Egress of B cells from secondary lymphoid organs depends on S1P1. This has been most clearly shown for differentiated antibody-secreting B cells, which leave the secondary lymphoid organs in which they were generated from naive B cells by antigen activation and home to bone marrow or tissue sites. S1PR1-deficient antibody-secreting cells have diminished ability to home from spleen to bone marrow or to form gut-associated lym-phoid tissues. Presumably, naive B cells that have entered secondary lymphoid tissues but do not become activated by antigen reenter the circulation, like naive T cells do, but how this process is controlled is not clear.

Subsets of B cells committed to producing particular types of antibodies migrate from secondary lymphoid organs into specific tissues. As we will describe in later chapters, different populations of activated B cells may secrete different types of antibodies, called isotypes, each of which performs a distinct set of effector functions. Many antibody-producing plasma cells migrate to the bone marrow, where they secrete antibodies for long periods. Most bone marrow-homing plasma cells produce IgG antibodies, which are then distributed throughout the body through the blood stream. B cells within mucosa-associated lymphoid tissues usually become committed to expression of the IgA isotype of antibody, and these committed cells may home specifically to epithelium-lined mucosal tissues. This homing pattern, combined with the local differentiation within the mucosa of B cells into IgA-secreting plasma cells, serves to optimize IgA responses to mucosal infections. As we will discuss in more detail in Chapter 13, IgA is efficiently excreted into the lumen of tissues lined by mucosal epi-thelia, such as the gut and respiratory tract. The mechanisms by which different B cell populations migrate to different tissues are, not surprisingly, similar to the mechanisms we described for tissue-specific migration of effector T cells and depend on expression of distinct combinations of adhesion molecules and chemokine receptors on each B cell subset. For example, bone marrow-homing IgG-secreting plasma cells express VLA-4 and CXCR4, which bind respectively to VCAM-1 and CXCL12 expressed on bone marrow sinusoidal endo-thelial cells. In contrast, mucosa-homing IgA-secreting plasma cells express a4p7, CCR9, and CCR10, which bind respectively to MadCAM-1, CCL25, and CCL28, expressed on mucosal endothelial cells. IgG-secreting B cells are also recruited to chronic inflammatory sites in various tissues, and this pattern of homing can be attributed to CXCR3 and VLA-4 on these B cells binding to VCAM-1, CXCL9, and CXCL10, which are often found on the endothelial surface at sites of chronic inflammation.

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