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Ligation of CD23 activates soluble guanylate cyclase in human monocytes via an L‐arginine–dependent mechanism
Author(s) -
PaulEugène Nathalie,
Kolb JeanPierre,
Sarfati Marika,
Arock Michel,
Ouaaz Fateh,
Debré Patrice,
Mossalayi Djavad M.,
Dugas Bernard
Publication year - 1995
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.57.1.160
Subject(s) - cd23 , immunoglobulin e , monoclonal antibody , biology , nitric oxide , antibody , microbiology and biotechnology , chemistry , immunology , endocrinology
Transduction through FcR 2 /CD23 was analyzed in normal human monocytes using immunoglobulin E (IgE)‐anti‐IgE immune complexes (IgE ICs) and monoclonal antibodies (mAbs) to CD23. Anti‐CD23 mAb and IgE IC triggered a time‐dependent increase in cGMP and cAMP in interleukin‐4–preincubated (CD23 + ) but not in unstimulated (CD23 ‐ ) monocytes. Maximal cGMP and cAMP accumulations were observed 10 and 20 min, respectively, after the onset of CD23 ligation. The increase in cGMP was inhibited with N ω ‐monomethyl‐l‐arginine (L‐NMMA), which also partially affected cAMP accumulation. Addition of an anti‐CD23 mAb Fab fragment inhibited the IgE IC– and the anti‐CD23 mAb–induced cGMP and cAMP accumulation, confirming the engagement of CD23. In addition, IgE IC and anti‐CD23 mAb induced, at least in some donors, a production of nitrite that was inhibited in the presence of L‐NMMA. Taken together, these findings suggest a possible involvement of the nitric oxide synthase pathway in IgE IC–mediated activation of CD23 + monocytes. J. Leukoc. Biol. 57: 160–167; 1995.