title: Treatment with Anti-FcεRIα (MAR-1) Antibody Prevents Acute Islet Allograft Rejection in a Murine Model.
abstract: OBJECTIVE
  Various immunological strategies for tolerance induction against allogeneic tissue grafts (allografts) have been tested in islet transplant recipients; for example, T cell activating co-stimulatory pathway blockade has been shown to prolong islet allograft survival. However, little is known about whether infiltrating inflammatory cells (e.g., basophils) affect islet allograft fates before antigen-specific immune cell development. Herein, we treated mice with a basophil-specific monoclonal antibody (mAb) and examined whether early acute-phase islet allograft rejection could be prevented in recipients.
  
  
  METHODS
  Pancreatic islets isolated from C57BL/6 (H-2b) or DBA/2 (H-2d) mice were transplanted under the renal capsules of C57BL/6 recipient mice. Recipients receiving allografts were administered the anti-basophil mAb MAR-1 to examine the antibody-mediated effect on graft survival. At days 4 and 7 post-transplantation, graft-bearing recipient kidneys were harvested for immunohistological analysis and stained with anti-insulin antibody to compare the sizes of grafted islets.
  
  
  RESULTS
  On day 7 post-transplantation, the transplanted pancreatic islet clusters in allograft-recipient kidneys had rapidly decreased in size, whereas those in syngeneic recipients remained larger in both size and number. However, MAR-1-treated recipients had increased the numbers of larger insulin-positive allograft islet cell clusters.
  
  
  CONCLUSIONS
  Basophil-specific mAb treatment contributes to enhance and prolong transplanted islet survival in allogeneic recipient mice.
authors.affiliation: Department of Surgery, Tokai University School of Medicine, 143 Shimokasuya, Isehara, Kanagawa 259-1193, Japan. naoki-y@poppy.ocn.ne.jp.
authors.forename: Naoki
authors.initials: N
authors.lastname: Yazawa
authors.forename: Toshihide
authors.initials: T
authors.lastname: Imaizumi
authors.forename: Hiroyasu
authors.initials: H
authors.lastname: Makuuchi
authors.forename: Izumi
authors.initials: I
authors.lastname: Tsuchiya
authors.forename: Makiko
authors.initials: M
authors.lastname: Tanaka
authors.forename: Sadaki
authors.initials: S
authors.lastname: Inokuchi
authors.forename: Sonoko
authors.initials: S
authors.lastname: Habu
authors.forename: Toshio
authors.initials: T
authors.lastname: Nakagohri
mesh_terms: D064591:Allografts; D000818:Animals; D000911:Antibodies, Monoclonal / Q000008:administration & dosage* / Q000494:pharmacology; D001491:Basophils / Q000276:immunology; D004195:Disease Models, Animal; D006084:Graft Rejection / Q000276:immunology / Q000517:prevention & control*; D006085:Graft Survival / Q000187:drug effects; D007165:Immunosuppression Therapy; D007166:Immunosuppressive Agents; D016381:Islets of Langerhans Transplantation; D008297:Male; D008810:Mice, Inbred C57BL; D008811:Mice, Inbred DBA; D017455:Receptors, IgE / Q000276:immunology*
chemical_list: D000911:Antibodies, Monoclonal; C579617:FcepsilonRIalpha protein, mouse; D007166:Immunosuppressive Agents; D017455:Receptors, IgE