Table 2: Effect of intestinal helminth infections or their products on DC function.

Intestinal helminth productDC subsetDC responseReferences

Ascaris suumHigh molecular weight components of adult wormsCD11c+ MLN DCsDownregulation of CD 40, CD 80, CD86, and MHCII induced by immunization. Production of IL-10.[40]
Heligmosomoides polygyrus InfectionCD11c+ Spleen and MLN DCsActivation with upregulation of CD80 and CD86. Production of IL-10. Inhibition of protective response against bacteria and exacerbated colonic inflammation (pasive transfer of Hp-DCs).[41, 42]
E/S productsBone marrow DCsInhibition of cytokine production. Inhibition of upregulation of CD40, CD86, and MHCII by TLR engagement. Induction of IL-10 producing T cells (regulatory T cells).[43]
Necator americanusE/S productsHuman monocyte-derived DCDownregulation of CD86, CD1a, HLA-ABC, and HLA-DR resulting in a diminished capacity to induce T cell proliferation.[44]
Nippostrongylus brasiliensisE/S productsBone marrow DCsUpregulation of CD86 and Ox40L. No effect on CD80 and MHCI. Production of IL-6, IL-10, and IL-12 p40. Inhibition of LPS-induced IL-12 p70.[45]
InfectionCD11c+ CD8 𝛼 i n t CD103+Reduction of this subpopulation during infection. Reduction of CD86 and Dec 205. Reduced production of ll-12 and increase in IL-6, TNF 𝛼 , and IL-10. In H. polygyrus infection reduction of this DC subset is more pronounced.[46]
Trichuris murisInfection (E-J isolate)CD11c+ MLN DCsExpansion of DCs correlates with worm expulsion. Production of IL-4, IL-13, and IL-10.[4749]
E/S products (S, J, E isolates)Bone marrow DCsS isolate induces higher levels of IL-6 and IL-10. Upregulation of CD 40 by all three isolates.[50]
InfectionCD11c+ MLN DCsThymic Stromal Lymphopoietin (TSLP) produced by intestinal epithelial cells (IECs) interacts with DCs inhibiting LPS-induced IL12/23p40 and increasing IL-13 production.[51, 52]