Neoplastic b-cell growth is impaired by hla-g/ilt2 interaction

Access through your institution Buy or subscribe Deregulation of B-cell proliferation may induce malignant growth causing various lymphoproliferative disorders including the most prevalent

hematological malignancies in adult, namely lymphoma, multiple myeloma (MM) and B-cell chronic lymphocytic leukemia.1 Inducing depletion through an apoptotic pathway or inhibiting B-cell

proliferation and differentiation constitutes a rational approach to cure B-cell-mediated disorders. One such modality used recently in B-cell malignancies is rituximab, a B-cell-depleting

monoclonal antibody against CD20.2 Nevertheless, efforts to identify novel therapeutic targets remain essential. Like NK, T and antigen-presenting cells, B cells express immunoreceptor

tyrosine-based inhibitory motif bearing receptors such as the leukocyte immunoglobulin-like receptor LILRB1/ILT2/CD85j.3 ILT2 is characterized by a broad specificity for HLA class-I

molecules, with the highest affinity for HLA-G. However, no information is currently available on the role of ILT2 and HLA-G in regulating neoplastic B-cell growth. The biological functions

of HLA-G have been originally described in maternal-fetal tolerance and more recently in allograft acceptance and tumor escape showing evidences for its tolerogenic properties.4 In contrast

to classical HLA-class I, HLA-G is expressed in a limited number of healthy tissues and can be expressed as seven isoforms including four membrane-bound (HLA-G1–HLA-G4) and three soluble

(HLA-G5–HLA-G7) proteins.4 This is a preview of subscription content, access via your institution ACCESS OPTIONS Access through your institution Subscribe to this journal Receive 12 print

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local taxes which are calculated during checkout ADDITIONAL ACCESS OPTIONS: * Log in * Learn about institutional subscriptions * Read our FAQs * Contact customer support REFERENCES *

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Commissariat à l’Energie Atomique et aux energies alternatives. We thank Drs N Mooney and JC Bories for providing us with the B-cell malignant cell lines. We thank Florent Montespan and

Chantal Schenowitz for technical help. AUTHOR INFORMATION Author notes * A Naji and C Menier: These authors contributed equally to this work. AUTHORS AND AFFILIATIONS * CEA, Institut des

Maladies Emergentes et des Therapies Innovantes (iMETI), Service de Recherche en Hemato-Immunologie (SRHI), Hopital Saint-Louis, Paris, France A Naji, C Menier, G Maki, E D Carosella & N

Rouas-Freiss * Univ Paris Diderot, Sorbonne Paris Cite, UMR E_5 Institut Univ.Hematologie, Hopital Saint Louis, Paris, France A Naji, C Menier, G Maki, E D Carosella & N Rouas-Freiss

Authors * A Naji View author publications You can also search for this author inPubMed Google Scholar * C Menier View author publications You can also search for this author inPubMed Google

Scholar * G Maki View author publications You can also search for this author inPubMed Google Scholar * E D Carosella View author publications You can also search for this author inPubMed 

Google Scholar * N Rouas-Freiss View author publications You can also search for this author inPubMed Google Scholar CORRESPONDING AUTHOR Correspondence to N Rouas-Freiss. ETHICS

DECLARATIONS COMPETING INTERESTS The authors declare no conflict of interest. ADDITIONAL INFORMATION Supplementary Information accompanies the paper on the Leukemia website SUPPLEMENTARY

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THIS ARTICLE Naji, A., Menier, C., Maki, G. _et al._ Neoplastic B-cell growth is impaired by HLA-G/ILT2 interaction. _Leukemia_ 26, 1889–1892 (2012). https://doi.org/10.1038/leu.2012.62

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