Primary immunodeficiency
Core of basic research: Clarify the genetic mechanisms of developmental, activation, or functional defects in immune cells (T/B cells, complement), focus on the impact of mutations in key genes (ADA, BTK, IL-2Rγ) on the immune network, providing a theoretical basis for gene therapy and replacement therapy.
Core key proteins: ADA (adenosine deaminase, deficiency causes T/B cell developmental disorders), IL-2Rγ (cytokine receptor subunit, deficiency causes severe combined immunodeficiency), BTK (Bruton tyrosine kinase, deficiency causes B cell maturation disorders), CD40L (T cell surface molecule, deficiency impairs B cell activation), STAT3 (signal factor, deficiency causes immune cell dysfunction), PI3K (signaling pathway, deficiency affects immune cell activation), MHC-II (antigen-presenting molecule, deficiency causes immune response defects), Complement components (C3/C5, deficiency increases susceptibility to infections).
Core key proteins: ADA (adenosine deaminase, deficiency causes T/B cell developmental disorders), IL-2Rγ (cytokine receptor subunit, deficiency causes severe combined immunodeficiency), BTK (Bruton tyrosine kinase, deficiency causes B cell maturation disorders), CD40L (T cell surface molecule, deficiency impairs B cell activation), STAT3 (signal factor, deficiency causes immune cell dysfunction), PI3K (signaling pathway, deficiency affects immune cell activation), MHC-II (antigen-presenting molecule, deficiency causes immune response defects), Complement components (C3/C5, deficiency increases susceptibility to infections).
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