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Robert L. Fairchild - One of the best experts on this subject based on the ideXlab platform.
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natural killer cells play a critical role in mediating inflammation and graft failure during antibody mediated rejection of kidney Allografts
Kidney International, 2016Co-Authors: Naoki Kohei, William M Baldwin, Toshiaki Tanaka, Kazunari Tanabe, Naoya Masumori, Nina Dvorina, Anna Valujskikh, Robert L. FairchildAbstract:While the incidence of antibody-mediated kidney graft rejection has increased, the key cellular and molecular participants underlying this graft injury remain unclear. Rejection of kidney Allografts in mice lacking the chemokine receptor CCR5 is dependent on production of donor-specific antibody. Here we determine if cells expressing cytotoxic function contributed to antibody-mediated kidney Allograft rejection in these recipients. Wild-type C57BL/6, B6.CCR5 -/- , and B6.CD8 -/- /CCR5 -/- mice were transplanted with complete MHC-mismatched A/J kidney grafts, and intragraft inflammatory components were followed to rejection. B6.CCR5 -/- and B6.CD8 -/- /CCR5 -/- recipients rejected kidney Allografts by day 35, whereas 65% of Allografts in wild-type recipients survived past day 80 post-transplant. Rejected Allografts in wild-type C57BL/6, B6.CCR5 -/- , and B6.CD8 -/- /CCR5 -/- recipients expressed high levels of VCAM-1 and MMP7 mRNA that was associated with high serum titers of donor-specific antibody. High levels of perforin and granzyme B mRNA expression peaked on day 6 post-transplant in Allografts in all recipients, but were absent in isografts. Depletion of natural killer cells in B6.CD8 -/- /CCR5 -/- recipients reduced this expression to background levels and promoted the long-term survival of 40% of the kidney Allografts. Thus, natural killer cells have a role in increased inflammation during antibody-mediated kidney Allograft injury and in rejection of the grafts.
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graft derived ccl2 increases graft injury during antibody mediated rejection of cardiac Allografts
American Journal of Transplantation, 2014Co-Authors: William M Baldwin, Robert L. Fairchild, Shoichi Iida, Toyofumi Abe, Norio Nonomura, Shiro TakaharaAbstract:The pathogenic role of macrophages in antibody-mediated rejection (AMR) remains unclear. Monocyte chemoattractant protein-1 (MCP-1/CCL2) is a potent chemotactic factor for monocytes and macrophages. The current studies used a murine model of AMR to investigate the role of graft-derived CCL2 in AMR and how macrophages may participate in antibody-mediated Allograft injury. B6.CCR5−/−/CD8−/− recipients rejected MHC-mismatched WT A/J Allografts with high donor-reactive antibody titers and diffuse C4d deposition in the large vessels and myocardial capillaries, features consistent with AMR. In contrast, A/J.CCL2−/− Allografts induced low donor-reactive antibody titers and C4d deposition at Day 7 posttransplant. Decreased donor-reactive CD4 T cells producing interferon gamma were induced in response to A/J.CCL2−/− versus WT Allografts. Consequently, A/J.CCL2−/− Allograft survival was modestly but significantly longer than A/J Allografts. Macrophages purified from WT Allografts expressed high levels of IL-1β and IL-12p40 and this expression and the numbers of classically activated macrophages were markedly reduced in CCL2-deficient Allografts on Day 7. The results indicate that Allograft-derived CCL2 plays an important role in directing classically activated macrophages into Allografts during AMR and that macrophages are important contributors to the inflammatory environment mediating graft tissue injury in this pathology, suggesting CCL2 as a therapeutic target for AMR.
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monokine induced by interferon γ mig cxcl9 is derived from both donor and recipient sources during rejection of class ii major histocompatibility complex disparate skin Allografts
American Journal of Pathology, 2009Co-Authors: Michael B Auerbach, Robert L. Fairchild, Naohiko Shimoda, Hiroyuki Amano, Joshua M Rosenblum, Danielle D Kish, Joshua M FarberAbstract:Chemokines, including monokine induced by interferon-γ (Mig/CXCL9), are produced both in Allografts and during the direct T-cell infiltration that mediates graft rejection. Neither the specific production nor contribution of Allograft donor versus recipient Mig in Allograft rejection is currently known. C57BL/6 mice with a targeted deletion in the Mig gene were used as both skin Allograft donors and recipients in a class II major histocompatibility complex-mismatched graft model to test the requirement for donor- versus recipient-derived Mig for acute rejection. B6.Mig −/− Allografts had a 10-day prolonged survival in B6.H-2 bm12 recipients when compared with wild-type C57BL/6 Allograft donors, and B6.H-2 bm12 skin Allografts had a 5-day prolonged survival in B6.Mig −/− versus wild-type recipients. Transplantation of B6.Mig −/− skin grafts onto B6.H-2 bm12 .Mig −/− recipients resulted in further prolonged Allograft survival with more than 30% of the grafts surviving longer than 60 days. Prolonged Allograft survival was also associated with delayed cellular infiltration into grafts but not with altered T-cell proliferative responses to donor stimulators. Immunohistochemical staining of Allograft sections indicated that Mig is produced by both donor- and recipient-derived sources, but Mig from each of these sources appeared in different areas of the Allograft tissue. These results therefore demonstrate the synergy of donor- and recipient-derived Mig in promoting T-cell infiltration into Allografts.
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inhibition of polymorphonuclear leukocyte mediated graft damage synergizes with short term costimulatory blockade to prevent cardiac Allograft rejection
Circulation, 2005Co-Authors: Tarek Elsawy, John A Belperio, Robert M Strieter, Daniel G Remick, Robert L. FairchildAbstract:BACKGROUND: The early inflammatory response during reperfusion of cardiac Allografts is initiated by the infiltration of polymorphonuclear leukocytes (PMNs) into the graft. The impact of early PMN infiltration on Allograft rejection compared with long-term graft survival remains poorly understood. METHODS AND RESULTS: We tested the role of CXCR2, the receptor for 2 PMN attractant chemokines, KC/CXCL1 and MIP-2/CXCL2, on intragraft inflammation and vascularized cardiac Allograft rejection in a murine model. Compared with Allografts retrieved from control recipients, both PMN infiltration and intragraft proinflammatory cytokine expression were significantly attenuated in Allografts from CXCR2-antisera-treated wild-type or from CXCR2(-/-) recipients. Adoptive transfer of alloantigen-primed T cells rapidly infiltrated and rejected Allografts in control recipients, but T-cell infiltration was significantly decreased in recipients depleted of PMNs at transplantation. The influence of early PMN-mediated inflammation on the therapeutic efficacy of costimulatory blockade to prevent Allograft rejection was tested. Short-term treatment of recipients with anti-CD154 mAb or CTLA-4 Ig induced modest prolongation of cardiac Allograft survival. However, CD154 mAb or CTLA-4 Ig treatment, combined with either peritransplantation PMN depletion or antibodies specific for KC/CXCL1 plus MIP-2/CXCL2, prolonged cardiac Allograft survival beyond 100 days. CONCLUSIONS: Results suggest that strategies attenuating PMN-mediated tissue damage during reperfusion significantly improve the efficacy of short-term costimulatory blockade to prevent T-cell-mediated rejection of cardiac Allografts.
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inhibition of polymorphonuclear leukocyte mediated graft damage synergizes with short term costimulatory blockade to prevent cardiac Allograft rejection
Circulation, 2005Co-Authors: Tarek Elsawy, John A Belperio, Robert M Strieter, Daniel G Remick, Robert L. FairchildAbstract:Background— The early inflammatory response during reperfusion of cardiac Allografts is initiated by the infiltration of polymorphonuclear leukocytes (PMNs) into the graft. The impact of early PMN infiltration on Allograft rejection compared with long-term graft survival remains poorly understood. Methods and Results— We tested the role of CXCR2, the receptor for 2 PMN attractant chemokines, KC/CXCL1 and MIP-2/CXCL2, on intragraft inflammation and vascularized cardiac Allograft rejection in a murine model. Compared with Allografts retrieved from control recipients, both PMN infiltration and intragraft proinflammatory cytokine expression were significantly attenuated in Allografts from CXCR2-antisera–treated wild-type or from CXCR2−/− recipients. Adoptive transfer of alloantigen-primed T cells rapidly infiltrated and rejected Allografts in control recipients, but T-cell infiltration was significantly decreased in recipients depleted of PMNs at transplantation. The influence of early PMN-mediated inflammati...
Robert M Strieter - One of the best experts on this subject based on the ideXlab platform.
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inhibition of polymorphonuclear leukocyte mediated graft damage synergizes with short term costimulatory blockade to prevent cardiac Allograft rejection
Circulation, 2005Co-Authors: Tarek Elsawy, John A Belperio, Robert M Strieter, Daniel G Remick, Robert L. FairchildAbstract:BACKGROUND: The early inflammatory response during reperfusion of cardiac Allografts is initiated by the infiltration of polymorphonuclear leukocytes (PMNs) into the graft. The impact of early PMN infiltration on Allograft rejection compared with long-term graft survival remains poorly understood. METHODS AND RESULTS: We tested the role of CXCR2, the receptor for 2 PMN attractant chemokines, KC/CXCL1 and MIP-2/CXCL2, on intragraft inflammation and vascularized cardiac Allograft rejection in a murine model. Compared with Allografts retrieved from control recipients, both PMN infiltration and intragraft proinflammatory cytokine expression were significantly attenuated in Allografts from CXCR2-antisera-treated wild-type or from CXCR2(-/-) recipients. Adoptive transfer of alloantigen-primed T cells rapidly infiltrated and rejected Allografts in control recipients, but T-cell infiltration was significantly decreased in recipients depleted of PMNs at transplantation. The influence of early PMN-mediated inflammation on the therapeutic efficacy of costimulatory blockade to prevent Allograft rejection was tested. Short-term treatment of recipients with anti-CD154 mAb or CTLA-4 Ig induced modest prolongation of cardiac Allograft survival. However, CD154 mAb or CTLA-4 Ig treatment, combined with either peritransplantation PMN depletion or antibodies specific for KC/CXCL1 plus MIP-2/CXCL2, prolonged cardiac Allograft survival beyond 100 days. CONCLUSIONS: Results suggest that strategies attenuating PMN-mediated tissue damage during reperfusion significantly improve the efficacy of short-term costimulatory blockade to prevent T-cell-mediated rejection of cardiac Allografts.
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inhibition of polymorphonuclear leukocyte mediated graft damage synergizes with short term costimulatory blockade to prevent cardiac Allograft rejection
Circulation, 2005Co-Authors: Tarek Elsawy, John A Belperio, Robert M Strieter, Daniel G Remick, Robert L. FairchildAbstract:Background— The early inflammatory response during reperfusion of cardiac Allografts is initiated by the infiltration of polymorphonuclear leukocytes (PMNs) into the graft. The impact of early PMN infiltration on Allograft rejection compared with long-term graft survival remains poorly understood. Methods and Results— We tested the role of CXCR2, the receptor for 2 PMN attractant chemokines, KC/CXCL1 and MIP-2/CXCL2, on intragraft inflammation and vascularized cardiac Allograft rejection in a murine model. Compared with Allografts retrieved from control recipients, both PMN infiltration and intragraft proinflammatory cytokine expression were significantly attenuated in Allografts from CXCR2-antisera–treated wild-type or from CXCR2−/− recipients. Adoptive transfer of alloantigen-primed T cells rapidly infiltrated and rejected Allografts in control recipients, but T-cell infiltration was significantly decreased in recipients depleted of PMNs at transplantation. The influence of early PMN-mediated inflammati...
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monokine induced by ifn γ is a dominant factor directing t cells into murine cardiac Allografts during acute rejection
Journal of Immunology, 2001Co-Authors: Masayoshi Miura, Robert L. Fairchild, Robert M Strieter, Ken Morita, Hirohito Kobayashi, Thomas A Hamilton, Marie D BurdickAbstract:The use of chemokine antagonism as a strategy to inhibit leukocyte trafficking into inflammatory sites requires identification of the dominant chemokines mediating recruitment. The chemokine(s) directing T cells into cardiac Allografts during acute rejection remain(s) unidentified. The role of the CXC chemokines IFN-γ inducible protein 10 (IP-10) and monokine induced by IFN-γ (Mig) in acute rejection of A/J (H-2 a ) cardiac grafts by C57BL/6 (H-2 b ) recipients was tested. Intra-Allograft expression of Mig was observed at day 2 posttransplant and increased to the time of rejection at day 7 posttransplant. IP-10 mRNA and protein production were 2.5- to 8-fold lower than Mig. Whereas Allografts were rejected at day 7–9 in control recipients, treatment with rabbit antiserum to Mig, but not to IP-10, prolonged Allograft survival up to day 19 posttransplant. At day 7 posttransplant, Allografts from Mig antiserum-treated recipients had marked reduction in T cell infiltration. At the time of rejection in Mig antiserum-treated recipients (i.e., days 17–19), intra-Allograft expression of macrophage-inflammatory protein-1α, -1β, and their ligand CCR5 was high, whereas expression of CXCR3, the Mig receptor, was virtually absent. Mig was produced by the Allograft endothelium as well as by recipient Allograft-infiltrating macrophages and neutrophils, indicating the synergistic interactions between innate and adaptive immune compartments during acute rejection. Collectively, these results indicate that Mig is a dominant recruiting factor for alloantigen-primed T cells into cardiac Allografts during acute rejection. Although Mig antagonism delays acute heart Allograft rejection, the results also suggest that the alloimmune response circumvents Mig antagonism through alternative mechanisms.
Tarek Elsawy - One of the best experts on this subject based on the ideXlab platform.
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inhibition of polymorphonuclear leukocyte mediated graft damage synergizes with short term costimulatory blockade to prevent cardiac Allograft rejection
Circulation, 2005Co-Authors: Tarek Elsawy, John A Belperio, Robert M Strieter, Daniel G Remick, Robert L. FairchildAbstract:BACKGROUND: The early inflammatory response during reperfusion of cardiac Allografts is initiated by the infiltration of polymorphonuclear leukocytes (PMNs) into the graft. The impact of early PMN infiltration on Allograft rejection compared with long-term graft survival remains poorly understood. METHODS AND RESULTS: We tested the role of CXCR2, the receptor for 2 PMN attractant chemokines, KC/CXCL1 and MIP-2/CXCL2, on intragraft inflammation and vascularized cardiac Allograft rejection in a murine model. Compared with Allografts retrieved from control recipients, both PMN infiltration and intragraft proinflammatory cytokine expression were significantly attenuated in Allografts from CXCR2-antisera-treated wild-type or from CXCR2(-/-) recipients. Adoptive transfer of alloantigen-primed T cells rapidly infiltrated and rejected Allografts in control recipients, but T-cell infiltration was significantly decreased in recipients depleted of PMNs at transplantation. The influence of early PMN-mediated inflammation on the therapeutic efficacy of costimulatory blockade to prevent Allograft rejection was tested. Short-term treatment of recipients with anti-CD154 mAb or CTLA-4 Ig induced modest prolongation of cardiac Allograft survival. However, CD154 mAb or CTLA-4 Ig treatment, combined with either peritransplantation PMN depletion or antibodies specific for KC/CXCL1 plus MIP-2/CXCL2, prolonged cardiac Allograft survival beyond 100 days. CONCLUSIONS: Results suggest that strategies attenuating PMN-mediated tissue damage during reperfusion significantly improve the efficacy of short-term costimulatory blockade to prevent T-cell-mediated rejection of cardiac Allografts.
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inhibition of polymorphonuclear leukocyte mediated graft damage synergizes with short term costimulatory blockade to prevent cardiac Allograft rejection
Circulation, 2005Co-Authors: Tarek Elsawy, John A Belperio, Robert M Strieter, Daniel G Remick, Robert L. FairchildAbstract:Background— The early inflammatory response during reperfusion of cardiac Allografts is initiated by the infiltration of polymorphonuclear leukocytes (PMNs) into the graft. The impact of early PMN infiltration on Allograft rejection compared with long-term graft survival remains poorly understood. Methods and Results— We tested the role of CXCR2, the receptor for 2 PMN attractant chemokines, KC/CXCL1 and MIP-2/CXCL2, on intragraft inflammation and vascularized cardiac Allograft rejection in a murine model. Compared with Allografts retrieved from control recipients, both PMN infiltration and intragraft proinflammatory cytokine expression were significantly attenuated in Allografts from CXCR2-antisera–treated wild-type or from CXCR2−/− recipients. Adoptive transfer of alloantigen-primed T cells rapidly infiltrated and rejected Allografts in control recipients, but T-cell infiltration was significantly decreased in recipients depleted of PMNs at transplantation. The influence of early PMN-mediated inflammati...
Kenji Chiba - One of the best experts on this subject based on the ideXlab platform.
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fty720 a novel immunosuppressant induces sequestration of circulating mature lymphocytes by acceleration of lymphocyte homing in rats ii fty720 prolongs skin Allograft survival by decreasing t cell infiltration into grafts but not cytokine production
Journal of Immunology, 1998Co-Authors: Yoshiki Yanagawa, Kunio Sugahara, Hirotoshi Kataoka, Takafumi Kawaguchi, Yumi Masubuchi, Kenji ChibaAbstract:FTY720, a novel immunosuppressant, prolonged the survival of WKAH skin Allografts transplanted into MHC-incompatible F344 rats. In this Allograft model, the median survival time of the control group was 7 days, whereas those of the groups given FTY720 orally at 0.1 mg/kg and cyclosporin A (CsA) at 10 mg/kg were 10.5 and 11 days, respectively. In contrast, FTY720 (0.1 mg/kg) combined with CsA (10 mg/kg) synergistically prolonged Allograft survival with a median survival time exceeding 70 days. To elucidate the mechanisms of this remarkable synergistic effect, mRNA expressions of IL-2 and IFN-gamma and that of CD3 (delta-chain), which reflects T cell infiltration, in Allografts were temporally analyzed using a semiquantitative PCR method. In WKAH skin Allografts, mRNA levels of IL-2, IFN-gamma, and CD3 were increased as compared with isograft controls, peaking on days 4 to 5. CsA (10 mg/kg) significantly inhibited elevations of IL-2 and IFN-gamma mRNA, while slightly inhibiting that of CD3 mRNA in Allografts. On the contrary, FTY720 (0.1 mg/kg) markedly inhibited the elevation of CD3 mRNA, while slightly inhibiting those of IL-2 and IFN-gamma mRNA. FTY720 (0.1 mg/kg) combined with CsA (10 mg/kg) almost completely suppressed the intragraft expressions of mRNA for IL-2, IFN-gamma, and CD3. Immunohistochemical staining and flow cytometric analysis also confirmed that FTY720 decreased T cell infiltration into Allografts. From these results, the synergistic effect of FTY720 combined with CsA on prolongation of Allograft survival is presumably based on the respective inhibitions of T cell infiltration and cytokine production in grafts.
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fty720 a novel immunosuppressant induces sequestration of circulating mature lymphocytes by acceleration of lymphocyte homing in rats ii fty720 prolongs skin Allograft survival by decreasing t cell infiltration into grafts but not cytokine production
Journal of Immunology, 1998Co-Authors: Yoshiki Yanagawa, Kunio Sugahara, Hirotoshi Kataoka, Takafumi Kawaguchi, Yumi Masubuchi, Kenji ChibaAbstract:FTY720, a novel immunosuppressant, prolonged the survival of WKAH skin Allografts transplanted into MHC-incompatible F344 rats. In this Allograft model, the median survival time of the control group was 7 days, whereas those of the groups given FTY720 orally at 0.1 mg/kg and cyclosporin A (CsA) at 10 mg/kg were 10.5 and 11 days, respectively. In contrast, FTY720 (0.1 mg/kg) combined with CsA (10 mg/kg) synergistically prolonged Allograft survival with a median survival time exceeding 70 days. To elucidate the mechanisms of this remarkable synergistic effect, mRNA expressions of IL-2 and IFN-γ and that of CD3 (δ-chain), which reflects T cell infiltration, in Allografts were temporally analyzed using a semiquantitative PCR method. In WKAH skin Allografts, mRNA levels of IL-2, IFN-γ, and CD3 were increased as compared with isograft controls, peaking on days 4 to 5. CsA (10 mg/kg) significantly inhibited elevations of IL-2 and IFN-γ mRNA, while slightly inhibiting that of CD3 mRNA in Allografts. On the contrary, FTY720 (0.1 mg/kg) markedly inhibited the elevation of CD3 mRNA, while slightly inhibiting those of IL-2 and IFN-γ mRNA. FTY720 (0.1 mg/kg) combined with CsA (10 mg/kg) almost completely suppressed the intragraft expressions of mRNA for IL-2, IFN-γ, and CD3. Immunohistochemical staining and flow cytometric analysis also confirmed that FTY720 decreased T cell infiltration into Allografts. From these results, the synergistic effect of FTY720 combined with CsA on prolongation of Allograft survival is presumably based on the respective inhibitions of T cell infiltration and cytokine production in grafts.
Rene Verdonk - One of the best experts on this subject based on the ideXlab platform.
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transplantation of viable meniscal Allograft surgical technique
Journal of Bone and Joint Surgery American Volume, 2006Co-Authors: Peter Verdonk, A Demurie, Karl Almqvist, Eric Veys, Gust Verbruggen, Rene VerdonkAbstract:BACKGROUND: Few medium-term or long-term reports on meniscal Allograft transplantations are available. In this study, we present the results of a survival analysis of the clinical outcomes of our first 100 procedures involving transplantation of viable medial and lateral meniscal Allografts performed in ninety-six patients. METHODS: Thirty-nine medial and sixty-one lateral meniscal Allografts were evaluated after a mean of 7.2 years. Survival analysis was based on specific clinical end points, with failure of the Allograft defined as moderate occasional or persistent pain or as poor function. An additional survival analysis was performed to assess the results of the sixty-nine procedures that involved isolated use of a viable Allograft (twenty of the thirty-nine medial Allograft procedures and forty-nine of the sixty-one lateral Allograft procedures) and of the thirteen viable medial meniscal Allografts that were implanted in combination with a high tibial osteotomy in patients with initial varus malalignment of the lower limb. RESULTS: Overall, eleven (28%) of the thirty-nine medial Allografts and ten (16%) of the sixty-one lateral Allografts failed. The mean cumulative survival time (11.6 years) was identical for the medial and lateral Allografts. The cumulative survival rates for the medial and lateral Allografts at ten years were 74.2% and 69.8%, respectively. The mean cumulative survival time and the cumulative survival rate for the medial Allografts used in combination with a high tibial osteotomy were 13.0 years and 83.3% at ten years, respectively. CONCLUSIONS: Transplantation of a viable meniscal Allograft can significantly relieve pain and improve function of the knee joint. Survival analysis showed that this beneficial effect remained in approximately 70% of the patients at ten years. This study identified the need for a prospective study comparing patients with similar symptoms and clinical findings treated with and without a meniscal Allograft and followed for a longer period with use of clinical evaluation as well as more objective documentation tools regarding the actual fate of the Allograft itself and the articular cartilage.
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transplantation of viable meniscal Allograft survivorship analysis and clinical outcome of one hundred cases
Journal of Bone and Joint Surgery American Volume, 2005Co-Authors: Peter Verdonk, A Demurie, Karl Almqvist, Eric Veys, Gust Verbruggen, Rene VerdonkAbstract:Background: Few medium-term or long-term reports on meniscal Allograft transplantations are available. In this study, we present the results of a survival analysis of the clinical outcomes of our first 100 procedures involving transplantation of viable medial and lateral meniscal Allografts performed in ninety-six patients. Methods: Thirty-nine medial and sixty-one lateral meniscal Allografts were evaluated after a mean of 7.2 years. Survival analysis was based on specific clinical end points, with failure of the Allograft defined as moderate occasional or persistent pain or as poor function. An additional survival analysis was performed to assess the results of the sixty-nine procedures that involved isolated use of a viable Allograft (twenty of the thirty-nine medial Allograft procedures and forty-nine of the sixty-one lateral Allograft procedures) and of the thirteen viable medial meniscal Allografts that were implanted in combination with a high tibial osteotomy in patients with initial varus malalignment of the lower limb. Results: Overall, eleven (28%) of the thirty-nine medial Allografts and ten (16%) of the sixty-one lateral Allografts failed. The mean cumulative survival time (11.6 years) was identical for the medial and lateral Allografts. The cumulative survival rates for the medial and lateral Allografts at ten years were 74.2% and 69.8%, respectively. The mean cumulative survival time and the cumulative survival rate for the medial Allografts used in combination with a high tibial osteotomy were 13.0 years and 83.3% at ten years, respectively. Conclusions: Transplantation of a viable meniscal Allograft can significantly relieve pain and improve function of the knee joint. Survival analysis showed that this beneficial effect remained in approximately 70% of the patients at ten years. This study identified the need for a prospective study comparing patients with similar symptoms and clinical findings treated with and without a meniscal Allograft and followed for a longer period with use of clinical evaluation as well as more objective documentation tools regarding the actual fate of the Allograft itself and the articular cartilage.