The Journal of Immunology · 2006 · 313 citations · 54 references
Life SciencesCell BiologyImmunologyAdaptive ImmunityCellular ImmunologyImmunoregulationAdaptive Immune ResponsesB Cell BiologyHumoral ImmunityImmunological MemoryLymphocyte ActivationLymphocyte DevelopmentB Cell Antigen PresentationClonal Expansion Of LymphocytesLymphoid Tissue ArchitectureMemory Effector T CellsMhc Class Ii DeficiencyT Cell Clonal ExpansionT Cell ExpansionTh2 Immune Response
B cells are well documented as APC; however, their role in supporting and programming the T cell response in vivo is still unclear. Studies using B cell-deficient mice have given rise to contradictory results. We have used mixed BM chimeric mice to define the contribution that B cells make as APC. When the B cell compartment is deficient in MHC class II, while other APC are largely normal, T cell clonal expansion is significantly reduced and the differentiation of T cells into cytokine-secreting effector cells is impaired (in particular, Th2 cells). The development of the memory T cell populations is also decreased. Although MHC class II-mediated presentation by B cells was crucial for an optimal T cell response, neither a B cell-specific lack of CD40 (influencing costimulation) nor lymphotoxin alpha (influencing lymphoid tissue architecture) had any effect on the T cell response. We conclude that in vivo B cells provide extra and essential Ag presentation capacity over and above that provided by dendritic cells, optimizing expansion and allowing the generation of memory and effector T cells.
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Life Sciences, Genetics, Immunology +12
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