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Published on: January 13, 2016
The role of ADAM17 in the T-cell response against bacterial pathogens
Moritz Andreas Link1, Karsten Lücke1, Joanna Schmid1
1Institute of Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Abstract:
ADAM17 is a member of the A Disintegrin And Metalloproteinase family of proteases. It is ubiquitously expressed and causes the shedding of a broad spectrum of surface proteins such as adhesion molecules, cytokines and cytokine receptors. By controlled shedding of these proteins from leukocytes, ADAM17 is able to regulate immune responses. Several ADAM17 targets on T cells have been implicated in T-cell migration, differentiation and effector functions. However, the role of ADAM17 in T-cell responses is still unclear. To characterize the function of ADAM17 in T cells, we used Adam17fl/fl×CD4cre+ mice with a T-cell restricted inactivation of the Adam17 gene. Upon stimulation, ADAM17-deficient CD4+ and CD8+ T cells were impaired in shedding of CD62L, IL-6Rα, TNF-α, TNFRI and TNFRII. Surprisingly, we could not detect profound changes in the composition of major T-cell subsets in Adam17fl/fl×CD4cre+ mice. Following infection with Listeria monocytogenes, Adam17fl/fl×CD4cre+ mice mounted regular listeria-specific CD4+ TH1 and CD8+ T-cell responses and were able to control primary and secondary infections. In conclusion, our study indicates that ADAM17 is either not required in T cells under homoeostatic conditions and for control of listeria infection or can be effectively compensated by other mechanisms.
Insights
ADAM17 (A Disintegrin And Metalloproteinase 17) deficiency in T cells did not impact immune responses during Listeria infection. These findings suggest ADAM17 may not be essential for T-cell function or can be compensated by other pathways.
Area of Science:
- Immunology
- Molecular Biology
- Protease Function
Background:
- ADAM17 (A Disintegrin And Metalloproteinase 17) is a protease involved in shedding surface proteins.
- It regulates immune responses by cleaving targets on leukocytes, including T cells.
- The precise role of ADAM17 in T-cell immunity remains incompletely understood.
Purpose of the Study:
- To investigate the function of ADAM17 in T cells.
- To determine the impact of T-cell-specific ADAM17 deficiency on immune responses.
- To elucidate the necessity of ADAM17 for T-cell migration, differentiation, and effector functions.
Main Methods:
- Utilized Adam17fl/fl×CD4cre+ mice for conditional T-cell-specific gene inactivation.
- Stimulated T cells to assess protein shedding and T-cell subset composition.
- Infected mice with Listeria monocytogenes to evaluate adaptive immune responses.
Main Results:
- ADAM17-deficient T cells showed impaired shedding of CD62L, IL-6Rα, TNF-α, TNFRI, and TNFRII upon stimulation.
- No significant alterations in major T-cell subset composition were observed in deficient mice.
- Mice lacking ADAM17 in T cells mounted effective CD4+ TH1 and CD8+ T-cell responses against Listeria monocytogenes.
Conclusions:
- ADAM17 is dispensable for T-cell homeostasis and controlling Listeria monocytogenes infection.
- T-cell-intrinsic ADAM17 function can be compensated by alternative mechanisms.
- Further research is needed to fully understand ADAM17's role in adaptive immunity.
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