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Interleukin-2 (IL-2) inducible T-cell kinase (ITK) is a non-receptor tyrosine kinase highly expressed in T-cell lineages and regulates multiple aspects of T-cell development and function, mainly through its function downstream of the T-cell receptor.  Itk  deficiency can lead to CD4 lymphopenia and Epstein-Bar virus (EBV)-associated lymphoproliferation and recurrent pulmonary infections in humans. However, the role of the ITK signaling pathway in pulmonary responses in active tuberculosis due to  Mtb  infection is not known. We show here that human lungs with active tuberculosis exhibit altered T-cell receptor/ITK signaling and that  Itk  deficiency impaired early protection against  Mtb  in mice, accompanied by defective development of IL-17A-producing γδ T cells in the lungs. These findings have important implications of human genetics associated with susceptibility to  Mtb  due to altered immune responses and molecular signals modulating host immunity that controls  Mtb  activity. Enhancing ITK signaling pathways may be an alternative strategy to target  Mtb  infection, especially in cases with highly virulent strains in which IL-17A plays an essential protective role.

Interleukin-2-Inducible T-Cell Kinase Deficiency Impairs Early Pulmonary Protection Against Mycobacterium tuberculosis Infection