1. Promote the activation and differentiation of T cells and enhance adaptive immunity.
Maintaining T cell survival and proliferation: During an immune response, T cells must rapidly proliferate to maximize their immune response. Spermidine inhibits T cell apoptosis (by downregulating pro-apoptotic genes such as Bax and upregulating anti-apoptotic genes such as Bcl-2) while also providing raw materials for cell division (polyamines are essential for nucleic acid and protein synthesis), ensuring T cell numerical dominance in immune responses.
Spermidine promotes Th1 cell differentiation (secreting cytokines such as IFN-γ), enhancing the clearance of intracellular pathogens (such as viruses and bacteria).
It also induces the differentiation and function of Treg cells (by upregulating Foxp3 expression), preventing autoimmune damage (such as allergies and autoimmune diseases) caused by excessive immune responses.
2. Enhance the phagocytic and bactericidal ability of macrophages and strengthen innate immunity.
(1) Promote phagocytosis: Spermidine enhances the recognition and phagocytosis efficiency of pathogens (such as bacteria, fungi) and foreign bodies by upregulating the expression of phagocytic receptors (such as Toll-like receptor TLR4 and scavenger receptor SR-A) on the surface of macrophages; at the same time, it promotes the fusion of phagosomes and lysosomes, accelerating the degradation of pathogens.
(2) Regulating macrophage polarization: Macrophages are divided into the pro-inflammatory "M1" type (which eliminates pathogens) and the anti-inflammatory "M2" type (which repairs tissues). Spermidine can adjust their polarization according to the body's needs:
In the early stages of infection, it promotes M1 differentiation, enhancing the release of pro-inflammatory cytokines (TNF-α, IL-6), and strengthening pathogen killing.
In the late stages of infection or during tissue repair, it induces M2 transformation, secreting anti-inflammatory cytokines (IL-10, TGF-β), reducing inflammatory tissue damage and promoting the restoration of immune homeostasis.
3. Protect immune organs and maintain the microenvironment for immune cell production.
(1) Delaying Immune Organ Aging: With aging, thymic atrophy and decreased bone marrow hematopoietic function are major contributors to immune decline. Spermidine protects the function of thymic epithelial cells and bone marrow hematopoietic stem cells by activating autophagy (clearing senescent cells and damaged organelles) and anti-oxidation (reducing cellular damage caused by reactive oxygen species), thereby maintaining the continuous production of immune cells.
(2) Improving the Splenic Immune Microenvironment: The spleen is the core of the peripheral immune system. Spermidine promotes the maturation of antigen-presenting cells (such as dendritic cells) within the spleen, enhancing their efficiency in presenting antigens to T cells and accelerating the initiation of immune responses.