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C57BL/6 Recipients (c57bl/6 + recipient)
Selected AbstractsGraft rejection mediated by CD4+ T cells via indirect recognition of alloantigen is associated with a dominant Th2 responseEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 3 2005Keri Csencsits Abstract CD4+ T cells that respond to indirectly presented alloantigen have been shown to mediate chronic rejection, however, the role of the indirect pathway in acute rejection has yet to be completely elucidated. To this end, BALB/c or C57BL/6 mice were depleted of CD8+ T cells and transplanted with class II transactivator (CIITA)-deficient cardiac allografts, which cannot directly present class II alloantigens to CD4+ T cells. In this manner, the rejection response by CD4+ cells was forced to rely upon the indirect recognition pathway. When not depleted of CD8+ cells, both BALB/c and C57BL/6 mice rejected CIITA,/, allografts and a polarized Th1 response was observed. In contrast, when BALB/c recipients of CIITA,/, allografts were depleted of CD8+ T cells, the grafts were acutely rejected and a strong Th2 response characterized by eosinophil influx into the graft was observed. Interestingly, CD8-depleted C57BL/6 recipients of CIITA,/, allografts did not acutely reject their transplants and a Th2 response was not mounted. These findings indicate that CD4+ T cells responding to indirectly presented alloantigens mediate graft rejection in a Th2-dominant manner, and provide further evidence for the role of Th2 responses in acute graft rejection. [source] Evidence of Temporary Airway Epithelial Repopulation and Rare Clonal Formation by BM-derived Cells Following Naphthalene Injury in MiceTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 9 2007Vladimir B. Serikov Abstract The goal of the study was to investigate participation of bone marrow (BM) cells in the process of airway epithelial restoration after naphthalene-induced injury. We transplanted sex-mismatched green fluorescent protein (GFP) -tagged BM-derived cultured plastic-adherent mesenchymal stem cells into 5Gy-irradiated C57BL/6 recipients. After 1 month of recovery, experimental animals were subjected to 250 mg/kg naphthalene IP. Animals were killed at 2,30 days after naphthalene. By immunofluorescence, immunohistochemistry, and by in situ hybridization for the Y-chromosome, we observed patches of donor-derived cells in the large and small conducting airways, mostly at 2,6 days after injury. GFP+ cells in the epithelium of airways were positive for pancytokeratin and some other epithelial markers. Although rare, GFP+ cells formed clear isolated patches of the bronchial epithelium, consistent with clonal formation; as some cells were also positive for proliferating cell nuclear antigen, a marker of proliferating cells. After day 12, only occasional GFP+ cells were present in the epithelium. These data confirm that bone marrow-derived cultured mesenchymal cells can participate in the recovery of the injured airway epithelium after naphthalene-induced injury with minimal long-term engraftment. Anat Rec, 2007. © 2007 Wiley-Liss, Inc. [source] CCR5 Is Required for Regulation of Alloreactive T-Cell Responses to Single Class II MHC-Mismatched Murine Cardiac GraftsAMERICAN JOURNAL OF TRANSPLANTATION, Issue 10 2009T. Nozaki The effector CD4 T-cell response in wild-type C57BL/6 recipients of single class II MHC-disparate B6.H-2bm12 cardiac allografts is restricted by CD4+CD25+ regulatory T cells (Tregs) resulting in long-term allograft survival. To investigate the role chemokine receptors might play in Treg function, this study tested the requirement for CCR5 on Tregs to suppress the alloimmune response in C57BL/6 recipients of B6.H-2bm12 cardiac allografts. In contrast to the long-term survival of B6.H-2bm12 allografts in wild-type recipients (>100 days), the allografts were acutely rejected within 25 days in CCR5,/, recipients with intense infiltration of CD4 T cells. Numbers and duration of donor-reactive CD4 T cells producing IFN-, and IL-4 were markedly increased in spleens of B6.CCR5,/, versus wild-type recipients. Wild-type and B6.CCR5,/, mice had equivalent numbers of splenic FoxP3+ Tregs before and following transplantation, and these Tregs were equivalently suppressive in vitro. However, diminished numbers of FoxP3+ Tregs infiltrated B6.H-2bm12 allografts in B6.CCR5,/, recipients. Adoptive transfer of wild-type, but not CCR5-deficient, CD4+CD25+ Tregs to CCR5,/, recipients restored long-term survival of B6.H-2bm12 cardiac grafts. Collectively, these results indicate that CCR5 expression is required for the regulatory functions of Tregs that restrict alloreactive CD4 T-cell responses to single class II MHC-mismatched cardiac allografts. [source] | ||||||||||