The pathophysiology of TB-IRIS is largely speculative but believed to be a type IV hypersensitivity reaction.4 The lymphocyte CD4-Th1 immune cells increase production of pro-inflammatory cytokines interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and in particular, interferon-γ (IFN-γ).6 These cytokines are known to lead to a widespread neutrophilic response.4 Other CD4 T-helper cells, such as Th17 cells, which are characterized by their production of IL-17, have been suggested to play a part in TB-IRIS but their role has not been well described.6 Here, IFNG is linked to tuberculosis.