This was demonstrated when evaluating IgG from atopic individuals that modulate the production of IFN-γ by CD4+ and CD8+ T cells (20), IgG from Atopic Dermatitis patients that modulates the production of IL-17 and IL-10 by CD4+ and CD8+ T cells (21), or IgG from HIV-1-exposed non-infected and infected individuals that modulates the production of IFN-γ by αβT (CD4+ and CD8+), γδT and B cells (22). This evidence concerns the gene IFNG and atopic eczema.