The Role of Chemokines in Regulating Cell Migration during Humoral Immune Responses

Switzerland cytokine secretion, which are necessary for the production of mature T cells, B cells, and APC. It is thought that HSC (Figure 1, cell type 1) divide asymmetrically to renew themselves, whereas the other cell in a division Three major types of hematopoietic cells cooperate in further differentiates and migrates to a new microenvi-the recognition of antigens in humoral adaptive immune ronment, perhaps with a different stroma. These latter responses: T lymphocytes, B lymphocytes, and antigen-cells change their hematopoietic potential, first becom-presenting cells (APC). All three types of cells originate ing erythroid-myeloid-lymphoid progenitors, which then from pluripotent hematopoietic stem cells (HSC), are made in the primary lymphoid organs (bone marrow and thymus), and are used for immune responses in secondary lymphoid organs (spleen, lymph nodes, and the gut-associated lymphoid tissues), and in nonlymphoid tissues. The essence of a properly functioning immune system is the high degree of cell motility during cell maturation and immune responses. Cell migration is controlled by multistep processes that include chemoattraction, cell–cell adhesion and, where needed, transmigration through cell layers (Springer, 1994; Butcher et al., 1999). In this review we will consider the trafficking of cells cooperating in the development of the immune system and in a humoral immune response. We will focus our attention on the role(s) of chemokines and their receptors during these processes. Travel begins at the stage of HSC (1) in the bone marrow and pro-their expression and by chemotactic activities measured ceeds through myeloid-lymphoid (2) to lymphoid (3) progenitors. At in vitro. For only a few has it been possible to determine this point two routes can be taken: either B lineage development their function in vivo either by naturally occurring defects through preB-I (4), large preB-II (5), small preB-II (6), and immature or by targeted inactivation of the chemokine or chemo-B cell (7) stages, and from there out into venous blood, the heart, and arterial blood (red lines and arrows; B-route, yellow marks), or kine receptor genes. This lack of functional insight is travel to the thymus (T route, green marks) via blood where T cell likely to be a consequence of redundancy in the system.