture with goat serum which contain goat Ig. These result suggest that G alpha M IgD treatment may modulate APC function in the G alpha M IgD-treated mice through Th2 type cytokine(s) produced by goat Ig-specific T cells, which results in changes of Th response against irrelevant antigen.
authors.affiliation: Department of Immunology, Kyushu University, Fukuoka, Japan.
authors.forename: F
authors.initials: F
authors.lastname: Song
authors.forename: G
authors.initials: G
authors.lastname: Matsuzaki
authors.forename: K
authors.initials: K
authors.lastname: Nomoto
mesh_terms: D000818:Animals; D000888:Antibodies, Anti-Idiotypic / Q000494:pharmacology*; D000938:Antigen-Presenting Cells / Q000378:metabolism; D001402:B-Lymphocytes / Q000276:immunology / Q000378:metabolism; D016207:Cytokines / Q000096:biosynthesis*; D015536:Down-Regulation / Q000276:immunology*; D005260:Female; D006041:Goats; D000949:Histocompatibility Antigens Class II / Q000096:biosynthesis; D007072:Immunoglobulin D / Q000276:immunology*; D016753:Interleukin-10 / Q000096:biosynthesis; D015847:Interleukin-4 / Q000096:biosynthesis; D008089:Listeria monocytogenes / Q000276:immunology*; D051379:Mice; D008807:Mice, Inbred BALB C; D018417:Th1 Cells / Q000276:immunology* / Q000378:metabolism*; D018418:Th2 Cells / Q000276:immunology / Q000378:metabolism
chemical_list: D000888:Antibodies, Anti-Idiotypic; D016207:Cytokines; D000949:Histocompatibility Antigens Class II; D007072:Immunoglobulin D; D016753:Interleukin-10; D015847:Interleukin-4