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Thymus‐independent type 2 (TI‐2) antigens are repetitive antigens capable of eliciting antibody responses without T cell help. They are important in the immune response against encapsulated bacteria and as a rapid first line of defense against pathogens. TI‐2 antigens induce strong proliferation in extrafollicular foci. However, any germinal centers forming in response to TI‐2 antigens involute synchronously 5 days after immunization. This is thought to be caused by the lack of T cell help. Surprisingly, immunization of mice deficient for the homeostatic chemokine receptor CCR7 with TI‐2 antigens resulted not only in the expected, vigorous extrafollicular plasma cell response but also in persisting splenic germinal centers. This was observed for two different TI‐2 antigens, heat‐killed Streptococcus pneumoniaeand (4‐hydroxy‐3‐nitrophenyl)acetyl‐Ficoll (NP‐Ficoll). Germinal centers induced by TI‐2 and thymus‐dependent (TD) antigens were located in the periarteriolar area of the white pulp in CCR7 knockout mice, corresponding to the T zone of wild‐type (WT) mice. The TI‐2‐induced germinal centers contained peripheral rings of follicular dendritic cells and unusually for TI‐2‐induced germinal centers, T cells. The licensing responsible for their atypical persistence did not endow TI‐2‐induced germinal centers with the full range of characteristics of classic germinal centers induced by TD antigens. Thus, class‐switching, affinity maturation, and memory B cell generation were not increased in CCR7‐deficient mice. It seems unlikely that a defect in regulatory T cell (Treg) location was responsible for the atypical persistence of TI‐2‐induced germinal centers, as Tregs were comparably distributed in germinal centers of CCR7‐deficient and WT mice.