Phenotypic and functional properties of γδ T Cells from patients with Guillain Barré syndrome
| Autor: | Giovanna Borsellino, Barbara Cipriani, Sabina Luchetti, Luca Battistini, Simona Bach, Giorgio Mancino, Fabrizio Poccia, Roberta Placido, Bruno Bonetti, Celia F. Brosnan, Daniela Tramonti, Simona Galgani |
|---|---|
| Rok vydání: | 2000 |
| Předmět: |
Adult
Multiple Sclerosis T-Lymphocytes T cell Immunology Biology Guillain-Barre Syndrome Ligands Natural killer cell Antigen Reference Values medicine Humans Immunology and Allergy Lectins C-Type Phosphorylation Receptors Immunologic Receptor Blood Cells Guillain-Barre syndrome Multiple sclerosis T-cell receptor Receptors Antigen T-Cell gamma-delta medicine.disease Phenotype Killer Cells Natural medicine.anatomical_structure Neurology Antigens Surface Cytokines Receptors Natural Killer Cell Neurology (clinical) NK Cell Lectin-Like Receptor Subfamily B |
| Zdroj: | Journal of Neuroimmunology. 102:199-207 |
| ISSN: | 0165-5728 |
| DOI: | 10.1016/s0165-5728(99)00165-4 |
| Popis: | In this study we have examined the phenotypic and functional properties of circulating gamma delta T cells in patients with Guillain Barre syndrome (GBS), in normal healthy controls, and in patients with active multiple sclerosis (MS). Cells expressing the Vdelta2 T cell receptor showed elevated expression of the C-lectin receptor NKRP1A in both GBS and MS, suggestive of an activated state. However, in patients with GBS these cells failed to respond to pyrenil-pyrophosphate derivatives and Vdelta2 + T cell clones derived from these patients released lower levels of IFNgamma than Vdelta2 + clones derived from controls and MS patients. In contrast, in patients with GBS the Vdelta1 + subset was expanded, showed elevated expression of NKRPIA and Vdelta1 + clones derived from these patients secreted high levels of IL-4. Our findings of expanded NKRP-1A +, IL-4-producing Vdelta1 T cells in the GBS patients suggests the possibility that these cells are activated by the recognition of non-protein antigens in an MHC-unrestricted manner and contribute to the humoral response to glycolipids that is a hallmark of this disease. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect