Mucosal associated invariant T cells from human breast ducts mediate a Th17-skewed response to bacterially exposed breast carcinoma cells

Breast Cancer Res. 2018 Sep 12;20(1):111. doi: 10.1186/s13058-018-1036-5.

Abstract

Background: Antimicrobial T cells play key roles in the disease progression of cancers arising in mucosal epithelial tissues, such as the colon. However, little is known about microbe-reactive T cells within human breast ducts and whether these impact breast carcinogenesis.

Methods: Epithelial ducts were isolated from primary human breast tissue samples, and the associated T lymphocytes were characterized using flow cytometric analysis. Functional assays were performed to determine T-cell cytokine secretion in response to bacterially treated human breast carcinoma cells.

Results: We show that human breast epithelial ducts contain mucosal associated invariant T (MAIT) cells, an innate T-cell population that recognizes specific bacterial metabolites presented by nonclassical MR1 antigen-presenting molecules. The MAIT cell population from breast ducts resembled that of peripheral blood in its innate lymphocyte phenotype (i.e., CD161, PLZF, and interleukin [IL]-18 receptor coexpression), but the breast duct MAIT cell population had a distinct T-cell receptor Vβ use profile and was markedly enriched for IL-17-producing cells compared with blood MAIT cells. Breast carcinoma cells that had been exposed to Escherichia coli activated MAIT cells in an MR1-dependent manner. However, whereas phorbol 12-myristate 13-acetate/ionomycin stimulation induced the production of both interferon-γ and IL-17 by breast duct MAIT cells, bacterially exposed breast carcinoma cells elicited a strongly IL-17-biased response. Breast carcinoma cells also showed upregulated expression of natural killer group 2 member D (NKG2D) ligands compared with primary breast epithelial cells, and the NKG2D receptor contributed to MAIT cell activation by the carcinoma cells.

Conclusions: These results demonstrate that MAIT cells from human breast ducts mediate a selective T-helper 17 cell response to human breast carcinoma cells that were exposed to E. coli. Thus, cues from the breast microbiome and the expression of stress-associated ligands by neoplastic breast duct epithelial cells may shape MAIT cell responses during breast carcinogenesis.

Keywords: Breast carcinoma; Breast duct; Microbe-reactive human T cells; Mucosal associated invariant T (MAIT) cells; NKG2D ligands; Th17 response.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Breast / cytology
  • Breast Neoplasms / immunology*
  • Breast Neoplasms / metabolism
  • Breast Neoplasms / microbiology
  • Cell Line, Tumor
  • Cells, Cultured
  • Cytokines / immunology
  • Cytokines / metabolism
  • Epithelial Cells / immunology*
  • Epithelial Cells / metabolism
  • Escherichia coli / immunology
  • Escherichia coli / physiology
  • Female
  • Histocompatibility Antigens Class I / genetics
  • Histocompatibility Antigens Class I / immunology
  • Humans
  • Interferon-gamma / immunology
  • Interferon-gamma / metabolism
  • Interleukin-17 / immunology*
  • Interleukin-17 / metabolism
  • Lymphocyte Activation / immunology
  • Minor Histocompatibility Antigens / genetics
  • Minor Histocompatibility Antigens / immunology
  • Mucosal-Associated Invariant T Cells / immunology*
  • Mucosal-Associated Invariant T Cells / metabolism

Substances

  • Cytokines
  • Histocompatibility Antigens Class I
  • IL17A protein, human
  • Interleukin-17
  • MR1 protein, human
  • Minor Histocompatibility Antigens
  • Interferon-gamma