The diagram of immune response mechanisms. The diagram is divided into two sections, each representing a different type of immune response. On the left, a helminth is shown interacting with the intestinal lining, triggering the release of I L-25, which binds to the I L-17 R B receptor on inflammatory I L C 2 cells. This interaction leads to increased proliferation and migration of these cells, marked as Type 3 effector. On the right, an allergen interacts with the intestinal lining, releasing I L-33, which binds to the S T 2 receptor on natural I L C 2 cells. This interaction enhances cytokine production, marked as Type 2 effector. The central cell shows internal signaling pathways involving N F-k B, P r d m 1, and I r f 4, which are activated by these interactions.
Blimp1 controls the phenotype and effector functions of ILC2 in response to alarmins. Alarmins such as IL-25 and IL-33 act to fine-tune ILC2 phenotype and function. IL-33 was found to induce the transcription factors Prdm1 (Blimp1) and Irf4 that in turn promoted enhanced effector cytokine secretion and optimal type 2 immunity. In contrast, genetic deletion of Prdm1 in ILC2s favored the dominance of iILC2—a subset induced by IL-25 and associated with enhanced proliferative and migratory function, as well as enhanced type 3 cytokine production. Together, these findings position Blimp1 as a key transcription factor in gating ILC2 phenotype and function following activation by helminth infection or during allergy (Forster et al., 2026). Created in BioRender.