The 3rd Beijing Union Allergic Disease International Summit was successfully held in Beijing in October, golden autumn. This year’s International Summit Forum invited a number of renowned allergists from Europe, America and Taiwan, as well as a number of renowned experts in the fields of digestion, respiratory, ENT and proteomics in China, who gave excellent presentations on the latest advances in clinical and basic research for nearly 400 participants who are engaged in the specialty of allergic reactions. Professor Zhu Zhou graduated from the University of Birmingham, completed his postdoctoral work at Yale University, and is currently working on the genetics of allergic diseases and experimental zoology at Johns Hopkins University School of Medicine. In this forum, Prof. Zhu Zhou gave an in-depth explanation of the pathogenesis of allergic diseases by summarizing a number of basic researches he has completed in recent years. First, Prof. Zhu Zhou led a review about Th2 type cytokines and the corresponding tissue responses. His group used transgenic mice to confirm the important role of the Th2-type cytokine interleukin-13 (IL-13) in the lung: excessive production of IL-13 leads to monocyte and eosinophil inflammation, thickening of airway epithelium, mucus proliferation, alveolar dilation or even destruction, airway subepithelial fibrosis, Charcot-Redden crystal-like deposition in the alveoli, and clinical manifestations of airway obstruction and increased airway reactivity. Then, Prof. Zhu Zhou introduced a special tyrosine phosphatase SHP-1 (protein tyrosine phosphatase-1 containing 2 oncogene Src homologous structural domains). This phosphatase is encoded by the hematopoietic cell phosphatase (hcp) gene and has a negative regulatory effect on a variety of growth factors and cytokines. Activated SHP-1 can terminate signaling by binding to target proteins and dephosphorylating phosphorylated tyrosine substrates. In order to better understand the function of SHP-1, Professor Zhu Zhou selected mev mice with SHP-1 deficiency as the subject of his study. mev mice have abnormal splicing during SHP-1 transcription due to gene mutations, resulting in decreased production of functional SHP-1 protein. The mev mice were found to develop spontaneous, progressive lung inflammation with macrophage, lymphocyte and eosinophil enrichment, along with increased production of Th2-type cytokines (IL-4, IL-5 and IL-13) and Th2-type chemokines (eosinophil chemokine and monocyte chemotactic protein-1). Meanwhile, enhanced mucin gene expression in mev mice leads to airway mucus hyperplasia, increased TGF-β production leads to subepithelial fibrosis, and clinical manifestations of airway obstruction and increased airway reactivity. Subsequently, Prof. Zhu Zhou introduced that reactive oxygen species can inactivate protein tyrosine phosphatases (PTPs) transiently, but corresponding antagonistic mechanisms exist in the normal organism. However, the ability of SHP-1-deficient mice to handle intracellular reactive oxygen species was significantly reduced, and the activity of Nrf2 and STAT6 transcription factors was increased. In the presence of oxidative stress, airway inflammation was increased in SHP-1-deficient mice, and the cellular and cytokine environment under allergen exposure favored the production of Th2-type responses, leading to the emergence of allergic reactions. Finally, Professor Zhu Zhou explored the regulation of SHP-1 on mast cells and severe allergic reactions. It was found that SHP-1 regulates the differentiation, maturation and proliferation of mast cells and is a key link in the mast cell response to environmental stimuli such as oxidative stress and LPS, that SHP-1 deficiency can lead to increased Th2-type cytokine production by mast cells, and that SHP-1 deficiency can lead to more severe symptoms of severe allergic reactions. Through Prof. Zhu Zhou’s excellent presentation, we learned that SHP-1 is necessary for maintaining homeostasis in the lung, and its deficiency leads to a Th2-type allergic inflammatory response in the lung. SHP-1 not only maintains airway tolerance to oxidative stress, but is also important in mast cell development, function, and in the control of severe allergic reactions.