MyDths and un-TOLLed truths: sensor, instructive and effector immunity to tuberculosis.

Abstract:

:Controversy exists concerning the role of Toll-like receptors and MyD88 in immunity to tuberculosis (TB). This mini-review argues that (i) Toll-like receptors are not essential for an effective immune response against TB, (ii) MyD88 is essential, but not because it transduces signals from TLRs, (iii) adaptive immunity to TB is largely TLR/MyD88-independent. Some of the discrepancies may be resolved by cogent attribution of distinct immune functions to the individual components of the TLR/MyD88 system. In mice, TLRs and MyD88 are fully dispensable in sensing Mtb infection and instructing T cell-mediated adaptive immunity, and while TLRs are also redundant during macrophage effector immunity, MyD88 is essential for efficient killing of mycobacteria. This distinction should help to molecularly pinpoint the MyD88-dependent, yet TLR-independent critical mechanisms of macrophage activation involved in intracellular growth restriction of Mtb. Disrupted IL-1R and/or IFN-gamma signaling pathways likely play a much more prominent role in explaining the exquisite susceptibility of MyD88-deficient mice to TB than the function of MyD88 as a TLR adaptor.

journal_name

Immunol Lett

journal_title

Immunology letters

authors

Reiling N,Ehlers S,Hölscher C

doi

10.1016/j.imlet.2007.11.015

subject

Has Abstract

pub_date

2008-02-15 00:00:00

pages

15-23

issue

1

eissn

0165-2478

issn

1879-0542

pii

S0165-2478(07)00298-2

journal_volume

116

pub_type

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