Collectively, our results demonstrate for the first time that activation of JAK2/STAT4/STAT5 signaling pathway by PBMT to regulate the function of peripheral CD4+ T lymphocytes has a certain contribute to promoting AHN, alleviating the pathological symptoms of AD, and ultimately rescuing cognitive impairment in AD mouse models, suggesting that PBMT has potential immunotherapeutic value in AD, which is likely reflected by regulating CD4+ T lymphocyte function. The gene discussed is JAK2; the disease is Alzheimer disease.