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Targeting natural killer cell reactivity by employing antibody to NKp46: implications for type 1 diabetes

Natural killer (NK) cells belong to the innate lymphoid cells. Their cytotoxic activity is regulated by the delicate balance between activating and inhibitory signals. NKp46 is a member of the primary activating receptors of NK cells. We previously reported that the NKp46 receptor is involved in the... Full description

Journal Title: PloS one 2015, Vol.10(2), pp.e0118936
Main Author: Yossef, Rami
Other Authors: Gur, Chamutal , Shemesh, Avishai , Guttman, Ofer , Hadad, Uzi , Nedvetzki, Shlomo , Miletić, Antonija , Nalbandyan, Karen , Cerwenka, Adelheid , Jonjic, Stipan , Mandelboim, Ofer , Porgador, Angel
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: E-ISSN: 1932-6203 ; PMID: 25719382 Version:1 ; DOI: 10.1371/journal.pone.0118936
Link: http://pubmed.gov/25719382
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recordid: medline25719382
title: Targeting natural killer cell reactivity by employing antibody to NKp46: implications for type 1 diabetes
format: Article
creator:
  • Yossef, Rami
  • Gur, Chamutal
  • Shemesh, Avishai
  • Guttman, Ofer
  • Hadad, Uzi
  • Nedvetzki, Shlomo
  • Miletić, Antonija
  • Nalbandyan, Karen
  • Cerwenka, Adelheid
  • Jonjic, Stipan
  • Mandelboim, Ofer
  • Porgador, Angel
subjects:
  • Antibodies, Blocking -- Immunology
  • Diabetes Mellitus, Experimental -- Therapy
  • Killer Cells, Natural -- Immunology
  • Natural Cytotoxicity Triggering Receptor 1 -- Immunology
ispartof: PloS one, 2015, Vol.10(2), pp.e0118936
description: Natural killer (NK) cells belong to the innate lymphoid cells. Their cytotoxic activity is regulated by the delicate balance between activating and inhibitory signals. NKp46 is a member of the primary activating receptors of NK cells. We previously reported that the NKp46 receptor is involved in the development of type 1 diabetes (T1D). Subsequently, we hypothesized that blocking this receptor could prevent or hinder disease development. To address this goal, we developed monoclonal antibodies for murine NKp46. One mAb, named NCR1.15, recognizes the mouse homologue protein of NKp46, named Ncr1, and was able to down-regulate the surface expression of NKp46 on primary murine NK cells following antibody injection in vivo. Additionally, NCR1.15 treatments were able to down-regulate cytotoxic activity mediated by NKp46, but not by other NK receptors. To test our primary assumption, we examined T1D development in two models, non-obese diabetic mice and low-dose streptozotocin. Our results show...
language: eng
source:
identifier: E-ISSN: 1932-6203 ; PMID: 25719382 Version:1 ; DOI: 10.1371/journal.pone.0118936
fulltext: fulltext
issn:
  • 19326203
  • 1932-6203
url: Link


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titleTargeting natural killer cell reactivity by employing antibody to NKp46: implications for type 1 diabetes
creatorYossef, Rami ; Gur, Chamutal ; Shemesh, Avishai ; Guttman, Ofer ; Hadad, Uzi ; Nedvetzki, Shlomo ; Miletić, Antonija ; Nalbandyan, Karen ; Cerwenka, Adelheid ; Jonjic, Stipan ; Mandelboim, Ofer ; Porgador, Angel
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descriptionNatural killer (NK) cells belong to the innate lymphoid cells. Their cytotoxic activity is regulated by the delicate balance between activating and inhibitory signals. NKp46 is a member of the primary activating receptors of NK cells. We previously reported that the NKp46 receptor is involved in the development of type 1 diabetes (T1D). Subsequently, we hypothesized that blocking this receptor could prevent or hinder disease development. To address this goal, we developed monoclonal antibodies for murine NKp46. One mAb, named NCR1.15, recognizes the mouse homologue protein of NKp46, named Ncr1, and was able to down-regulate the surface expression of NKp46 on primary murine NK cells following antibody injection in vivo. Additionally, NCR1.15 treatments were able to down-regulate cytotoxic activity mediated by NKp46, but not by other NK receptors. To test our primary assumption, we examined T1D development in two models, non-obese diabetic mice and low-dose streptozotocin. Our results show...
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descriptionNatural killer (NK) cells belong to the innate lymphoid cells. Their cytotoxic activity is regulated by the delicate balance between activating and inhibitory signals. NKp46 is a member of the primary activating receptors of NK cells. We previously reported that the NKp46 receptor is involved in the development of type 1 diabetes (T1D). Subsequently, we hypothesized that blocking this receptor could prevent or hinder disease development. To address this goal, we developed monoclonal antibodies for murine NKp46. One mAb, named NCR1.15, recognizes the mouse homologue protein of NKp46, named Ncr1, and was able to down-regulate the surface expression of NKp46 on primary murine NK cells following antibody injection in vivo. Additionally, NCR1.15 treatments were able to down-regulate cytotoxic activity mediated by NKp46, but not by other NK receptors. To test our primary assumption, we examined T1D development in two models, non-obese diabetic mice and low-dose streptozotocin. Our results show...
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abstractNatural killer (NK) cells belong to the innate lymphoid cells. Their cytotoxic activity is regulated by the delicate balance between activating and inhibitory signals. NKp46 is a member of the primary activating receptors of NK cells. We previously reported that the NKp46 receptor is involved in the development of type 1 diabetes (T1D). Subsequently, we hypothesized that blocking this receptor could prevent or hinder disease development. To address this goal, we developed monoclonal antibodies for murine NKp46. One mAb, named NCR1.15, recognizes the mouse homologue protein of NKp46, named Ncr1, and was able to down-regulate the surface expression of NKp46 on primary murine NK cells following antibody injection in vivo. Additionally, NCR1.15 treatments were able to down-regulate cytotoxic activity mediated by NKp46, but not by other NK receptors. To test our primary assumption, we examined T1D development in two models, non-obese diabetic mice and low-dose streptozotocin. Our results show...
doi10.1371/journal.pone.0118936
pmid25719382