![]() ![]() If the antigen is a protein, the B cell processes the antigen into smaller peptides, binds some of those peptides to MHC class II molecules, and presents the peptide–class II complexes on the cell surface. When a BCR binds antigen, it may pull the antigen into the cell. Each B cell expresses many BCRs on its surface, each with the same specificity. The B cell receptor (BCR) is an attached form of antibody, which has specificity for particular epitopes. The interaction between B cells and T cells happens roughly as follows. Major expansion of a B cell clone and transition to IgG production typically depend on stimulation from helper T cells, although some nonprotein antigens can stimulate IgM response without T cell help ( Janeway et al. ![]() Review of Processes by Which Antibody Response Develops The final section takes up promising issues for future research. Original antigenic sin has been observed in both antibody and CTL responses. Sometimes the cross-reaction is rather weak, causing the host to respond weakly to the second antigen because of interference by its memory against the first variant. In this case, A′ recalls the memory against an earlier cross-reacting epitope rather than generating a primary, specific response against itself. If a host first encounters a variant A and then a later variant A′, the second variant will sometimes restimulate the initial response against A rather than a new, specific response against A′. The third section describes original antigenic sin, in which the specificity of the immune response depends on the sequence of exposure to antigenic variants. Dominant lineages may repress subdominant lineages by pushing the abundance of pathogens below the threshold needed to trigger weaker, subdominant responses. Earlier stimulation of T cell lineages in response to infection rather than more rapid T cell division seems to determine the dominance of lineages. Among this potential set, some epitopes dominate others in stimulating a CTL response. Aspects of specificity such as MHC binding and avoidance of self-recognition determine which epitopes could potentially be recognized. The second section discusses cytotoxic T lymphocyte (CTL) immunodominance. The later phases of B cell competition and maturation of IgG favor antibodies with increased on-rates of association to epitopes rather than increased equilibrium binding affinity. However, antibodies that bind too strongly clear the matching antigens quickly and prevent feedback stimulation to their B cells. On initial infection, B cells that bind epitopes with relatively high equilibrium affinity divide rapidly and dominate the early phase of the immune response by outcompeting other B cells. The diverse, naive B cells secrete IgM antibodies that bind to nearly any epitope. The first section reviews antibody immunodominance. In this chapter, I describe how immunodominance develops by competition among B and T cell lineages with different specificities. Immunodominant focus determines which epitopes are favored to vary antigenically to escape immune pressure. The immune response focuses on only a few of the many potential epitopes, a process called immunodominance. Each parasite presents a large number of epitopes to the host's immune system. ![]()
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