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Lewis-antigen-containing ICAM-2/3 on Jurkat leukemia cells interact with DC-SIGN to regulate DC functions

Xin Jin1, Qingpan Bu2, Yingying Zou1

  • 1Key Laboratory of Molecular Epigenetics of the Ministry of Education (MOE), Northeast Normal University, 5268 Renmin Street, Changchun, Jilin, 130024, People's Republic of China.

Glycoconjugate Journal
|April 20, 2018
PubMed

Insights

Dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin (DC-SIGN) binds malignant T lymphocytes via ICAM-2/3 and Lewis antigens. This interaction impacts dendritic cell maturation and T cell differentiation.

Area of Science:

  • Immunology
  • Cell Biology
  • Oncology

Background:

  • Dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin (DC-SIGN) is a C-type lectin involved in pathogen and self-antigen recognition.
  • DC-SIGN's interaction with acute T lymphoblastic leukemia (T-ALL) cells has been observed, but the underlying mechanisms and functional consequences remain unclear.

Purpose of the Study:

  • To elucidate the mechanism of DC-SIGN-mediated association with T-ALL cells.
  • To investigate the role of DC-SIGN in regulating dendritic cell (DC) function and T cell differentiation in the context of T-ALL.

Main Methods:

  • Binding assays to assess DC-SIGN interaction with various T-ALL cell lines (Jurkat, CCRF-HSB2, CCRF-CEM).
  • Blocking experiments using antibodies against ICAM-2/3 and analysis of Lewis antigen expression.
  • Transcriptome analysis to identify genes involved in DC-SIGN ligand expression, focusing on fucosyltransferase 4 (FUT4).
  • Assessment of DC maturation markers and T cell differentiation markers upon co-culture with T-ALL cells.

Main Results:

  • DC-SIGN preferentially binds to malignant T lymphocytes, notably Jurkat cells.
  • ICAM-2/3 on Jurkat cells serve as ligands for DC-SIGN, and their blockade significantly reduces binding.
  • ICAM-2/3 display Lewis X, Lewis Y, and Lewis A residues crucial for DC-SIGN recognition.
  • FUT4 is upregulated in Jurkat cells, and its downregulation limits DC-SIGN binding, highlighting its role in Lewis antigen expression.
  • Jurkat cells impair DC maturation, and blocking DC-SIGN enhances these effects on DC function and T cell differentiation.

Conclusions:

  • DC-SIGN mediates the association of dendritic cells with acute T lymphoblastic leukemia cells.
  • The interaction is dependent on ICAM-2/3 and their Lewis antigen residues, regulated by FUT4.
  • DC-SIGN plays a significant role in orchestrating DC functions and T cell responses in the context of T-ALL.

Keywords:
DC-SIGNFUT4ICAM-2ICAM-3Immune responseLewis antigens

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