| First Author | Xia F | Year | 2018 |
| Journal | Autophagy | Volume | 14 |
| Issue | 3 | Pages | 450-464 |
| PubMed ID | 29297752 | Mgi Jnum | J:281835 |
| Mgi Id | MGI:6363853 | Doi | 10.1080/15548627.2017.1421884 |
| Citation | Xia F, et al. (2018) IL4 (interleukin 4) induces autophagy in B cells leading to exacerbated asthma. Autophagy 14(3):450-464 |
| abstractText | Allergic asthma is a common airway inflammatory disease in which B cells play important roles through IgE production and antigen presentation. SNP (single nucleotide polymorphism) analysis showed that Atg (autophagy-related) allele mutations are involved in asthma. It has been demonstrated that macroautophagy/autophagy is essential for B cell survival, plasma cell differentiation and immunological memory maintenance. However, whether B cell autophagy participates in asthma pathogenesis remains to be investigated. In this report, we found that autophagy was enhanced in pulmonary B cells from asthma-prone mice. Autophagy deficiency in B cells led to attenuated immunopathological symptoms in asthma-prone mice. Further investigation showed that IL4 (interleukin 4), a key effector Th2 cytokine in allergic asthma, was critical for autophagy induction in B cells both in vivo and in vitro, which further sustained B cell survival and enhanced antigen presentation by B cells. Moreover, IL4-induced autophagy depended on JAK signaling via an MTOR-independent, PtdIns3K-dependent pathway. Together, our data indicate that B cell autophagy aggravates experimental asthma through multiple mechanisms. |
