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West Ashley Library
9 a.m. – 7 p.m.
Phone: (843) 766-6635
Folly Beach Library
Closed
Phone: (843) 588-2001
Edgar Allan Poe/Sullivan's Island Library
Closed for renovations
Phone: (843) 883-3914
Wando Mount Pleasant Library
9 a.m. – 8 p.m.
Phone: (843) 805-6888
Village Library
9 a.m. – 6 p.m.
Phone: (843) 884-9741
St. Paul's/Hollywood Library
9 a.m. – 8 p.m.
Phone: (843) 889-3300
Otranto Road Library
9 a.m. – 8 p.m.
Phone: (843) 572-4094
Mt. Pleasant Library
9 a.m. – 8 p.m.
Phone: (843) 849-6161
McClellanville Library
9 a.m. - 6 p.m.
Phone: (843) 887-3699
Keith Summey North Charleston Library
9 a.m. – 8 p.m.
Phone: (843) 744-2489
John's Island Library
9 a.m. – 8 p.m.
Phone: (843) 559-1945
Hurd/St. Andrews Library
9 a.m. – 8 p.m.
Phone: (843) 766-2546
Miss Jane's Building (Edisto Library Temporary Location)
9 a.m. – 6 p.m.
Phone: (843) 869-2355
Dorchester Road Library
9 a.m. – 8 p.m.
Phone: (843) 552-6466
John L. Dart Library
9 a.m. – 7 p.m.
Phone: (843) 722-7550
Baxter-Patrick James Island
9 a.m. – 8 p.m.
Phone: (843) 795-6679
Main Library
9 a.m. – 8 p.m.
Phone: (843) 805-6930
Bees Ferry West Ashley Library
9 a.m. – 8 p.m.
Phone: (843) 805-6892
Mobile Library
9 a.m. - 5 p.m.
Phone: (843) 805-6909
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Targeting NKG2A to boost anti-tumor CD8 T-cell responses in human colorectal cancer.
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- Author(s): Ducoin, Kathleen; Oger, Romain; Mutala, Linda Bilonda; Deleine, Cécile; Jouand, Nicolas; Desfrançois, Juliette; Podevin, Juliette; Duchalais, Emilie; Cruard, Jonathan; Benlalam, Houssem; Labarrière, Nathalie; Bossard, Céline; Jarry, Anne; Gervois-Segain, Nadine
- Source:
OncoImmunology; 2022, Vol. 11 Issue 1, p1-16, 16p- Subject Terms:
- Source:
- Additional Information
- Abstract: The concept of exploiting tumor intrinsic deficiencies in DNA damage repair mechanisms by inhibiting compensatory DNA repair pathways is well established. For example, ATM-deficient cells show increased sensitivity to the ATR inhibitor ceralasertib. DNA damage response (DDR)-deficient cells are also more Recently, the inhibitory CD94/NKG2A receptor has joined the group of immune checkpoints (ICs) and its expression has been documented in NK cells and CD8+ T lymphocytes in several cancers and some infectious diseases. In colorectal cancer (CRC), we previously reported that NKG2A+ tumor-infiltrating lymphocytes (TILs) are predominantly CD8+ αβ T cells and that CD94 overexpression and/or its ligand HLA-E were associated with a poor prognosis. This study aimed to thoroughly characterize the NKG2A+ CD8+ TIL subpopulation and document the impact of NKG2A on anti-tumor responses in CRC. Our findings highlight new features of this subpopulation: (i) enrichment in colorectal tumors compared to paired normal colonic mucosa, (ii) their character as tissue-resident T cells and their majority terminal exhaustion status, (iii) co-expression of other ICs delineating two subgroups differing mainly in the level of NKG2A expression and the presence of PD-1, (iv) high functional avidity despite reduced proliferative capacity and finally (v) inhibition of anti-tumor reactivity that is overcome by blocking NKG2A. From a clinical point of view, these results open a promising alternative for immunotherapies based on NKG2A blockade in CRC, which could be performed alone or in combination with other IC inhibitors, adoptive cell transfer or therapeutic vaccination. [ABSTRACT FROM AUTHOR]
- Abstract: Copyright of OncoImmunology is the property of Taylor & Francis Ltd and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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