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. 2019 May 3;10:961. doi: 10.3389/fimmu.2019.00961

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Copyright © 2019 Poggi, Benelli, Venè, Costa, Ferrari, Tosetti and Zocchi.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Crohn Disease (CD) and Ulcerative colitis (UC) pathogenesis: possible role of NK cells. Different Th1/Th2 responses in CD and UC. Mϕ, macrophages; DC, dendritic cells; NK, natural killer cells; NKT, natural killer-like T cells. (A) Crohn's Disease is mainly a Th1/Th17 IBD, linked to a KIR2DL3/HLA-C1 genotype in NK cells. Mucosal NK cells are RORC, CD127 (IL7Rα), NKG2D and NKp46 positive, produce IL22 and IFNγ when activated via IL23 and contribute to the expansion of CD4⁺ Th1/Th17 lymphocytes that, in turn, secrete both IFNγ and TNFα, in addition to IL17. (B) Ulcerative Colitis is mainly an atypical Th2 IBD, linked to a KIR2DL5/2DS1 genotype in NK cells. Atypical NKT produce IL13, which induces epithelial damage. In turn, NK cells are unable to induce an efficient TNFα IFNγ response to reduce the Th1/Th2 imbalance, contrasting excessive IL13 secretion.