6533b85afe1ef96bd12b8d3e
RESEARCH PRODUCT
In vitro model for the activation of CD4 and CD8 T cell receptors.
Borros Arnethsubject
CD4-Positive T-LymphocytesCytoplasmImmunologyReceptors Antigen T-CellAutoimmunityCell SeparationCD8-Positive T-Lymphocytesmedicine.disease_causeLymphocyte ActivationHemoglobinsAlbuminsmedicineExtracellularImmunology and AllergyCytotoxic T cellHumansInsulinReceptorGlyceraldehyde 3-phosphate dehydrogenaseCells CulturedbiologyAlbuminModels ImmunologicalGlyceraldehyde-3-Phosphate DehydrogenasesGeneral MedicineImmune dysregulationFlow CytometryActinsCell biologyProtein Transportbiology.proteinCell activationExtracellular SpaceIntracellulardescription
Previously, most models that sought to explain the misregulation of immune cell function assumed molecular similarities between the disease-causing pathogens and the host's proteins. In recent time several different models have been proposed and in this study, these concepts are compared to a new hypothesis proposing another explanation for this immune dysregulation: the possibility that the mislocalization of proteins may be responsible for autoimmune activity. Based on this hypothesis, proteins are recognized as self or non-self depending on where they appear in sufficiently high concentrations. To examine this new idea, the intracellular human proteins beta-actin, GAPDH, and hemoglobin as well as the extracellular human proteins insulin and albumin, were added to human whole blood samples. After an incubation period, the activation of whole-blood T lymphocytes in the samples was measured. The observed activation pattern of the T lymphocytes fit well with the proposed hypothesis. Therefore, these data suggest that protein mislocalization and/or errors within protein trafficking might be important in the development of autoimmune diseases.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2008-09-25 | Human immunology |