Mincle is not essential for controlling Mycobacterium tuberculosis infection

Area of Science:

• Immunology
• Microbiology
• Infectious Diseases

Background:

• Toll-like receptors (TLR) and NOD-like receptors contribute limitedly to the innate immune response against Mycobacterium tuberculosis (Mtb).
• Trehalose-6,6'-dimycolate (TDM), a mycobacterial glycolipid, is implicated in early Mtb infection responses.
• Macrophage inducible C-type lectin (Mincle) is a known TDM receptor, but its role during live Mtb infection is unclear.

Purpose of the Study:

• To investigate the significance of Mincle in the host immune response to Mtb infection.
• To determine if Mincle is essential for sensing Mtb and initiating protective immunity.

Main Methods:

• Mtb infection was analyzed in Mincle-deficient mice.
• Macrophage responses to TDM were assessed in the absence of Mincle.
• Granuloma formation, T helper cell responses (TH1, TH17), and control of mycobacterial growth were evaluated.

Main Results:

• Mincle-deficient macrophages did not respond to TDM.
• Mincle-deficient mice exhibited efficient granulomatous and protective immune responses to Mtb infection.
• Normal TH1 and TH17 responses, effective macrophage effector mechanisms, and control of Mtb growth were observed in mutant mice.

Conclusions:

• The absence of Mincle can be fully compensated for in vivo regarding Mtb sensing and mounting protective immune responses.
• Mincle is not essential for initiating an effective innate and adaptive immune response to Mtb infection.