Infection with helminths and exposure to antigens induce a strong type 2 immune response resulting in the secretion of the cytokines IL‐4 and IL‐13 by CD4⁺ T cells and several innate cell types. IL‐4 and IL‐13 promote class switch recombination to IgG1 and IgE while their role for germinal center (GC) formation is poorly understood. We found a dramatic reduction in the numbers of GC B cells when investigating different type 2 immune responses in IL‐4/IL‐13‐deficient mice. IL‐4/IL‐13 from T cells located outside B‐cell follicles was sufficient for GC formation. We further revealed that IL‐4/IL‐13 acts directly on B cells for the formation of a robust GC response. The frequency of apoptotic GC B cells was not altered in the absence of IL‐4/IL‐13 and proliferation was even enhanced. However, deficiency of signal transducer and activator of transcription 6 signaling in B cells resulted in failure to downregulate the chemotactic receptor Gpr183 (Ebi2) and downregulation of this receptor has been shown to be essential for proper GC B‐cell differentiation. Thus, T‐cell‐derived extrafollicular IL‐4/IL‐13 and signal transducer and activator of transcription 6‐regulated genes in B cells play a critical role for orchestration of the GC response in type 2 immunity.