Generation and characterization of an antagonistic monoclonal antibody against an extracellular domain of mouse DP2 (CRTH2/GPR44) receptors for prostaglandin D2

PLoS One. 2017 Apr 10;12(4):e0175452. doi: 10.1371/journal.pone.0175452. eCollection 2017.

Abstract

Prostaglandin D2 (PGD2) is a lipid mediator involved in sleep regulation and inflammation. PGD2 interacts with 2 types of G protein-coupled receptors, DP1 and DP2/CRTH2 (chemoattractant receptor homologous molecule expressed on T helper type 2 cells)/GPR44 to show a variety of biological effects. DP1 activation leads to Gs-mediated elevation of the intracellular cAMP level, whereas activation of DP2 decreases this level via the Gi pathway; and it also induces G protein-independent, arrestin-mediated cellular responses. Activation of DP2 by PGD2 causes the progression of inflammation via the recruitment of lymphocytes by enhancing the production of Th2-cytokines. Here we developed monoclonal antibodies (MAbs) against the extracellular domain of mouse DP2 by immunization of DP2-null mutant mice with DP2-overexpressing BAF3, murine interleukin-3 dependent pro-B cells, to reduce the generation of antibodies against the host cells by immunization of mice. Moreover, we immunized DP2-KO mice to prevent immunological tolerance to mDP2 protein. After cell ELISA, immunocytochemical, and Western blot analyses, we successfully obtained a novel monoclonal antibody, MAb-1D8, that specifically recognized native mouse DP2, but neither human DP2 nor denatured mouse DP2, by binding to a particular 3D receptor conformation formed by the N-terminus and extracellular loop 1, 2, and 3 of DP2. This antibody inhibited the binding of 0.5 nM [3H]PGD2 to mouse DP2 (IC50 = 46.3 ± 18.6 nM), showed antagonistic activity toward 15(R)-15-methyl PGD2-induced inhibition of 300 nM forskolin-activated cAMP production (IC50 = 16.9 ± 2.6 nM), and gave positive results for immunohistochemical staining of DP2-expressing CD4+ Th2 lymphocytes that had accumulated in the kidney of unilateral ureteral obstruction model mice. This monoclonal antibody will be very useful for in vitro and in vivo studies on DP2-mediated diseases.

MeSH terms

  • Animals
  • Antibodies, Monoclonal / biosynthesis*
  • Antibodies, Monoclonal / chemistry
  • Antibodies, Monoclonal / immunology*
  • Antibody Specificity
  • CD4-Positive T-Lymphocytes / metabolism
  • CHO Cells
  • COS Cells
  • Cricetulus
  • Cyclic AMP / metabolism
  • Disease Models, Animal
  • Epitope Mapping
  • HEK293 Cells
  • Humans
  • Hybridomas / metabolism
  • Immunization
  • Immunohistochemistry
  • Kidney / metabolism
  • Kidney / pathology
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Precursor Cells, B-Lymphoid / immunology
  • Prostaglandin D2 / analogs & derivatives
  • Prostaglandin D2 / antagonists & inhibitors
  • Receptors, Immunologic / genetics
  • Receptors, Immunologic / immunology*
  • Receptors, Prostaglandin / genetics
  • Receptors, Prostaglandin / immunology*
  • Ureteral Obstruction / immunology
  • Ureteral Obstruction / metabolism
  • Ureteral Obstruction / pathology
  • beta-Arrestins / metabolism

Substances

  • Antibodies, Monoclonal
  • Receptors, Immunologic
  • Receptors, Prostaglandin
  • beta-Arrestins
  • 15-methylprostaglandin D2
  • Cyclic AMP
  • Prostaglandin D2
  • prostaglandin D2 receptor

Grants and funding

This work was supported in part by the Program for Development of New Functional Antibody Technologies of the New Energy and Industrial Technology Development Organization (NEDO, http://www.nedo.go.jp/) of Japan (to TH); by Takeda Science Foundation (http://www.takeda-sci.or.jp/assist/) (to YU); by Osaka City (http://www.city.osaka.lg.jp/) (to YU); and by the program Grants-in-Aid for Scientific Research (A) to Y.U. (16H01881), (B) to KA (26293051), and (C) to HK (14463492) from Japan Society for the Promotion of Science (JSPS, https://www.jsps.go.jp/). The funders had no role in the study design, data collection and analysis, decision to publish or preparation of the manuscript.