Find articles by Hess, C. Find articles by Winkler, A. Find articles by Lorenz, A. Find articles by Holecska, V. Find articles by Blanchard, V. Find articles by Eiglmeier, S. Find articles by Schoen, A. Find articles by Bitterling, J. Find articles by Stoehr, A.
Find articles by Petzold, D. Find articles by Schommartz, T. Find articles by Mertes, M. Find articles by Schoen, C. Find articles by Tiburzy, B.
Find articles by Herrmann, A. Find articles by Manz, R. Find articles by Madaio, M. Find articles by Berger, M. Find articles by Wardemann, H. Find articles by Ehlers, M. Published August 27, - More info. Antigen-specific Abs are able to enhance or suppress immune responses depending on the receptors that they bind on immune cells.
Recent studies have shown that pro- or antiinflammatory effector functions of IgG Abs are also regulated through their Fc N-linked glycosylation patterns. IgG Abs that are agalactosylated non-galactosylated and asialylated are proinflammatory and induced by the combination of T cell—dependent TD protein antigens and proinflammatory costimulation.
Sialylated IgG Abs, which are immunosuppressive, and Tregs are produced in the presence of TD antigens under tolerance conditions. We found in mouse experiments that TI immune responses induced suppressive sialylated IgGs, in contrast to TD proinflammatory Th1 and Th17 immune responses, which induced agalactosylated and asialylated IgGs. Transfer of low amounts of antigen-specific sialylated IgG Abs was sufficient to inhibit B cell activation and pathogenic immune reactions.
These findings suggest an immune regulatory function for TI immune responses through the generation of immunosuppressive sialylated IgGs and may provide insight on the role of TI immune responses during infection, vaccination, and autoimmunity.
Abs regulate the production of new Abs specific for the same antigen via positive or negative feedback mechanisms 1 — 5. As a result of helper T cell recognition of antigen on the B cell surface, the T cell becomes activated and in turn activates the B cell.
T cell help has two components: lymphokines which act as growth and differentiation factors for B cells, and additional signals which require cell contact and enable B cells to respond to lymphokines. Increased IL-2 production was facilitated when culture conditions afforded the opportunity for contact between B cells and activated T cells. These results indicate that the establishment of interactions between B cells and anti-CD3-stimulated T4 or T8 cells provides all of the signals necessary for proliferation and differentiation of B cells without other stimuli and also augments the production of lymphokines by the activated T cells.
The data emphasize the role of Ag-nonspecific interactions between B cells and T cells in promoting polyclonal responses of both cell types. Antigens that are expressed on the surface of pathogens in an organized, highly repetitive form can activate specific B cells by cross-linking of antigen receptors in a multivalent fashion.
B cells respond to these multivalent antigens in the absence of MHC class II-restricted T-cell help by a mechanism that depends on the expression of a functional Bruton's tyrosine kinase Btk.
Accordingly, this class of immunogens has been designated T-cell-independent type 2 TI-2 antigens.
0コメント