Prolonged physical interaction between helper T cells and antibody-producing B cells is crucial for efficient immune responses. Mutations in a protein that underlies this process cause human disease. The production of antibodies by B cells is essential for protective immunity following vaccination or exposure to infectious pathogens. The development of antibody-secreting B cells occurs in discrete areas of lymphoid tissues called germinal centres, the formation of which depends on interactions between B cells and T cells bearing the CD4 molecule on their surface (CD4~+ T cells). But several steps in the orchestration of T- and B-cell activation, differentiation and 'homing' to germinal centres during an immune response remain incompletely defined. For example, mutations in the protein SAP, which is involved in signalling by the SLAM family of cell-surface receptors, leads to defects in the formation of germinal centres and the generation of long-lived antibody-secreting B cells. These defects result in a human immunodeficiency condition called X-linked lymphoproliferative disease. But the mechanism associated with loss of SAP function has remained unknown. On page 764 of this issue, Qi et al. shed light on how SAP functions in CD4~+ T cells to efficiently engage B cells and to provide appropriate signals for both the formation of germinal centres and the differentiation of B cells into antibody-secreting cells.
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