Aim: The aim of the present study was to explore the tolerance march in children and establish probable factors that affect the prognosis of an egg allergy (EA). Methods: Two hundred children 6 months to 2.5 years old with atopic dermatitis (AD) were recruited into our study from 2018 to 2019. EA was diagnosed based on medical history, the skin prick test (SPT), and the oral food challenge test (OFC) ,EA was diagnosed in 78，among those, 7 were allergic only to egg yolk (OnlyEYA), 20 to egg white (OnlyEWA), and 51 to whole egg (WEA). Logistic regression analysis was used to detect the disease course and related risk factors of outcomes. The receiver operating characteristic curve was used to establish a predicting model. Results:The Scoring Atopic Dermatitis score in the WEA group was more severe and persistent than that in the other groups. Forty-three cases of EA developed clinical tolerance (average age, 32.3 ± 8.7 months). The tolerance rate of EYA was 75.9% and EWA was 56.3%. The SPT wheal diameter at initial diagnosis (SPT diag) was the risk factor for persistent EA. The SPT wheal diameter after 6 months (△SPT 6mo) in the tolerant group decreased markedly compared to that in the persistent EA group. Tolerance was higher when △EW-SPT 6mo ≥ 39.5% or △EY-SPT 6mo ≥ 27%. Conclusion: The initial SPT diag and SPT 6mo values were significantly correlated with and can predict outcomes of EA. Key words: Egg allergy, atopic dermatitis, outcome, related factors.

Hyperactivation of NLRP3 inflammasome contributes to the neuroinflammation in autoimmune disorders, but the underlying regulating mechanism remains to be elucidated. We here demonstrate that mice lacking thymic stromal lymphopoietin receptor gene (Tslpr-/-) exhibit significant decreases in experimental autoimmune encephalitis (EAE) score, reduced CD4+ T cells infiltration, and restored expression of myelin basic protein (MBP) in the brain after induction of EAE by injection of myelin oligodendrocyte glycoprotein35-55 (MOG35-55) . TSLPR signals through Janus Kinase 2 (JAK2) to activate NLRP3. Tslpr-/- mice of EAE show decreased phosphorylation of JAK2 and expression of NLRP3 in the brain. In wild type (WT) mice after induction of EAE, inhibition of JAK2 by ruxolitinib inflammatory and CD4+ cell infiltration, decreased expression of NLRP3, and restored BMP expression in the brain. Ruxolitinib also decreased levels of IL-1β and TSLP in brain of EAE mouse when compared to that without ruxolitinib treatment. Further results with NLRP3 inhibitor MCC950 in EAE mouse of WT verified the proinflammatory role of NLRP3 by showing decreased inflammatory cells and CD4+ T cells, restored MBP expression, and declined levels of IL-1β and TSLP in the brain. In patients with anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis we found increased level of NLRP3 and IL-1β in CSF when compared to that in control subjects. These findings highlight TSLP as a prospective target for treating JAK2-NLRP3 axis-associated autoimmune inflammatory disorders.