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10.7759/cureus.19401 Nazia Khan, Irma Hashmi, Liana Atallah, Hamid Shaaban, Gunwant Guron, Andre Fedida

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The ability of IL-12/IL-23 cytokines and IL-18 to induce NK-1R expression can be explained due to the ability of both of these cytokines to elicit cellular effects via NF-kB activation (Weinstock et al., 2003a), and the fact that the promoter region of the NK-1R gene contains a binding site for this transcription factor (Takahashi et al., 1992)

Evaluations of relapse timing, integrated with immune phenotyping data, further link early resistance to insufficient effector function and late-onset relapse to progressive loss of memory-sustaining T-cell subsets

This experiment was repeated, and data was combined