Nrf2 activation by sulforaphane restores the age-related decrease of TH1 immunity: Role of dendritic cells

Abstract

SFN and NAC upregulate T(H)1 immunity in aging through a restoration of redox equilibrium.

An increased need for dietary cysteine in support of glutathione synthesis may underlie the increased risk for mortality associated with low protein intake in the elderly

“…With respect to the impact of NAC on cell-mediated immunity-the efficiency of which typically declines with aging-there is evidence that glutathione is crucially important to efficient function of dendritic cells, the central coordinators of cell-mediated immunity (Kim et al 2007). Moreover, administration of NAC to aging mice has been shown to restore the delayed-type hypersensitivity to more youthful levels, in precise parallel to the findings of the Italian clinical trial with NAC (Kim et al 2008). …”

Association of Systemic Oxidative Stress with Suppressed Serum IgG to Commensal Oral Biofilm and Modulation by Periodontal Infection

“…Overall, it appears that oxidative stress is associated with suppression of Th1-mediated responses and increased Th2-mediated responses. Recent findings indicate that Nrf2, a redox-sensitive transcription factor that enhances expression of antioxidant genes, has an important role in the molecular mechanism whereby oxidative stress modifies Th1 responses mediated by APCs (34). In preclinical testing, Nrf2 pathway activation in dendritic cells enhanced Th1 immunity (34), whereas disruption of Nrf2 expression promoted prooxidative dendritic cells that led to increased Th2 responses (62).…”

Keratinocytes, Innate Immunity and Allergic Contact Dermatitis - Opportunities for the Development of In Vitro Assays to Predict the Sensitizing Potential of Chemicals

“…The ear swelling in response to DNFB and oxazolone was reduced but not completely prevented in old (but not young) Nrf2 deficient mice. Furthermore, in these old mice it was shown that IFN- but not IL-4 production was absent, indicating that Nrf2 plays a role in the type 1 T cell response (Kim et al, 2008).…”

“…In Nrf2 deficient mice, the severity of disease in a colitis model was aggravated and this was attributed to increased levels of IL1-, IL-6, IL12p40, and TNF-, (Khor et al, 2006). In old mice deficient of Nrf2, skin sensitization was less pronounced, meaning that Nrf2 is essential for the skin sensitization process (Kim et al, 2008). Hence, Nrf2 has an important role in regulating immune responses.…”