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A common inhibitory receptor for major histocompatibility complex class I molecules on human lymphoid and myelomonocytic cells.

Colonna M, Navarro F, Bellón T, Llano M, García P, Samaridis J, Angman L, Cella M, López-Botet M - J. Exp. Med. (1997)

Bottom Line: In this study, we characterize a novel inhibitory MHC class I receptor of the immunoglobulin-superfamily, expressed not only by subsets of NK and T cells, but also by B cells, monocytes, macrophages, and dendritic cells.This receptor, called Ig-like transcript (ILT)2, binds MHC class I molecules and delivers a negative signal that inhibits killing by NK and T cells, as well as Ca2+ mobilization in B cells and myelomonocytic cells triggered through the B cell antigen receptor and human histocompatibility leukocyte antigens (HLA)-DR, respectively.In addition, myelomonocytic cells express receptors homologous to ILT2, which are characterized by extensive polymorphism and might recognize distinct HLA class I molecules.

View Article: PubMed Central - PubMed

Affiliation: Basel Institute for Immunology, Basel CH-4005, Switzerland.

ABSTRACT
Natural killer (NK) cell-mediated lysis is negatively regulated by killer cell inhibitory receptors specific for major histocompatibility complex (MHC) class I molecules. In this study, we characterize a novel inhibitory MHC class I receptor of the immunoglobulin-superfamily, expressed not only by subsets of NK and T cells, but also by B cells, monocytes, macrophages, and dendritic cells. This receptor, called Ig-like transcript (ILT)2, binds MHC class I molecules and delivers a negative signal that inhibits killing by NK and T cells, as well as Ca2+ mobilization in B cells and myelomonocytic cells triggered through the B cell antigen receptor and human histocompatibility leukocyte antigens (HLA)-DR, respectively. In addition, myelomonocytic cells express receptors homologous to ILT2, which are characterized by extensive polymorphism and might recognize distinct HLA class I molecules. These results suggest that diverse leukocyte lineages have adopted recognition of self-MHC class I molecules as a common strategy to control cellular activation during an immune response.

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Related in: MedlinePlus

Inhibition of IgE-induced serotonin release in ILT2-transfected RBL cells. Transfected and control cells were stimulated with purified mouse IgE (20 μg/ml) alone and in combination with either HP-F1  [20 μg/ml of whole antibody or F(ab′)2 fragments] or with the isotype-matched antibody HP-1F7 [20 μg/ml of whole antibody or F(ab′)2 fragments] immobilized on plastic. The percentage of serotonin release, as  compared to total and spontaneous release, was determined after 1 h at  37°C. The expression of ILT2 on transfected RBL cells was assessed by  indirect immunofluorescence with HP-F1 mAb (not shown).
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Figure 5: Inhibition of IgE-induced serotonin release in ILT2-transfected RBL cells. Transfected and control cells were stimulated with purified mouse IgE (20 μg/ml) alone and in combination with either HP-F1 [20 μg/ml of whole antibody or F(ab′)2 fragments] or with the isotype-matched antibody HP-1F7 [20 μg/ml of whole antibody or F(ab′)2 fragments] immobilized on plastic. The percentage of serotonin release, as compared to total and spontaneous release, was determined after 1 h at 37°C. The expression of ILT2 on transfected RBL cells was assessed by indirect immunofluorescence with HP-F1 mAb (not shown).

Mentions: To further demonstrate that ILT2 delivers a negative signal and is sufficient to inhibit cell activation triggered via a stimulatory receptor, ILT2 cDNA was stably transfected in the RBL cell line, which constitutively expresses the FcR for IgE (FcεRI; reference 34). As shown in Fig. 5, ILT2-transfected RBL cells released serotonin when triggered through the FcεRI with mouse IgE bound to a plastic surface. Conversely, serotonin secretion was clearly inhibited by cocross-linking of FcεRI with ILT2 using mouse IgE and the HP-F1 antibody [or its F(ab′)2 fragments] coated on plastic. These results indicate that recruitment of ILT2 to a stimulatory receptor by antibody ligation can inhibit cellular activation.


A common inhibitory receptor for major histocompatibility complex class I molecules on human lymphoid and myelomonocytic cells.

Colonna M, Navarro F, Bellón T, Llano M, García P, Samaridis J, Angman L, Cella M, López-Botet M - J. Exp. Med. (1997)

Inhibition of IgE-induced serotonin release in ILT2-transfected RBL cells. Transfected and control cells were stimulated with purified mouse IgE (20 μg/ml) alone and in combination with either HP-F1  [20 μg/ml of whole antibody or F(ab′)2 fragments] or with the isotype-matched antibody HP-1F7 [20 μg/ml of whole antibody or F(ab′)2 fragments] immobilized on plastic. The percentage of serotonin release, as  compared to total and spontaneous release, was determined after 1 h at  37°C. The expression of ILT2 on transfected RBL cells was assessed by  indirect immunofluorescence with HP-F1 mAb (not shown).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2199153&req=5

Figure 5: Inhibition of IgE-induced serotonin release in ILT2-transfected RBL cells. Transfected and control cells were stimulated with purified mouse IgE (20 μg/ml) alone and in combination with either HP-F1 [20 μg/ml of whole antibody or F(ab′)2 fragments] or with the isotype-matched antibody HP-1F7 [20 μg/ml of whole antibody or F(ab′)2 fragments] immobilized on plastic. The percentage of serotonin release, as compared to total and spontaneous release, was determined after 1 h at 37°C. The expression of ILT2 on transfected RBL cells was assessed by indirect immunofluorescence with HP-F1 mAb (not shown).
Mentions: To further demonstrate that ILT2 delivers a negative signal and is sufficient to inhibit cell activation triggered via a stimulatory receptor, ILT2 cDNA was stably transfected in the RBL cell line, which constitutively expresses the FcR for IgE (FcεRI; reference 34). As shown in Fig. 5, ILT2-transfected RBL cells released serotonin when triggered through the FcεRI with mouse IgE bound to a plastic surface. Conversely, serotonin secretion was clearly inhibited by cocross-linking of FcεRI with ILT2 using mouse IgE and the HP-F1 antibody [or its F(ab′)2 fragments] coated on plastic. These results indicate that recruitment of ILT2 to a stimulatory receptor by antibody ligation can inhibit cellular activation.

Bottom Line: In this study, we characterize a novel inhibitory MHC class I receptor of the immunoglobulin-superfamily, expressed not only by subsets of NK and T cells, but also by B cells, monocytes, macrophages, and dendritic cells.This receptor, called Ig-like transcript (ILT)2, binds MHC class I molecules and delivers a negative signal that inhibits killing by NK and T cells, as well as Ca2+ mobilization in B cells and myelomonocytic cells triggered through the B cell antigen receptor and human histocompatibility leukocyte antigens (HLA)-DR, respectively.In addition, myelomonocytic cells express receptors homologous to ILT2, which are characterized by extensive polymorphism and might recognize distinct HLA class I molecules.

View Article: PubMed Central - PubMed

Affiliation: Basel Institute for Immunology, Basel CH-4005, Switzerland.

ABSTRACT
Natural killer (NK) cell-mediated lysis is negatively regulated by killer cell inhibitory receptors specific for major histocompatibility complex (MHC) class I molecules. In this study, we characterize a novel inhibitory MHC class I receptor of the immunoglobulin-superfamily, expressed not only by subsets of NK and T cells, but also by B cells, monocytes, macrophages, and dendritic cells. This receptor, called Ig-like transcript (ILT)2, binds MHC class I molecules and delivers a negative signal that inhibits killing by NK and T cells, as well as Ca2+ mobilization in B cells and myelomonocytic cells triggered through the B cell antigen receptor and human histocompatibility leukocyte antigens (HLA)-DR, respectively. In addition, myelomonocytic cells express receptors homologous to ILT2, which are characterized by extensive polymorphism and might recognize distinct HLA class I molecules. These results suggest that diverse leukocyte lineages have adopted recognition of self-MHC class I molecules as a common strategy to control cellular activation during an immune response.

Show MeSH
Related in: MedlinePlus