PubMed Health⌕ Search

Biomedical subjects

D Mossalayi

Publications and source records attributed to D Mossalayi.

9 recordsLinked to original sources

Mechanism of extracellular thiol nitrosylation by N(2)O(3) produced by activated macrophages.

Reactive nitrogen intermediates are synthesized by activated macrophages. These molecules, and nitrous anhydride (N(2)O(3)) in particular, are known to be potent nitrosylating species. We investigated the role of macrophage-derived N(2)O(3) in extracellular nitrosylation. We used dilution experiments to demonstrate the intracellular production of N(2)O(3) and its export into the extracellular medium, with a rate constant k(ex) = 6.8 x 10(6) M s(-1). The kinetics of the competition between extracellular hydrolysis of N(2)O(3) and its reaction with added glutathione were also studied. We obtained a value of the rate constant k(GSH) for the latter reaction of 4.4 x 10(7) M(-1) s(-1), consistent with earlier determinations in cell-free systems. The implications of these results in human albumin nitrosylation were investigated. Nitrosylated albumin was detected in activated macrophages supernatants using an anti-NO-acetylated cysteine antibody. It was estimated that 10% of N(2)O(3) produced by activated cells participate in extracellular nitrosylation. N(2)O(3) thus appears to be a new effector molecule of the immune system, as an agent for the nitrosylation of albumin, the main nitric oxide carrier in vivo.

Animals↗

Evidence for a role of Fc epsilon RII/CD23 in the IL-4-induced nitric oxide production by normal human mononuclear phagocytes.

IL-4 stimulates NO production by human monocytes. After 6 days of culture with IL-4, human monocytes released detectable amounts of nitrite and L-citrulline that were inhibited in the presence of nitro-L-arginine (1 mM). Incubation with an anti-CD23 mAb Fab fragment that suppressed the biological effect of CD23 led to a strong reduction (50 to 70%) of the IL-4-induced nitrite and L-citrulline production. Ligation of membrane-associated CD23 or stimulation with recombinant soluble CD23 elicited monocytes to release nitrite and L-citrulline that was suppressed by nitro-L-arginine. Preactivation of human monocytes with IFN-gamma led to subsequent increased IL-4- and CD23-driven nitrite and L-citrulline productions that were also suppressed in the presence of either nitro-L-arginine or the anti-CD23 mAb Fab fragment. The CD23 molecule under its membrane or soluble form thus regulates NO generation by human monocytes. In addition, the IL-4-induced NO production could be mediated, at least in part, by CD23.

Antibodies, Monoclonal↗

[Physiopathological role of low affinity IgE receptor (CD23) in hematopoietic cells].

Ligation of the low affinity IgE receptor by specific monoclonal antibodies or multivalent IgE complexes result in the transduction of signals which differ according to the CD23 isotype expressed by the various cell types. In B lymphocytes, it elicits the early activation of phospholipase C through a mechanism involving a G-protein insensitive to Pertussis toxin, followed by a late phase of cAMP accumulation. In monocytes, which express the CD23b isoform, ligation of CD23 was also found to induce a delayed accumulation of cAMP, that was largely dependent on a prior cGMP increase through a mechanism involving the activation of a NO synthase. This pathway, which appears to be exacerbated in allergic diseases, seems to play an important role in the differentiation of cells of the monocytic lineage, their capacity to release proinflammatory mediators and their cytotoxic functions.

Amino Acid Oxidoreductases↗

Effect of CD23 on purified human hematopoietic cells.

We report herein the effect of soluble CD23 (sCD23) on the differentiation of lymphoid and myeloid precursors. CD23 is known as the low affinity receptor for IgE. In addition to it, our results indicate that sCD23 in synergy with IL1 is able to promote the maturation of normal and leukemic hematopoietic progenitor cells.

Antigens, Differentiation, B-Lymphocyte↗

The differentiation of human pro-thymocytes along the TCR-alpha/beta pathway in vitro is accompanied by the site-specific deletion of the TCR-delta locus.

The nested location of the TCR-delta gene within the TCR-alpha locus is a common feature of both mouse and human. Yet alpha/beta and gamma/delta T cells represent two separate lineages. We have previously proposed that a specific rearrangement event (delta Rec--psi J alpha) resulting in the specific deletion of the TCR-delta gene could be responsible for the independent usage of these two loci. We used an in vitro model of T cell differentiation to test this hypothesis. We show that in culture conditions (IL-1 + sCD23) which promote the development of alpha/beta expressing T cells exclusively, the specific deletion of the TCR-delta locus occurs very rapidly, probably before the productive rearrangement of the TCR-alpha gene. These results clearly demonstrate that the specific deletion of the TCR-delta gene could be the initial regulatory event that imprints the irreversible commitment of T cell differentiation along the alpha/beta pathway.

Base Sequence↗

[Contribution of immunologic technics to the characterization of lethal midline granuloma of unknown origin].

The lethal midline granuloma is a clinical entity characterized by a relentless ulceration of the upper airway involving the nose, the palate and the face, without any demonstrable etiology. We have applied the cell membrane immunostaining techniques to twelve cases. According to the results, it seems that most of the cases are in fact T-cell lymphomas with membrane staining consistent with either precursor or mature lymphoid T-cells. Some cases, however, exhibit an immunostaining pattern compatible with other origins, the proliferating cells belonging either to the B lymphoid or to the histio-monocytic lineages. We conclude that the lethal midline granuloma is an heterogeneous group of neoplastic diseases, in the most part close to a T cell lymphoma, but with a remarkable clinical unity.

Granuloma, Lethal Midline↗