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000178063 041__ $$aEnglish
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000178063 1001_ $$0P:(DE-He78)1c2351213e0199e6bd4efaceac511917$$aHanna, Bola S$$b0$$eFirst author
000178063 245__ $$aInterleukin-10 receptor signaling promotes the maintenance of a PD-1int TCF-1+ CD8+ T cell population that sustains anti-tumor immunity.
000178063 260__ $$aNew York, NY$$bElsevier$$c2021
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000178063 500__ $$a#EA:B060#LA:B060# / 2021 Dec 14;54(12):2825-2841.e10
000178063 520__ $$aT cell exhaustion limits anti-tumor immunity and responses to immunotherapy. Here, we explored the microenvironmental signals regulating T cell exhaustion using a model of chronic lymphocytic leukemia (CLL). Single-cell analyses identified a subset of PD-1hi, functionally impaired CD8+ T cells that accumulated in secondary lymphoid organs during disease progression and a functionally competent PD-1int subset. Frequencies of PD-1int TCF-1+ CD8+ T cells decreased upon Il10rb or Stat3 deletion, leading to accumulation of PD-1hi cells and accelerated tumor progression. Mechanistically, inhibition of IL-10R signaling altered chromatin accessibility and disrupted cooperativity between the transcription factors NFAT and AP-1, promoting a distinct NFAT-associated program. Low IL10 expression or loss of IL-10R-STAT3 signaling correlated with increased frequencies of exhausted CD8+ T cells and poor survival in CLL and in breast cancer patients. Thus, balance between PD-1hi, exhausted CD8+ T cells and functional PD-1int TCF-1+ CD8+ T cells is regulated by cell-intrinsic IL-10R signaling, with implications for immunotherapy.
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000178063 650_7 $$2Other$$aCD8(+) T cells
000178063 650_7 $$2Other$$aCLL
000178063 650_7 $$2Other$$aIL-10
000178063 650_7 $$2Other$$aIL-10R
000178063 650_7 $$2Other$$aNFAT
000178063 650_7 $$2Other$$aPD-1 heterogeneity
000178063 650_7 $$2Other$$aSTAT3
000178063 650_7 $$2Other$$aT cell exhaustion
000178063 650_7 $$2Other$$aTCF-1
000178063 650_7 $$2Other$$atumor microenvironment
000178063 7001_ $$0P:(DE-HGF)0$$aLlaó-Cid, Laura$$b1
000178063 7001_ $$0P:(DE-He78)f28fcc92d5c00f3ee511e3319c699b38$$aIskar, Murat$$b2
000178063 7001_ $$0P:(DE-HGF)0$$aRoessner, Philipp M$$b3
000178063 7001_ $$0P:(DE-He78)dd57fd8197d9c5e0290f104db294e019$$aKlett, Lara C$$b4
000178063 7001_ $$0P:(DE-HGF)0$$aWong, John K L$$b5
000178063 7001_ $$0P:(DE-He78)1cd5686a9bcef9182c18a1cb799637d3$$aPaul, Yashna$$b6
000178063 7001_ $$0P:(DE-HGF)0$$aIoannou, Nikolaos$$b7
000178063 7001_ $$0P:(DE-He78)c3e32dca3eea6c46d4d140757aaf6e18$$aÖztürk, Selcen$$b8
000178063 7001_ $$0P:(DE-He78)e73a0a4fab40344d89d693cbe1df3109$$aMack, Norman$$b9
000178063 7001_ $$0P:(DE-He78)ece9c40a97e047bf607a89f04fcc7466$$aKalter, Verena$$b10
000178063 7001_ $$0P:(DE-HGF)0$$aColomer, Dolors$$b11
000178063 7001_ $$0P:(DE-HGF)0$$aCampo, Elías$$b12
000178063 7001_ $$0P:(DE-HGF)0$$aBloehdorn, Johannes$$b13
000178063 7001_ $$0P:(DE-HGF)0$$aStilgenbauer, Stephan$$b14
000178063 7001_ $$0P:(DE-He78)6333b389d0abc96ef7f2f6e049a8f8c4$$aDietrich, Sascha$$b15
000178063 7001_ $$0P:(DE-He78)b91bec47a4148ba68a58ab292d5860f2$$aSchmidt, Manfred$$b16
000178063 7001_ $$0P:(DE-He78)647431b5ca55b04fdf3c2fce31ef1915$$aGabriel, Richard$$b17
000178063 7001_ $$0P:(DE-He78)94de5f7413279464b6e738d91dfae1eb$$aRippe, Karsten$$b18
000178063 7001_ $$0P:(DE-He78)f0638edf1d3f61c0d7ebb587f511733f$$aFeuerer, Markus$$b19
000178063 7001_ $$0P:(DE-HGF)0$$aRamsay, Alan G$$b20
000178063 7001_ $$0P:(DE-He78)e13b4363c5fe858044ef8a39c02c870c$$aLichter, Peter$$b21
000178063 7001_ $$0P:(DE-He78)1beba8f953e7ae7e96e8d3e9a48f10f7$$aZapatka, Marc$$b22
000178063 7001_ $$0P:(DE-He78)e67f907703fcb2cf909f4d72d50268b5$$aSeiffert, Martina$$b23$$eLast author
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