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전체 게시물

작성자 사진Jun Young Hong

2021년 7월과 8월, 면역생리 발달프로그래밍 연구실과 분자구조및 신호전달 연구실 (신동혁 교수) Joint로 대학원생과 학부 연구생을 위한 기초 연구 교육이 진행됩니다. 기본적인 분자생물학적 실험의 기법과 원리를 배우고 실전 트레이닝이 두 명의 PI로 부터 직접 제공될 예정입니다. 다루게 될 내용은, 논문 검색 및 공부, 클로닝, 단백질 실험, 유전자 분석, 포유류세포 배양, 데이터 해석, 분석 장비에 대한 이해등을 포함합니다.




Early life environmental exposure, particularly during perinatal period, can have a life-long impact on organismal development and physiology. The biological rationale for this phenomenon is to promote physiological adaptations to the anticipated environment based on early life experience. However, perinatal exposure to adverse environments can also be associated with adult-onset disorders. Multiple environmental stressors induce glucocorticoids, which prompted us to investigate their role in developmental programming. Here, we report that perinatal glucocorticoid exposure had long-term consequences and resulted in diminished CD8 T cell response in adulthood and impaired control of tumor growth and bacterial infection. We found that perinatal glucocorticoid exposure resulted in persistent alteration of the hypothalamic-pituitary-adrenal (HPA) axis. Consequently, the level of the hormone in adults was significantly reduced, resulting in decreased CD8 T cell function. Our study thus demonstrates that perinatal stress can have long-term consequences on CD8 T cell immunity by altering HPA axis activity.


최종 수정일: 2021년 1월 13일


Early-life respiratory infection has been associated with asthma in later-life. Particularly, early-life human rhinovirus (RV) infection has been linked to asthma development in high risk infants and children. Nevertheless, the role of RV infection in the initiation of asthma remains unclear. In Dr. Hong's doctoral research, RV infection in neonatal mice induces type 2 immune response, while infection in adult mice elicits type 1 immune response. Age-dependent induction of type 2 cytokines, such as IL-25, IL-33, and IL-33 leads to the increase of type 2 innate lymphoid cells (ILC2). Type 1 cytokine, IFN-γ, is able to reduce the function of ILC2 in type 2 immune response. Finally, neonatal RV infection provokes persistent mucous metaplasia and airway hyperresponsiveness, the asthma-phenotype, which is not observed in adulthood infection. These results suggest that early-life RV infection can contribute to the initiation of persistent asthma by provoking age-dependent type 2 immune response.

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