Central Tolerance in B Cells

Immature B lymphocytes that recognize self antigens in the bone marrow with high affinity either change their specificity or are deleted. The mechanisms of central B cell tolerance have been best described in experimental models (Fig. 14-8).

• Receptor editing. If immature B cells recognize self antigens that are present at high concentration in the bone marrow and especially if the antigen is displayed in multivalent form (e.g., on cell surfaces), many antigen receptors on each B cell are cross-linked, thus delivering strong signals to the cells. One consequence of such signaling is that the B cells reactivate their RAG1 and RAG2 genes and initiate a new round of VJ recombination in the immunoglobulin (Ig) k light chain gene locus. A Vk segment upstream of the already rearranged VkJk unit is joined to a downstream Jk. As a result, the previously rearranged VkJk exon in the self-reactive immature B cell is deleted and a new Ig light chain is expressed, thus creating a B cell receptor with a new specificity. This process is called receptor editing (see Chapter 8) and is an important

FIGURE 14-8 Central tolerance in B cells.

Immature B cells that recognize self antigens in the bone marrow with high avidity (e.g., multivalent arrays of antigens on cells) die by apoptosis or change the specificity of their antigen receptors (receptor editing). Weak recognition of self antigens in the bone marrow may lead to anergy (functional inactivation) of the B cells.

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