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Identification and Biochemical Characterization of Human Plasma Soluble IL-7R: Lower Concentrations in HIV-1-Infected Patients¹

Thierry Rose^*, Olivier Lambotte, Coralie Pallier, Jean-François Delfraissy and Jean-Hervé Colle^2,

^* Institut Pasteur, Unité d’Immunogénétique Cellulaire, Paris France; Hôpital Bicêtre, Service de Médecine Interne, Le Kremlin-Bicêtre, France; Centre Hospitalier de l’Université Bicêtre, Laboratoire de Virologie, Le Kremlin-Bicêtre, France; and Institut Pasteur, Unité de Biologie des Populations Lymphocytaires, Centre National de la Recherche Scientifique, Unité de Recherche Associée 1961, Paris, France

The IL-7R -chain and the common -chain (_c) are both components of IL-7R. Human plasma harbors soluble forms of IL-7R (sIL-7R and s_c) that are detected and assayed by Western blotting, showing that the levels of sIL-7R are higher than the levels of s_c (47.5 ng/ml and 1.5 ng/ml, respectively). Gel electrophoresis and tandem mass spectrometry used to analyze deglycosylated, affinity-purified protein showed that sIL-7R is generated through differentially spliced mRNA, not by membrane receptor shedding. Plasma sIL-7R and s_c are present as heterocomplexes and s_c was found to be mainly associated with sIL-7R. The affinities of two IL-7 binding sites (K_d = 35 ± 8 pM and K_d = 3 ± 1 nM) were similar to that of the membrane receptor, suggesting that the sIL-7R/s_c complex retains high affinity for IL-7. sIL-7R mRNA is constitutively present among peripheral T lymphocytes and is down-modulated in vitro by IL-7. Chronically HIV-1-infected patients (n = 20) showed no significant (p > 0.714) variation in s_c levels and a significant (p < 0.0014) 2-fold decrease in plasma sIL-7R levels compared with those in control healthy individuals. Plasma IL-7 and sIL-7R levels did not show any obvious relationship.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by grants from the Agence Nationale de la Recherche sur le SIDA (to J.-H.C.).

² Address correspondence and reprint requests to Dr. Jean-Hervé Colle, Unité de Biologie des Populations Lymphocytaires, Département d’Immunologie, Institut Pasteur, 25 Rue du Dr. Roux, 75724, Paris Cedex 15, France. E-mail address: jhcolle{at}pasteur.fr

³ Abbreviations used in this paper: _c, CD132, common cytokine receptor -chain; aa res., amino acid residue; iso, isoform (prefix); MS, mass spectrometry; MS/MS, tandem MS; m/z, mass-to-charge ratio; s, soluble (prefix); PNGase, peptide N-glycanase; SNP, single nuclear polymorphism.

⁴ The online version of this article contain supplemental material.