Abstract
In populations where vitamin A availability from food is low, infectious diseases can precipitate vitamin A deficiency by decreasing intake, decreasing absorption, and increasing excretion. Infectious diseases that induce the acute-phase response also impair the assessment of vitamin A status by transiently depressing serum retinol concentrations. Vitamin A deficiency impairs innate immunity by impeding normal regeneration of mucosal barriers damaged by infection, and by diminishing the function of neutrophils, macrophages, and natural killer cells. Vitamin A is also required for adaptive immunity and plays a role in the development of both T-helper (Th) cells and B-cells. In particular, vitamin A deficiency diminishes antibody-mediated responses directed by Th2 cells, although some aspects of Th1-mediated immunity are also diminished. These changes in mucosal epithelial regeneration and immune function presumably account for the increased mortality seen in vitamin A-deficient infants, young children, and pregnant women in many areas of the world today.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 167-192 |
| Number of pages | 26 |
| Journal | Annual Review of Nutrition |
| Volume | 21 |
| DOIs | |
| State | Published - 2001 |
Fingerprint
Keywords
- Acute phase response
- Immunity
- Retinoic acid
- T-cells
ASJC Scopus subject areas
- Medicine (miscellaneous)
Cite this
Vitamin A, infection, and immune function. / Stephensen, C. B.
In: Annual Review of Nutrition, Vol. 21, 2001, p. 167-192.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Vitamin A, infection, and immune function
AU - Stephensen, C. B.
PY - 2001
Y1 - 2001
N2 - In populations where vitamin A availability from food is low, infectious diseases can precipitate vitamin A deficiency by decreasing intake, decreasing absorption, and increasing excretion. Infectious diseases that induce the acute-phase response also impair the assessment of vitamin A status by transiently depressing serum retinol concentrations. Vitamin A deficiency impairs innate immunity by impeding normal regeneration of mucosal barriers damaged by infection, and by diminishing the function of neutrophils, macrophages, and natural killer cells. Vitamin A is also required for adaptive immunity and plays a role in the development of both T-helper (Th) cells and B-cells. In particular, vitamin A deficiency diminishes antibody-mediated responses directed by Th2 cells, although some aspects of Th1-mediated immunity are also diminished. These changes in mucosal epithelial regeneration and immune function presumably account for the increased mortality seen in vitamin A-deficient infants, young children, and pregnant women in many areas of the world today.
AB - In populations where vitamin A availability from food is low, infectious diseases can precipitate vitamin A deficiency by decreasing intake, decreasing absorption, and increasing excretion. Infectious diseases that induce the acute-phase response also impair the assessment of vitamin A status by transiently depressing serum retinol concentrations. Vitamin A deficiency impairs innate immunity by impeding normal regeneration of mucosal barriers damaged by infection, and by diminishing the function of neutrophils, macrophages, and natural killer cells. Vitamin A is also required for adaptive immunity and plays a role in the development of both T-helper (Th) cells and B-cells. In particular, vitamin A deficiency diminishes antibody-mediated responses directed by Th2 cells, although some aspects of Th1-mediated immunity are also diminished. These changes in mucosal epithelial regeneration and immune function presumably account for the increased mortality seen in vitamin A-deficient infants, young children, and pregnant women in many areas of the world today.
KW - Acute phase response
KW - Immunity
KW - Retinoic acid
KW - T-cells
UR - http://www.scopus.com/inward/record.url?scp=0034938825&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0034938825&partnerID=8YFLogxK
U2 - 10.1146/annurev.nutr.21.1.167
DO - 10.1146/annurev.nutr.21.1.167
M3 - Article
VL - 21
SP - 167
EP - 192
JO - Annual Review of Nutrition
JF - Annual Review of Nutrition
SN - 0199-9885
ER -