| Cell death is also induced by TNF via the TNF receptor; CTLA-4 has recently also been implicated in cell death. The subsequent signalling cascade activates proteases, such as IL-1beta Converting Enzyme (ICE), that leads to cell apoptosis. | | Cell death is also induced by TNF via the TNF receptor; CTLA-4 has recently also been implicated in cell death. The subsequent signalling cascade activates proteases, such as IL-1beta Converting Enzyme (ICE), that leads to cell apoptosis. |
− | '''Immune deviation'''can be described as one immune response being selectively induced over another potential response - examples include Th2-derived cytokines, such as IL-10, which typically support antibody production, but can also down-regulate macrophage effector functions, such as antigen presentation, thereby suppressing the inflammatory response. Likewise, Th1-derived gamma-IFN can prevent Th0-Th2 differentiation. In the case of self-antigens, autoimmune diseases such as diabetes which are caused by Th1 cells can theoretically be prevented by 'antigen-primed' Th2 cells. | + | '''Immune deviation''' can be described as one immune response being selectively induced over another potential response - examples include Th2-derived cytokines, such as IL-10, which typically support antibody production, but can also down-regulate macrophage effector functions, such as antigen presentation, thereby suppressing the inflammatory response. Likewise, Th1-derived gamma-IFN can prevent Th0-Th2 differentiation. In the case of self-antigens, autoimmune diseases such as diabetes which are caused by Th1 cells can theoretically be prevented by 'antigen-primed' Th2 cells. |