Changes

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===

'''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.

* Th2-derived cytokines, such as IL-10, typically support antibody production, but also down-regulate macrophage effector functions, such as antigen presentation, thereby suppressing inflammatory responses

* Likewise, Th1-derived gamma-IFN can prevent Th0-Th2 differentiation

** This process is described as '''immune deviation''', i.e. one response being selectively induced over the other

* In the case of self-antigens, autoimmune diseases such as diabetes are caused by Th1 cells and can be prevented by 'antigen-primed' Th2 cells.

==Mucosal tolerance==

==Mucosal tolerance==