REDUCED ANTIBODY RESPONSE

Th1-bias in vitamin A deficiency leads to reduced antibody response

Charles B Stephensen: VITAMIN A, INFECTION, AND IMMUNE FUNCTION Annu. Rev. Nutr. 2001. 21:167–92

Figure Effects of retinoic acid (RA) on cytokine production and of vitamin A deficiency (VAD) on mechanisms of immunity.
An antigen-presenting cell (APC) arrives in a lymph node carrying processed antigen from an invading pathogen. The antigen-naive T-helper (Th0) cell recognizes the antigen via its T-cell receptor. This recognition, in combination with interleukin (IL)-12 produced by the APC (green dashed →), stimulates development of Th1 memory cells or, in the presence of IL-4 (from Th2 cells mast cells or basophils), stimulates development of Th2 memory cells. Th1 cells produce interferon (IFN)-γ to stimulate immunity to intracellular pathogens and IL-2 to promote Th1 cell growth (blue dashed →). Th2 cells produce IL-4, which stimulates immunity to extracellular pathogens and Th2 cell growth, as well as other cytokines, such as IL-5. IFN-γ promotes development of Th1 cells (black → with red + sign) and blocks development of Th2 cells (black ┴ with red − sign). IL-4 has the opposite effects. RA blocks IL-12 and IFN-γ production and may enhance development of Th2 cells and IL-4 production (black → with question mark and red + sign). Immune mechanisms are either enhanced (↑), diminished (↓), or not-changed (↔) by vitamin A deficiency (? indicates equivocal data).
M, macrophage; NK, natural killer; CTL, cytotoxic T-lymphocyte; DTH, delayed-type hypersensitivity; Ig, immunoglobulin.