Vitamin A and Immune Specificity
Homeostasis — literally ‘standing still’ — describes the mechanisms by which all biological systems maintain stability. In effect this is the position at which human health is maintained and may also be described as a homeostatic set point, in which as circumstances change so does the set point. In simple parlance the idea that someone may be in a stable state of homeostasis but one that induces illness is a concept still developing. In effect all illness generates a change in homeostasis but not all changes in homeostasis results in illness.
In the immune system, although a great deal is known about responses to the ‘extreme’ situation of an acute infection, it is also important to also understand how immune pathways operate in steady-state conditions. When they function correctly, these homeostatic immune responses are barely visible, but like a graceful swan, the surface calm belies much hidden activity, and the consequences of dysfunction are significant. So much so that virtually all chronic illness is attributed to an inappropriate release of inflammation which over time cause systemic illness.
In a paper published in the journal Science Belkaid and colleagues report that a lack of vitamin A results in altered intestinal immune homeostasis, with a decrease in the frequency of group 3 innate lymphoid cells (ILC3s) and an increase in that of ILC2s. Whilst this is a mouse study, humans equally require access to and production of vitamin A inside the mucosal immune system to maintain homeostasis.
The shift in cell populations produce differing effects, with the ILC2 cells exerting barrier repair and parasite defending outcomes, but increased risk of bacterial infection. This study shows that nutrient deficiency is not only associated with a global immunosuppression, but can result in the specific activation of a distinct branch of barrier immunity and create changes in immune competence locally and systemically. The discoveries that retinoic acid (RA) imprints the homing of leukocytes to the gut and enhances the induction of regulatory T cells, highlighted a potential role for RA in mucosal tolerance. However, more recently emerging data tell of a more profound systemic impact of RA on leukocyte function and commitment. 
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