From:  Vitamin B12 as an immunometabolic regulator: bridging one-carbon metabolism, mitochondrial function and immunity

 Clinical and immunological consequences of vitamin B12 deficiency [4, 1921, 2327].

ConditionImmune effectMechanism/ObservationsReferences
Autoimmune diseases (multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus)Reduced Treg numbers, impaired toleranceFOXP3 hypomethylation; dysregulated Th1/Th2 balance[4, 19, 20, 23]
Immunosenescence/AgingReduced T cell repertoire, decreased NK activity, poor vaccine responseDeficient vitamin B12 → impaired proliferation, elevated homocysteine[4, 19, 21, 2325]
Infectious diseasesIncreased susceptibility to bacterial and viral infectionsImpaired macrophage activation, reduced interferon production[4, 1921, 23, 25]
Chronic inflammatory diseases (diabetes, atherosclerosis)Endothelial inflammation, oxidative stressElevated homocysteine; impaired nitric oxide (NO) metabolism[4, 1921, 23, 25]
Dysbiosis/Gut immune dysregulationAltered SCFA production, Treg differentiationReduced beneficial microbiota, increased pro-inflammatory taxa[21, 2427]

Summary of major clinical conditions associated with vitamin B12 deficiency and immunological consequences. FOXP3: forkhead box P3; NK: natural killer; SCFA: short-chain fatty acid; Treg: regulatory T cell.