Rapamycin combined with anti-CD45RB mAb and IL-10 or with G-CSF induces tolerance in a stringent mouse model of islet transplantation

PLoS One. 2011;6(12):e28434. doi: 10.1371/journal.pone.0028434. Epub 2011 Dec 9.

Abstract

Background: A large pool of preexisting alloreactive effector T cells can cause allogeneic graft rejection following transplantation. However, it is possible to induce transplant tolerance by altering the balance between effector and regulatory T (Treg) cells. Among the various Treg-cell types, Foxp3(+)Treg and IL-10-producing T regulatory type 1 (Tr1) cells have frequently been associated with tolerance following transplantation in both mice and humans. Previously, we demonstrated that rapamycin+IL-10 promotes Tr1-cell-associated tolerance in Balb/c mice transplanted with C57BL/6 pancreatic islets. However, this same treatment was unsuccessful in C57BL/6 mice transplanted with Balb/c islets (classified as a stringent transplant model). We accordingly designed a protocol that would be effective in the latter transplant model by simultaneously depleting effector T cells and fostering production of Treg cells. We additionally developed and tested a clinically translatable protocol that used no depleting agent.

Methodology/principal findings: Diabetic C57BL/6 mice were transplanted with Balb/c pancreatic islets. Recipient mice transiently treated with anti-CD45RB mAb+rapamycin+IL-10 developed antigen-specific tolerance. During treatment, Foxp3(+)Treg cells were momentarily enriched in the blood, followed by accumulation in the graft and draining lymph node, whereas CD4(+)IL-10(+)IL-4(-) T (i.e., Tr1) cells localized in the spleen. In long-term tolerant mice, only CD4(+)IL-10(+)IL-4(-) T cells remained enriched in the spleen and IL-10 was key in the maintenance of tolerance. Alternatively, recipient mice were treated with two compounds routinely used in the clinic (namely, rapamycin and G-CSF); this drug combination promoted tolerance associated with CD4(+)IL-10(+)IL-4(-) T cells.

Conclusions/significance: The anti-CD45RB mAb+rapamycin+IL-10 combined protocol promotes a state of tolerance that is IL-10 dependent. Moreover, the combination of rapamycin+G-CSF induces tolerance and such treatment could be readily translatable into the clinic.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antibodies, Monoclonal / immunology*
  • CD4 Antigens / metabolism
  • Drug Therapy, Combination
  • Epitopes / immunology
  • Female
  • Forkhead Transcription Factors / metabolism
  • Granulocyte Colony-Stimulating Factor / pharmacology*
  • Humans
  • Immune Tolerance / drug effects*
  • Interleukin-10 / pharmacology*
  • Interleukin-2 Receptor alpha Subunit / metabolism
  • Islets of Langerhans Transplantation*
  • Leukocyte Common Antigens / immunology*
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Models, Animal
  • Sirolimus / pharmacology*
  • Spleen / drug effects
  • Spleen / immunology
  • T-Lymphocytes, Regulatory / drug effects
  • T-Lymphocytes, Regulatory / metabolism
  • Time Factors
  • Transplantation, Homologous

Substances

  • Antibodies, Monoclonal
  • CD4 Antigens
  • Epitopes
  • Forkhead Transcription Factors
  • Foxp3 protein, mouse
  • Interleukin-2 Receptor alpha Subunit
  • Interleukin-10
  • Granulocyte Colony-Stimulating Factor
  • Leukocyte Common Antigens
  • Sirolimus