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. Author manuscript; available in PMC: 2016 Jan 1.

Published in final edited form as: Trends Immunol. 2014 Sep 20;36(1):3–12. doi: 10.1016/j.it.2014.08.003

(A) In Tregs, TCR and IL-2 signaling promotes Treg proliferation and function by activating mTORC1-dependent lipid biosynthesis, particularly the mevalonate pathway. mTORC1 also promotes Treg function through inhibition of mTORC2 activity. VAT-associated Tregs exhibit increased expression of PPAR-γ, which promotes fatty acid metabolism and hence stimulates the accumulation and suppressive phenotypes of Tregs residing in adipose tissue. (B) In conventional T cells, mTOR signaling inhibits Foxp3 induction partly by inducing HIF1α expression and HIF1α-dependent glycolysis. mTOR signaling promotes T_H1, T_H2, T_H17 and effector CD8⁺ T cell differentiation. However, mTORC1 signaling negatively regulates memory CD8⁺ T cell differentiation. Whether and how mTOR signaling controls Tfh differentiation is currently unknown.

(A) In Tregs, TCR and IL-2 signaling promotes Treg proliferation and function by activating mTORC1-dependent lipid biosynthesis, particularly the mevalonate pathway. mTORC1 also promotes Treg function through inhibition of mTORC2 activity. VAT-associated Tregs exhibit increased expression of PPAR-γ, which promotes fatty acid metabolism and hence stimulates the accumulation and suppressive phenotypes of Tregs residing in adipose tissue. (B) In conventional T cells, mTOR signaling inhibits Foxp3 induction partly by inducing HIF1α expression and HIF1α-dependent glycolysis. mTOR signaling promotes T_H1, T_H2, T_H17 and effector CD8⁺ T cell differentiation. However, mTORC1 signaling negatively regulates memory CD8⁺ T cell differentiation. Whether and how mTOR signaling controls Tfh differentiation is currently unknown.