Regulation of high-affinity IgE receptor-mediated mast cell activation by murine low-affinity IgG receptors.

Daëron, Marc; Malbec, Odile; Latour, Sylvain; Arock, Michel; Fridman, Wolf‐Herman

doi:10.1172/jci117701

Cited by 331 publications

(235 citation statements)

References 39 publications

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“…A family of receptors endowed with the capacity of inhibiting the activation processes triggered by the antigen receptors has been characterized during recent years [1,2,3]. The inhibitory receptors carry in their cytosolic tails one or more sequence motifs generally referred to as immunoreceptor tyrosine-based inhibition motif (ITIM).…”

Section: Introductionmentioning

confidence: 99%

“…The inhibitory receptors carry in their cytosolic tails one or more sequence motifs generally referred to as immunoreceptor tyrosine-based inhibition motif (ITIM). These inhibitory receptors include amongst other the CTLA-4 and CD22 expressed by T and B cells, respectively, murine FccRIIB on B and mast cells or the killer cell inhibitory receptors (KIR) on natural killer (NK) cells [1,2,3]. These receptors, upon being co-clustered with the activating receptors undergo phosphorylation of their ITIM tyrosine residues and recruit SH2 domain containing phosphatases, which interfere with the activating receptors' stimulus-response coupling cascade [1,3,4,5].…”

Section: Introductionmentioning

confidence: 99%

“…Clustering was found to be required and sufficient for inhibiting the secretory response to the type 1 receptor for IgE (FceRI) [7][8][9]. This is one important feature, which distinguishes MAFA as an inhibitory receptor from the majority of the other that require their coclustering with the activating receptors in order to induce inhibition [1][2][3][4].…”

Section: Introductionmentioning

confidence: 99%

“…(2) If so, can one correlate this association with the inhibitory action? To answer these questions we have now investigated the inhibition of the RBL-2H3 cells' secretory response as a function of co-clustering MAFA with the FceRI-IgE complexes.…”

Section: Introductionmentioning

confidence: 99%

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Regulation of mast cells’ secretory response by co‐clustering the Type 1 Fcϵ receptor with the mast cell function‐associated antigen

2005

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The mast cell function-associated antigen (MAFA) is a type II membrane glycoprotein first identified on rat mast cells and basophils. Clustering MAFA inhibits these cells' secretory response to the type 1 Fce receptor (FceRI) stimulus. To quantitatively characterize this inhibition and its dependence on MAFA-FceRI co-clustering, we investigated the secretory response of rat mucosal-type mast cells of the RBL 2H3 line carrying an IgE class, 2,4 dinitrophenyl (DNP) specific monoclonal antibody to DNPconjugated Fab and F(ab 0 ) 2 fragments of (1) mouse IgG, and (2) of the MAFA-specific, monoclonal antibody G63. The first reagent clusters FceRI-IgE complexes into oligomers by reacting with the DNP residues. The DNP conjugated G63 Fab and F(ab 0 ) 2 fragments, additionally aggregate MAFA and form FceRI-IgE-MAFA co-clusters. All experiments using these ligands were performed in the absence or presence of an excess of intact mAb G63, which clusters MAFA molecules. Empirical Hill functions were used to relate the secretory response of mast cells to the equilibrium concentrations of FceRI-IgE or MAFA clusters and co-clusters calculated as function of the employed ligands concentrations. This analysis of the experimental results indicates that coclustered MAFA molecules have a markedly higher inhibitory capacity than MAFAclusters alone. The molecular basis of the enhanced inhibition observed upon coclustering MAFA with the FceRI is most probably the increased concentration of the inhibitory cell components in the immediate proximity of the activation coupling elements.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Regulation of mast cells’ secretory response by co‐clustering the Type 1 Fcϵ receptor with the mast cell function‐associated antigen

2005

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“…However, the adaptive response provides an early counterregulatory signal by also producing Ag-specific IgG that, when bound to Fc + RIIB on mast cells, inhibits mast cell activation in vitro and in vivo [1,2]. This suppression is transduced through the immunoreceptor tyrosine-based inhibitory motif (ITIM) in the cytoplasmic domain of Fc + RIIB [3].…”

Section: Introductionmentioning

confidence: 99%

gp49B1 suppresses stem cell factor‐induced mast cell activation‐secretion and attendant inflammation in vivo

et al. 2003

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We report that gp49B1, a mast cell membrane receptor with two immunoreceptor tyrosinebased inhibitory motifs (ITIM), constitutively inhibits mast cell activation-secretion induced by stem cell factor (SCF), a tissue-derived cytokine that also regulates mast cell development. The intradermal injection of SCF into the ears of gp49B1 null (gp49B -/-) mice elicited 4-and 2.5-fold more degranulating mast cells and tissue swelling caused by edema, respectively, than in gp49B +/+ mice. SCF did not induce tissue swelling in mast cell-deficient mice, and the responsiveness of gp49B -/-mice to mast cell-associated amine and lipid mediators was unaltered. When gp49B +/+ and gp49B -/-mice were pretreated with antagonists of the amines, SCF-induced tissue swelling was reduced by G 90% and 60%, respectively, and it was reduced by G 90% in both genotypes when a cysteinyl leukotriene receptor antagonist was also provided. Hence, the dominant contribution of secretory granule amines to SCF-induced tissue swelling is the result of gp49B1-mediated inhibition of the production of cysteinyl leukotrienes by mast cells. Our findings also provide the first example of an ITIMbearing receptor that constitutively suppresses inflammation generated in vivo independently of the adaptive immune response by a receptor that signals through intrinsic tyrosine kinase activity rather than immunoreceptor tyrosine-based activation motifs.

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Inhibition of antigen-induced T cell response and antibody-induced NK cell cytotoxicity by NKG2A: association of NKG2A with SHP-1 and SHP-2 protein-tyrosine phosphatases

et al. 1998

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Subsets of T and natural killer (NK) lymphocytes express the CD94-NKG2A heterodimer, a receptor for major histocompatibility complex class I molecules. We show here that engagement of the CD94-NKG2A heterodimer inhibits both antigen-driven tumor necrosis factor (TNF) release and cytotoxicity on melanoma-specific human T cell clones. Similarly, CD16-mediated NK cell cytotoxicity is extinguished by cross-linking of the CD94-NKG2A heterodimer. Combining in vivo and in vitro analysis, we report that both I/VxYxxL immunoreceptor tyrosine-based inhibition motifs (ITIM) present in the NKG2A intracytoplasmic domain associate upon tyrosine phosphorylation with the protein tyrosine phosphatases SHP-1 and SHP-2, but not with the polyinositol phosphatase SHIP Determination of the dissociation constant, using surface plasmon resonance analysis, indicates that NKG2A phospho-ITIM interact directly with the SH2 domains of SHP-1 and SHP-2 with a high affinity. Engagement of the CD94-NKG2A heterodimer therefore appears as a protein-tyrosine phosphatase-based strategy that negatively regulates both antigen-induced T cell response and antibody-induced NK cell cytotoxicity. Our results suggest that this inhibitory pathway sets the threshold of T and NK cell activation.

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Regulation of high-affinity IgE receptor-mediated mast cell activation by murine low-affinity IgG receptors.

Abstract: Invest. 1995. 95:577-585.)

Cited by 331 publications

References 39 publications

Regulation of mast cells’ secretory response by co‐clustering the Type 1 Fcϵ receptor with the mast cell function‐associated antigen

Regulation of mast cells’ secretory response by co‐clustering the Type 1 Fcϵ receptor with the mast cell function‐associated antigen

gp49B1 suppresses stem cell factor‐induced mast cell activation‐secretion and attendant inflammation in vivo

Inhibition of antigen-induced T cell response and antibody-induced NK cell cytotoxicity by NKG2A: association of NKG2A with SHP-1 and SHP-2 protein-tyrosine phosphatases

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