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Increasing dietary vitamin A can enhance the effect of the vaccine? Science reveals the underlying mechanism.
Vitamin A is a fat-soluble nutrient that can be absorbed from the diet by intestinal epithelial cells and converted into retinol. Retinol promotes the development of B cells and T cells and promotes their recruitment to the intestinal tract, which is essential for intestinal adaptive immunity. Therefore, vitamin A deficiency can lead to increased susceptibility to intestinal infectious diseases.
Previous studies have shown that intestinal myeloid cells play an important role in the development of vitamin A-dependent intestinal immunity. Certain myeloid cells convert retinol to retinoic acid (RA), and then transmit RA to developing B cells and T cells, thereby activating RA-dependent gene expression, guiding B cells and T cells to return to the intestine and Induces B cells to produce immunoglobulin A (IgA). So, how do intestinal myeloid cells obtain retinol and convert it into RA? Retinol is lipophilic and needs to be transported by a retinol binding protein, which has not yet been identified.
Serum amyloid A (SAA) is a retinol-binding protein expressed in the intestinal epithelium, and its epithelial cell expression needs to be mediated by the intestinal microbiota and dietary vitamin A. SAA is produced by the liver and binds to retinol after systemic bacterial infections and circulates in the blood. However, the cellular target of the SAA-retinol complex is still unclear.
The international academic journal “Science” published online a new achievement named “Serum amyloid A delivers retinol to intestinal myeloid cells to promote adaptive immunity” by Lora V. Hooper’s team at the University of Texas Southwestern Medical Center. This study identified the receptor for the SAA-retinol complex, which mediates the uptake of retinol into the intestinal myeloid cells and promotes the adaptive immunity of the intestine.
Researchers used chemical cross-linking, mass spectrometry and other biochemical methods to identify cell lines cultured in vitro, and found that among the several subtypes of SAA, SAA1 had the highest expression.
Therefore, the researchers measured the binding protein of SAA1 and found that it preferentially binds to low-density lipoprotein (LDL) receptor-related protein 1 (LRP1). As the cell surface receptor of SAA protein, LRP1 promotes the endocytosis of SAA1-retinol complex.
So, who is the target cell of the SAA-retinol complex? The researchers tested the expression of LRP1 in intestinal cells and found that it has the highest expression in CD11c+MHCII+ myeloid cells compared to immune cells such as B cells, T cells, and CD11c-. LRP1 effectively binds to SAA1-retinol complex, promotes myeloid cells to take retinol from SAA1-retinol complex, and converts retinol to RA.
Subsequently, the researchers verified the role of SAA and LRP1 in the retinol acquisition of small intestinal CD11c+ myeloid cells in myeloid cell-specific LRP1 knockout mice.
At the same time, it was found that LRP1 promotes vitamin A-dependent adaptive immunity in the intestine, regulates the homing of intestinal B cells and CD4+ T cells, and the production of IgA. They also enhance the effector function of TH17 cells by stimulating the production of IL-17A, but they are not necessary for the production of intestinal Treg cells.
Therefore, researchers believe that SAA-mediated delivery of retinol is related to vitamin A-dependent intestinal immunity, which can promote specific immunity after oral intake of pathogens and increase the resistance of the intestine to pathogen infection.
(source:internet, reference only)