Dipeptidyl peptidase IV (DPPIV/CD26) inhibition does not improve engraftment of unfractionated syngeneic or allogeneic bone marrow after nonmyeloablative.

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Dipeptidyl peptidase IV (DPPIV/CD26) inhibition does not improve engraftment of unfractionated syngeneic or allogeneic bone marrow after nonmyeloablative conditioning Elisabeth Schwaiger, Christoph Klaus, Veerle Matheeussen, Ulrike Baranyi, Nina Pilat, Haley Ramsey, Stephan Korom, Ingrid De Meester, Thomas Wekerle Experimental Hematology Volume 40, Issue 2, Pages 97-106 (February 2012) DOI: 10.1016/j.exphem.2011.10.010 Copyright © 2012 ISEH - Society for Hematology and Stem Cells Terms and Conditions

Figure 1 Chimerism following transplantation of congenic BMCs pretreated in vitro with Diprotin A. Recipient mice were conditioned with 1 Gy TBI and received 15 × 106 congenic CD45.2 BMCs (n = 9/control group A, n = 9/Diprotin A–treated group B). BMCs of group B were treated in vitro with 5 mM Diprotin A before transplantation. The levels of chimerism in blood over time (A), was determined by flow cytometry and is presented as means for Diprotin A–treated (squares) and untreated (dotted line with diamonds) groups. In (B) chimerism in BM and spleen at the end of follow-up is depicted in box and whisker plots. No significant differences were noted between both groups. Experimental Hematology 2012 40, 97-106DOI: (10.1016/j.exphem.2011.10.010) Copyright © 2012 ISEH - Society for Hematology and Stem Cells Terms and Conditions

Figure 2 Chimerism after transplantation of congenic BMCs after combined treatment with Diprotin A in vitro and in vivo and after in vivo treatment with sitagliptin. Recipient mice were conditioned with 1 Gy TBI and received 10 × 106 congenic CD45.2 BMCs (n = 6/control group C, n = 5/Diprotin A–treated group D, n = 7/sitagliptin-treated group E). In group D, BMC were treated in vitro with 5 mM Diprotin A before transplantation and, in addition, recipients were treated in vivo with Diprotin A (4 μmol IV day 0 and 5 μmol Diprotin A subcutaneously every 12 hours for 3 days). Recipients of group E were treated with sitagliptin orally. Levels of chimerism in blood over time (A) were determined by flow cytometry and are presented as means for Diprotin A–treated (squares), sitagliptin-treated (dotted line with triangle) and untreated (dotted line with diamonds) groups. In (B) chimerism in BM and spleen at the end of follow-up is depicted in box and whisker plots. No significant differences were noted between both groups. Experimental Hematology 2012 40, 97-106DOI: (10.1016/j.exphem.2011.10.010) Copyright © 2012 ISEH - Society for Hematology and Stem Cells Terms and Conditions

Figure 3 DPPIV enzymatic activity in serum after in vivo inhibition with Diprotin A or sitagliptin. DPPIV enzymatic activity in serum was measured 2 (peak) and 12 hours (trough) after in vivo treatment with Diprotin A (group D) or sitagliptin (group E). DPPIV enzymatic activity at peak and trough exposure is depicted for Diprotin A– (A) and sitagliptin-treated [(B) congenic, (C) allogeneic model] groups (n = 3–4 randomly selected mice per group, congenic BMT). Experimental Hematology 2012 40, 97-106DOI: (10.1016/j.exphem.2011.10.010) Copyright © 2012 ISEH - Society for Hematology and Stem Cells Terms and Conditions

Figure 4 Chimerism and skin graft survival following transplantation of allogeneic BMCs after in vivo treatment with sitagliptin. Recipient mice were transplanted with 15 × 106 allogeneic BMCs after 1 Gy TBI (day –1) and costimulation blockade consisting of anti CD-154 monoclonal antibody (day 0) and CTLA4Ig (day 2). Four milligrams sitagliptin per mouse were administered twice a day (day 0–2). (A) Mean percent of blood chimerism among different cell lineages over time are depicted for sitagliptin-treated (bold lines with squares) and untreated (dotted lines with triangles) groups. No significant differences were noted between both groups. (B) Chimerism in spleen was similar in both groups at the end of follow-up. (C) Approximately 8 weeks post-BMT, mice were grafted with donor and third-party skin. Skin graft survival was comparable in both groups (p = 0.5). Experimental Hematology 2012 40, 97-106DOI: (10.1016/j.exphem.2011.10.010) Copyright © 2012 ISEH - Society for Hematology and Stem Cells Terms and Conditions