Cellular interactions as a hallmark of immunity

Few immunological responses are mediated by one cell type alone: two examples of some important cellular interactions regulating immunological responsiveness follow. Others are discussed later in the context of effector mechanisms.

T-cell help

B cells can produce antibody independently of T cells when many of their cell-surface Ig receptors are simultaneously bound to antigens which contain repeated identical recognition sites. These are mainly lipopolysaccharide or polysaccharide components of bacterial cell wall (T-independent antigens). However, most antigens also need to stimulate a CD4 T-cell response, which in turn 'helps' the B cells to differentiate into antibody-producing cells. Such antigens are bound by B cells, processed, and then presented to T cells via class II MHC. Because B cells only effectively present antigen bound by their own surface Ig, the epitope recognized by a B cell and the epitope recognized by a T cell helping it must be physically linked on the same molecule or within the same molecular complex. This process helps to prevent the production of autoreactive antibodies.

Once B and T cells interact via antigen, the most important signal mediating help is that given by the CD40 ligand on the surface of the T cell binding CD40 on the B-cell surface, which rescues B cells from apoptosis and stimulates them to divide. The T cell can also secrete many different cytokines (mostly belonging to the interleukin family) which regulate B-cell activation, differentiation, and proliferation. One major regulatory step in antibody formation is class-switching. IgM is expressed by all mature naive B cells, but B cells can switch their constant-chain usage to synthesize antibody of all five classes. The class switched to is determined by the cytokines secreted by the helper T cell. One very important example of this is that the cytokine IL-4 is absolutely essential for IgE production.

Tolerance to self

Because the process which generates antigen receptor diversity is random, mechanisms exist to avoid the initiation of a response to self-antigens. The acquisition of tolerance is a good example of the high degree of complexity of cellular interactions in immune function.

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