Cited by 167Immune Cell Function and InteractionImmune cells in cancerPhagocytosis and Immune Regulation

LILRB receptor-mediated regulation of myeloid cell maturation and function

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van der Touw, William, Chen, Hui-Ming, Pan, Ping-Ying, Chen, Shu-Hsia·2017·Cancer Immunology, Immunotherapy

Abstract

The leukocyte immunoglobulin-like receptor (LILR) family comprises a set of paired immunomodulatory receptors expressed among human myeloid and lymphocyte cell populations. While six members of LILR subfamily A (LILRA) associate with membrane adaptors to signal via immunoreceptor tyrosine-based activating motifs (ITAM), LILR subfamily B (LILRB) members signal via multiple cytoplasmic immunoreceptor tyrosine-based inhibitory motifs (ITIM). Ligand specificity of some LILR family members has been studied in detail, but new perspective into the immunoregulatory aspects of this receptor family in human myeloid cells has been limited. LILRB receptors and the murine ortholog, paired immunoglobulin-like receptor B (PIRB), have been shown to negatively regulate maturation pathways in myeloid cells including mast cells, neutrophils, dendritic cells, as well as B cells. Our laboratory further demonstrated in mouse models that PIRB regulated functional development of myeloid-derived suppressor cell and the formation of a tumor-permissive microenvironment. Based on observations from the literature and our own studies, our laboratory is focusing on how LILRs modulate immune homeostasis of human myeloid cells and how these pathways may be targeted in disease states. Integrity of this pathway in tumor microenvironments, for example, permits a myeloid phenotype that suppresses antitumor adaptive immunity. This review presents the evidence supporting a role of LILRs as myeloid cell regulators and ongoing efforts to understand the functional immunology surrounding this family.

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  • LILRB proteins are type I transmembrane receptors predominantly expressed on hematopoietic cells.

    “The LILRB proteins are type I transmembrane receptors predominantly expressed on hematopoietic cells14–20.”

    From Oligomeric cystatin C supports the immunosuppressive activity of myeloid cells through interaction with inhibitory receptors (2025) · cites this paper as [17]

    The Introduction (page unavailable) says LILRB expression is enriched in myeloid cells and also occurs in other immune cells, supporting predominant expression on hematopoietic cells. It describes LILRBs as receptors with cytoplasmic signaling domains, but does not identify them as type I transmembrane receptors. (LLM, conf=0.82)

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Authors
van der Touw, W., Chen, H.-M., Pan, P.-Y., & Chen, S.-H.
Affiliations
  • Houston Methodist Research Institute (US)
  • Houston Methodist (US)
Corresponding author
Chen, Shu-Hsia
Venue
Cancer Immunology, Immunotherapy
Published
2017-06-21
Volume
66
Issue
8
Pages
1079-1087
ISSN
  • 0340-7004 (ISSN-L)
  • 1432-0851
OpenAlex
W2677663897
Cited by
167
References
0
Citations by year
2026: 16 · 2025: 23 · 2024: 23 · 2023: 33 · 2022: 19 · 2021: 16 · 2020: 22 · 2019: 9 · 2018: 4 · 2017: 1
FWCI
1.01
Type
journal article
Language
en
Open access
Locations
  • Cancer Immunology Immunotherapy (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Cancer Institute (CA 127483; CA 208703, CA140243;CA188610)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Cell Function and Interaction
  • Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
  • Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
Keywords
myeloid cell maturation, ITIM, myeloid-derived suppressor cells, tumor microenvironment, mast cells, neutrophils, dendritic cells, B cells, immune homeostasis, antitumor immunity
MeSH terms
Myeloid-Derived Suppressor Cells, Leukocyte Immunoglobulin-like Receptor B1, Animals, Humans, Leukocytes, Neoplasms, Receptors, Immunologic, Signal Transduction, Antigens, CD, Gene Expression Regulation, Neoplastic, Mice, Immunomodulation, Tumor Microenvironment

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