| First Author | Kobayashi T | Year | 2023 |
| Journal | J Allergy Clin Immunol | PubMed ID | 36720287 |
| Mgi Jnum | J:336325 | Mgi Id | MGI:7441745 |
| Doi | 10.1016/j.jaci.2023.01.016 | Citation | Kobayashi T, et al. (2023) Lung-resident CD69(+)ST2(+) T(H)2 cells mediate long-term type 2 memory to inhaled antigen in mice. J Allergy Clin Immunol |
| abstractText | BACKGROUND: Chronic airway diseases such as asthma are characterized by persistent type 2 immunity in the airways. We know little about the mechanisms that explain why type 2 inflammation continues in these diseases. OBJECTIVE: We used mouse models to investigate the mechanisms involved in long-lasting immune memory. METHODS: Naive mice were exposed intranasally to ovalbumin (OVA) antigen with Alternaria extract as an adjuvant. Type 2 memory was analyzed by parabiosis model, flow cytometry with in vivo antibody labeling, and intranasal OVA recall challenge. Gene-deficient mice were used to analyze the mechanisms. RESULTS: In the parabiosis model, mice previously exposed intranasally to OVA with Alternaria showed more robust antigen-specific immune responses and airway inflammation than mice with circulating OVA-specific T cells. After a single airway exposure to OVA with Alternaria, CD69(+)ST2(+) T(H)2-type T cells, which highly express type 2 cytokine messenger RNA and lack CD62L expression, appeared in lung tissue within 5 days and persisted for at least 84 days. When exposed again to OVA in vivo, these cells produced type 2 cytokines quickly without involving circulating T cells. Development of tissue-resident CD69(+)ST2(+) T(H)2 cells and long-term memory to an inhaled antigen were abrogated in mice deficient in ST2 or IL-33, but not TSLP receptor. CONCLUSION: CD69(+)ST2(+) T(H)2 memory cells develop quickly in lung tissue after initial allergen exposure and persist for a prolonged period. The ST2/IL-33 pathway may play a role in the development of immune memory in lung to certain allergens. |
