ArticleProceedings of the National Academy of Sciences of the United States of America2003
Human inhibitory receptors Ig-like transcript 2 (ILT2) and ILT4 compete with CD8 for MHC class I binding and bind preferentially to HLA-G.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 229 papers.
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Who cites it
229 citing papers in PubMed, 541 citations in OpenAlex.
- Immunoglobulin-like transcript receptors on human dermal CD14+ dendritic cells act as a CD8-antagonist to control cytotoxic T cell priming.Proceedings of the National Academy of Sciences of the United States of America · 2012Trial
- LILRB2 inhibition by blocking antibody ES009 reprograms immunosuppressive myeloid cells and enhances T-cell-mediated tumor immunity.Human vaccines & immunotherapeutics · 2026Article
- Article
- Immunology of Normal Pregnancy and Preeclampsia and the Role of Placental Non-Classical HLA and Decidual NK Cells.International journal of molecular sciences · 2026Review
- The challenge and promise of studying human antigen-specific T cells.Nature reviews. Immunology · 2026Review
- Role of soluble human leukocyte antigen-G in virus-associated cancers: A focused minireview.World journal of virology · 2026Review
- Review
- Nonclassical MHC-I Molecules: Emerging Therapeutic Targets in Next-Generation Immunotherapy.MedComm · 2026Review
- Molecular basis of fibrinogen recognition by the innate immune receptor LILRA2.The Journal of biological chemistry · 2026Article
- LILRB1 Is a Prognostic-Related Biomarker Correlated With Immune Infiltration in Head-Neck Squamous Cell Carcinoma.Cancer medicine · 2026Article
- Unlocking the promise of innate biology through the HLA-G/ILT2/ILT4 pathway.Journal for immunotherapy of cancer · 2026Review
- A Subset of Pro-inflammatory CXCL10+ LILRB2+ Macrophages Derives From Recipient Monocytes and Drives Renal Allograft Rejection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Human leukocyte antigen-G in solid tumors: from immunotolerance to immunotherapy.Frontiers in immunology · 2026Review
- Hampered CD8 + ILT2 + T cell activation by HLA-G suggests a new immune checkpoint in gastric adenocarcinoma.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2026Article
- Targeting MHC-E as a new strategy for vaccines and immunotherapeutics.Nature reviews. Immunology · 2026Review
- The non-classical immune checkpoint HLA-G: a regulatory master switch governing tolerance, evasion, and translational frontiers.Frontiers in oncology · 2026Review
- Article
- Antibody-Mediated Inhibition of HLA/LILR Interactions Breaks Innate Immune Tolerance and Induces Antitumor Immunity.Cancer immunology research · 2025Article
- Article
- The progression of multiple myeloma is regulated by LILRB1 via the GATA2-SAGE1 pathway.British journal of haematology · 2025Article
169 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ig-like transcript 4 (ILT4) (also known as leukocyte Ig-like receptor 2, CD85d, and LILRB2) is a cell surface receptor expressed mainly on myelomonocytic cells, whereas ILT2 (also known as leukocyte Ig-like receptor 1, CD85j, and LILRB1) is expressed on a wider range of immune cells including subsets of natural killer and T cells. Both ILTs contain immunoreceptor tyrosine-based inhibitory receptor motifs in their cytoplasmic tails that inhibit cellular responses by recruiting phosphatases such as SHP-1 (Src homology 2 domain containing tyrosine phosphatase 1). Although these ILTs have been shown to recognize a broad range of classical and nonclassical human MHC class I molecules (MHCIs), their precise binding properties remain controversial. We have used surface plasmon resonance to analyze the interaction of soluble forms of ILT4 and ILT2 with several MHCIs. Although the range of affinities measured was quite broad (Kd = 2-45 microM), some interesting differences were observed. ILT2 generally bound with a 2- to 3-fold higher affinity than ILT4 to the same MHCI. Furthermore, ILT2 and ILT4 bound to HLA-G with a 3- to 4-fold higher affinity than to classical MHCIs, suggesting that ILT/HLA-G recognition may play a dominant role in the regulation of natural killer, T, and myelomonocytic cell activation. Finally, we show that ILT2 and ILT4 effectively compete with CD8 for MHCI binding, raising the possibility that ILT2 modulates CD8+ T cell activation by blocking the CD8 binding as well as by recruiting inhibitory molecules through its immunoreceptor tyrosine-based inhibitory receptor motif.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.