1) Many pathogens developed complex and efficient anti-immune strategies to interfere with host immune responses, which can result in diseases or chronic infections. How do these “smart” pathogens evade from the host immune response? Our goal is to clarify the interaction mechanism of pathogen and host proteins during infection process at molecular, cellular and animal levels, which will not only provide new molecular basis for the pathogenic mechanism of pathogen proteins in immune system, but also supply important theoretical evidence for the development of clinical strategies for infection diseases. 2) FoxP3+ T regulatory (Treg) cells help maintain lymphoid homeostasis in many immunological contexts: tolerance to self versus autoimmune deviation, foeto-maternal tolerance, allergy, responses to pathogens, and interactions with commensal microbes. Our group mainly focuses on the role of phosphatases on Treg signaling transduction with the tumor, EAE and IBD model, which will provide strategies for not only basic research but also clinical study. 3) As malignant cells, which can be distorted by gene mutation, tumor can escape immune surveillance, which leads to tumor tolerance and ultimately destroys human health. In our group, we focus on the role of these proteins in immune escape, which could provide new theoretical basis and drug targets for the prevention, diagnosis and treatment of tumors.