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A Gamma Interferon Independent Mechanism of CD4 T Cell Mediated
Control of Infection


CD4 T cell deficiency or defective IFNγ signaling render humans and mice

highly susceptible to Mycobacterium tuberculosis (Mtb)

infection. The prevailing model is that Th1 CD4 T cells produce IFNγ to

activate bactericidal effector mechanisms of infected macrophages. Here we test

this model by directly interrogating the effector functions of Th1 CD4 T cells

required to control Mtb in vivo. While Th1 CD4 T cells specific for the Mtb

antigen ESAT-6 restrict in vivo Mtb growth, this inhibition is independent of

IFNγ or TNF and does not require the perforin or FAS effector pathways.

Adoptive transfer of Th17 CD4 T cells specific for ESAT-6 partially inhibited

Mtb growth while Th2 CD4 T cells were largely ineffective. These results imply a

previously unrecognized IFNγ/TNF independent pathway that efficiently

controls Mtb and suggest that optimization of this alternative effector function

may provide new therapeutic avenues to combat Mtb through vaccination.


Vyšlo v časopise: A Gamma Interferon Independent Mechanism of CD4 T Cell Mediated Control of Infection. PLoS Pathog 7(5): e32767. doi:10.1371/journal.ppat.1002052
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.ppat.1002052

Souhrn

CD4 T cell deficiency or defective IFNγ signaling render humans and mice

highly susceptible to Mycobacterium tuberculosis (Mtb)

infection. The prevailing model is that Th1 CD4 T cells produce IFNγ to

activate bactericidal effector mechanisms of infected macrophages. Here we test

this model by directly interrogating the effector functions of Th1 CD4 T cells

required to control Mtb in vivo. While Th1 CD4 T cells specific for the Mtb

antigen ESAT-6 restrict in vivo Mtb growth, this inhibition is independent of

IFNγ or TNF and does not require the perforin or FAS effector pathways.

Adoptive transfer of Th17 CD4 T cells specific for ESAT-6 partially inhibited

Mtb growth while Th2 CD4 T cells were largely ineffective. These results imply a

previously unrecognized IFNγ/TNF independent pathway that efficiently

controls Mtb and suggest that optimization of this alternative effector function

may provide new therapeutic avenues to combat Mtb through vaccination.


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Štítky
Hygiena a epidemiológia Infekčné lekárstvo Laboratórium

Článok vyšiel v časopise

PLOS Pathogens


2011 Číslo 5
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Autori: MUDr. Tomáš Ürge, PhD.

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