A proline deletion in IFNAR1 impairs IFN-signaling and underlies increased resistance to tuberculosis in humans

Abstract

The role of type I interferons in bacterial infection is less clear than it is in viral infection. Here, the authors show that genetic variation of the human IFNAR1 gene is associated with decreased susceptibility to tuberculosis and identify a role for the IFNAR1 inter-domain region in the cytokine response.