In childhood TB, the immune inhibitory molecules, IL1RN and IL1R2 which inhibit functional IL1 signaling, and molecules involved in generation of an adaptive immune response (CD40LG, HAL‐DOB, CD28) that were downregulated is consistent with emerging evidence linking the cross talk between IL1 and type 1 IFN to TB and which provide potential targets for host directed therapy. This evidence concerns the gene CD28 and tuberculosis.