Editing Vitamin A (section)

=== Immune functions ===
Vitamin A deficiency has been linked to compromised resistance to infectious diseases.<ref name="Ross2012">{{cite journal | vauthors = Ross AC | title = Vitamin A and retinoic acid in T cell-related immunity | journal = The American Journal of Clinical Nutrition | volume = 96 | issue = 5 | pages = 1166S–1172S | date = November 2012 | pmid = 23053562 | pmc = 3471201 | doi = 10.3945/ajcn.112.034637 }}</ref><ref name="Pino2010">{{cite journal | vauthors = Pino-Lagos K, Guo Y, Noelle RJ | title = Retinoic acid: a key player in immunity | journal = BioFactors | volume = 36 | issue = 6 | pages = 430–436 | date = 2010 | pmid = 20803520 | pmc = 3826167 | doi = 10.1002/biof.117 }}</ref> In countries where early childhood vitamin A deficiency is common, vitamin A supplementation public health programs initiated in the 1980s were shown to reduce the incidence of diarrhea and measles, and all-cause mortality.<ref name="Imdad2017"/><ref name=Brown2015>{{cite journal | vauthors = Brown CC, Noelle RJ | title = Seeing through the dark: New insights into the immune regulatory functions of vitamin A | journal = European Journal of Immunology | volume = 45 | issue = 5 | pages = 1287–1295 | date = May 2015 | pmid = 25808452 | pmc = 4426035 | doi = 10.1002/eji.201344398 }}</ref><ref name="Guo2015">{{cite journal | vauthors = Guo Y, Brown C, Ortiz C, Noelle RJ | title = Leukocyte homing, fate, and function are controlled by retinoic acid | journal = Physiological Reviews | volume = 95 | issue = 1 | pages = 125–148 | date = January 2015 | pmid = 25540140 | pmc = 4281589 | doi = 10.1152/physrev.00032.2013 }}</ref> Vitamin A deficiency also increases the risk of immune system over-reaction, leading to chronic inflammation in the intestinal system, stronger allergic reactions and autoimmune diseases.<ref name="Ross2012"/><ref name="Pino2010"/><ref name=Bono2016/>

[[Lymphocyte]]s and [[monocyte]]s are types of [[white blood cell]]s of the [[immune system]].<ref name=Janeway>{{cite book |vauthors = Janeway C, Travers P, Walport M, Shlomchik M |author-link = Charles Janeway |title = Immunobiology |edition = 5th |publisher = Garland Science |year = 2001 |location = New York and London |url = https://www.ncbi.nlm.nih.gov/books/bv.fcgi?call=bv.View..ShowTOC&rid=imm.TOC&depth=10 |isbn = 0-8153-4101-6 |access-date = 15 January 2022 |archive-date = 28 June 2009 |archive-url = https://web.archive.org/web/20090628195820/http://www.ncbi.nlm.nih.gov/books/bv.fcgi?call=bv.View..ShowTOC&rid=imm.TOC&depth=10 |url-status = live }}</ref> Lymphocytes include [[natural killer cell]]s, which function in [[innate immune system|innate immunity]], [[T cell]]s for [[adaptive immune system|adaptive cellular immunity]] and [[B cell]]s for [[antibody]]-driven [[adaptive immune system|adaptive humoral immunity]]. Monocytes differentiate into [[macrophage]]s and [[dendritic cell]]s. Some lymphocytes migrate to the [[thymus]] where they differentiate into several types of T cells, in some instances referred to as "killer" or "helper" T cells and further differentiate after leaving the thymus. Each subtype has functions driven by the types of [[cytokine]]s secreted and organs to which the cells preferentially migrate, also described as trafficking or homing.<ref name=Omman>{{cite book | vauthors = Omman RA, Kini AR | veditors = Keohane EM, Otto CN, Walenga JN |title=Rodak's Hematology: Clinical Principles and Applications |date=2020 |publisher=Elsevier |location=St. Louis, Missouri |isbn=978-0-323-53045-3 |pages=117–135 |edition=6th |chapter=Leukocyte development, kinetics, and functions}}</ref><ref name=Cohn>{{cite book | title=Middleton's Allergy: Principles and Practice | date=2014 | doi=10.1016/B978-0-323-08593-9.00013-9 | chapter-url=https://www.sciencedirect.com/science/article/pii/B9780323085939000139 | pages=203–14 | vauthors=Cohn L, Hawrylowicz C, Ray A | isbn=9780323085939 | edition=8th | chapter=Biology of Lymphocytes | publisher=Saunders | location=Philadelphia | access-date=15 January 2022 | archive-date=15 January 2022 | archive-url=https://web.archive.org/web/20220115201856/https://www.sciencedirect.com/science/article/pii/B9780323085939000139 | url-status=live }}</ref>

Retinoic acid (RA) triggers receptors in bone marrow, resulting in generation of new white blood cells.<ref>{{cite journal | vauthors = Cañete A, Cano E, Muñoz-Chápuli R, Carmona R | title = Role of Vitamin A/Retinoic Acid in Regulation of Embryonic and Adult Hematopoiesis | journal = Nutrients | volume = 9 | issue = 2 | page = 159 | date = February 2017 | pmid = 28230720 | pmc = 5331590 | doi = 10.3390/nu9020159 | doi-access = free | title-link = doi }}</ref> RA regulates proliferation and differentiation of white blood cells, the directed movement of T cells to the [[Gastrointestinal tract|intestinal system]], and to the up- and down-regulation of lymphocyte function.<ref name="Ross2012"/><ref name="Pino2010"/><ref name=Brown2015/><ref name="Guo2015"/><ref name="Bono2016">{{cite journal | vauthors = Bono MR, Tejon G, Flores-Santibañez F, Fernandez D, Rosemblatt M, Sauma D | title = Retinoic Acid as a Modulator of T Cell Immunity | journal = Nutrients | volume = 8 | issue = 6 | page = 349 | date = June 2016 | pmid = 27304965 | pmc = 4924190 | doi = 10.3390/nu8060349 | doi-access = free | title-link = doi }}</ref><ref name="Czarn2017">{{cite journal | vauthors = Czarnewski P, Das S, Parigi SM, Villablanca EJ | title = Retinoic Acid and Its Role in Modulating Intestinal Innate Immunity | journal = Nutrients | volume = 9 | issue = 1 | page = 68 | date = January 2017 | pmid = 28098786 | pmc = 5295112 | doi = 10.3390/nu9010068 | doi-access = free | title-link = doi }}</ref> If RA is adequate, T helper cell subtype Th1 is suppressed and subtypes Th2, Th17 and iTreg (for regulatory) are induced. Dendritic cells located in intestinal tissue have enzymes that convert retinal to ''all-trans''-retinoic acid, to be taken up by retinoic acid receptors on lymphocytes. The process triggers gene expression that leads to T cell types Th2, Th17 and iTreg moving to and taking up residence in [[mesenteric lymph node]]s and [[Peyer's patch]]es, respectively outside and on the inner wall of the small intestine.<ref name=Brown2015/><ref name="Guo2015"/> The net effect is a down-regulation of immune activity, seen as tolerance of food [[allergen]]s, and tolerance of resident bacteria and other organisms in the [[microbiome]] of the large intestine.<ref name="Ross2012"/><ref name="Pino2010"/><ref name=Bono2016/> In a vitamin A deficient state, innate immunity is compromised and pro-inflammatory Th1 cells predominate.<ref name="Ross2012"/><ref name="Czarn2017"/>

====Measles prevention====
"Vitamin A deficiency (VAD) is a major public health problem in low- and middle-income countries, affecting 190 million children under five years of age and leading to many adverse health consequences, including death."<ref name="Cochrane2022"/> Vitamin A deficiency is rare in the United States.<ref name=":8">{{Cite web |title=Office of Dietary Supplements - Vitamin A and Carotenoids |url=https://ods.od.nih.gov/factsheets/VitaminA-HealthProfessional/ |access-date=2025-04-08 |website=ods.od.nih.gov |language=en}}</ref> A meta-analysis of clinical trials conducted in countries where VAD is prevalent concluded that when children were supplemented with vitamin A, there was a 50% reduction in incidence of contracting measles.<ref name="Cochrane2022">{{cite journal |vauthors=Imdad A, Mayo-Wilson E, Haykal MR, Regan A, Sidhu J, Smith A, Bhutta ZA |title=Vitamin A supplementation for preventing morbidity and mortality in children from six months to five years of age |journal=Cochrane Database Syst Rev |volume=3 |issue=3 |pages=CD008524 |date=March 2022 |pmid=35294044 |pmc=8925277 |doi=10.1002/14651858.CD008524.pub4 |url=}}</ref>  Vitamin A supplementation is not thought to reduce the risk of death from measles.<ref name=":8" /> Young children given high doses of vitamin A from supplements or [[cod liver oil]] can accumulate to toxic levels and this can lead to [[hypervitaminosis A]] and [[Liver disease|liver damage]].<ref name=":8" /> In the [[2025 Southwest United States measles outbreak]], centered in [[West Texas]], some families continued to refuse vaccines and instead opted for giving vitamin A supplements or vitamins A- and D-containing cod liver oil to their children after [[Robert F. Kennedy Jr.]], promoted vitamin A as prevention and treatment.<ref name="NYTimes">{{cite web | last=Rosenbluth | first=Teddy | title=For Some Measles Patients, Vitamin A Remedy Supported by RFK Jr. Leaves Them More Ill | website=The New York Times | date=2025-03-25 | url=https://www.nytimes.com/2025/03/25/health/measles-kennedy-vitamin-a.html | access-date=2025-03-26}}</ref> Multiple children hospitalized for measles at Covenant Children's Hospital in Lubbock also showed signs of [[liver damage]], a symptom of vitamin A toxicity.<ref name=":8" /><ref name="NYTimes" /><ref name="Davies2025">{{cite web | last=Davies | first=David Martin | title=West Texas children treated for vitamin A toxicity as medical disinformation spreads alongside measles outbreak | website=TPR | date=2025-03-28 | url=https://www.tpr.org/public-health/2025-03-27/west-texas-children-treated-for-vitamin-a-toxicity-as-medical-disinformation-spreads-alongside-measles-outbreak | access-date=2025-03-28}}</ref>