A previous study showed that a tolerogenic gene vaccine based on a IgG1Fc-pCons chimera (here named GX101) protects NZB/NZW mice from SLE development. The present study was aimed at identifying the most effective schedule of immunization and the possible involvement of CD4(+) Foxp3(+) Treg in the mechanism of action, in view of its eventual translation to the human studies. NZB/NZW mice were vaccinated with B lymphocytes made transgenic by spontaneous transgenesis with a gene coding for a chimeric IgG1Fc-pCons construct.
View Article and Find Full Text PDFConflicting observations have been reported about the role of CTLA-4 gene polymorphisms in the clinical outcome of allogeneic hematopoietic stem cell transplantation (HSCT). We have investigated three polymorphisms of the CTLA-4 gene (-318C>T, +49A>G, CT60G>A) in 133 donor/recipient pairs who underwent HLA-matched sibling donor HSCT for hematological malignancies. We found no association of the clinical outcome of the HSCT with either recipient or donor -318C>T and CT60G>A polymorphisms.
View Article and Find Full Text PDFInvestigation is lacking regarding the clinical impact of human leukocyte antigen (HLA) class I downregulation in breast cancer and results are inconsistent. In this study, we investigated the expression of HLA class I, the heavy chain, and beta2-microglobulin (beta2-m) by immunohistochemistry in 67 breast carcinomas (BC) and correlated results with clinical-pathologic parameters and patient outcomes. Seventy-six percent of BC were downregulated for HLA class I, whereas downregulation of heavy chain and beta2-m was observed in 57 and 46% of BC, respectively.
View Article and Find Full Text PDFWe have previously reported that about 80% of acute myeloid leukaemia (AML) samples tested at diagnosis constitutively expressed cytotoxic T-lymphocyte-associated antigen-4 (CTLA-4). The present study compared CTLA-4 expression and function of leukaemic cells from AML patients at diagnosis with those from AML patients resistant to conventional chemotherapy. We also explored the possibility of targeting CTLA-4 for apoptosis induction in chemoresistant AML cells.
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