Innate lymphoid cells: NK and cytotoxic ILC3 subsets infiltrate metastatic breast cancer lymph nodes

Oncoimmunology. 2022 Mar 30;11(1):2057396. doi: 10.1080/2162402X.2022.2057396. eCollection 2022.

Abstract

Innate lymphoid cells (ILCs) - which include cytotoxic Natural Killer (NK) cells and helper-type ILC - are important regulators of tissue immune homeostasis, with possible roles in tumor surveillance. We analyzed ILC and their functionality in human lymph nodes (LN). In LN, NK cells and ILC3 were the prominent subpopulations. Among the ILC3s, we identified a CD56+/ILC3 subset with a phenotype close to ILC3 but also expressing cytotoxicity genes shared with NK. In tumor-draining LNs (TD-LNs) and tumor samples from breast cancer (BC) patients, NK cells were prominent, and proportions of ILC3 subsets were low. In tumors and TD-LN, NK cells display reduced levels of NCR (Natural cytotoxicity receptors), despite high transcript levels and included a small subset CD127- CD56- NK cells with reduced function. Activated by cytokines CD56+/ILC3 cells from donor and patients LN acquired cytotoxic capacity and produced IFNg. In TD-LN, all cytokine activated ILC populations produced TNFα in response to BC cell line. Analyses of cytotoxic and helper ILC indicate a switch toward NK cells in TD-LN. The local tumor microenvironment inhibited NK cell functions through downregulation of NCR, but cytokine stimulation restored their functionality.

Keywords: Innate lymphoid cells; breast cancers; natural killer cells; tumor draining lymph nodes.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents*
  • Breast Neoplasms* / metabolism
  • Female
  • Humans
  • Immunity, Innate
  • Killer Cells, Natural / metabolism
  • Lymph Nodes / pathology
  • Tumor Microenvironment

Substances

  • Antineoplastic Agents

Grants and funding

EP, and CS received funds from Agence Nationale de la Recherche (ANR) ANR-10-IDEX-0001-02 PSL* and ANR-11-LABX-0043; CIC IGR-Curie 1428 (Center for Clinical Investigation) and INCa-DGOSInserm_10.13039/501100006364 Institut National Du Cancer 12554.