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Analysis of dendritic-cell-induced primary T-cell responses between HLA genotypically identical individuals
DCs are known for their superior antigenprocessing and antigen-presenting capacities. They are capable of processing intact protein: either endocytosed exogenous proteins or newly synthesized endogenous viral and bacterial proteins. They are potent inducers of primary T-cell immune responses such as...
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Published in: | Human immunology 1995-11, Vol.44 (3), p.181-188 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | DCs are known for their superior antigenprocessing and antigen-presenting capacities. They are capable of processing intact protein: either endocytosed exogenous proteins or newly synthesized endogenous viral and bacterial proteins. They are potent inducers of primary T-cell immune responses such as in allogeneic MLRs. It is also known that DCs can provide a strong stimulus for autologous T-cell proliferation. So far no information exists on the capacity of DCs to induce primary mH antigen-specific T-cell responses. Therefore, we investigated whether human DCs, isolated from peripheral blood, were able to generate specific T-cell responses between MLR-negative HLA genotypically identical individuals in vitro. To this end, unfractionated cells, monocytes, and B cells were assayed in parallel with DCs to compare their capacity to activate unprimed T cells in a primary MLR. DCs indeed induced significant proliferation between HLA genotypically identical siblings, whereas the other APCs were unable to evoke any T-cell response at all. As expected, besides these allogeneic T-cell responses, autologous T-cell responses were initiated by the DCs as well. Nonetheless, despite further detailed analyses of the responding T cells, neither proliferative nor cytotoxic mH antigen-specific reactivities could yet be detected using the stimulation protocols described herein. |
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ISSN: | 0198-8859 1879-1166 |
DOI: | 10.1016/0198-8859(94)00123-5 |