Initiation and development of experimental autoimmune neuritis in Lewis rats is independent of the cytotoxic capacity of NKR-P1A+ cells
| Autor: | Mats Alheim, Jie Zhu, Anna Klarare Ljungberg, Yu Zhu, Shuo Yu, Zhiguo Chen |
|---|---|
| Rok vydání: | 2002 |
| Předmět: |
Cytotoxicity
Immunologic Male medicine.drug_class Spleen Guillain-Barre Syndrome Monoclonal antibody Cellular and Molecular Neuroscience Interleukin 21 Splenocyte medicine Animals Cytotoxic T cell Lectins C-Type Peripheral Nerves business.industry Antibodies Monoclonal Flow Cytometry Natural killer T cell Neuritis Autoimmune Experimental Peptide Fragments Rats Killer Cells Natural medicine.anatomical_structure Rats Inbred Lew Antigens Surface Immunology Interleukin 12 business Myelin P0 Protein Demyelinating Diseases NK Cell Lectin-Like Receptor Subfamily B K562 cells |
| Zdroj: | Journal of Neuroscience Research. 67:823-828 |
| ISSN: | 1097-4547 0360-4012 |
| Popis: | Natural killer (NK) cells are implicated in T cell-mediated autoimmune diseases. Experimental autoimmune neuritis (EAN) is a CD4+ T cell-mediated animal model of the Guillain-Barre syndrome in human. The role of NK cells in the initiation and development of EAN remains unclear. In the present study, we demonstrate that anti-NKR-P1A monoclonal antibody (mAb) treatment in vivo did not affect the initiation and development of clinical EAN in Lewis rats induced by immunization with peripheral nerve myelin P0 protein peptide 180–199 and Freund's complete adjuvant, as well as the proportion of NKR-P1A+ cells (including NK cells and NKT cells) in the spleen. Furthermore, inflammatory cell infiltrations and demyelination in the peripheral nervous system (PNS) and in vitro P0 peptide 180–199-specific splenocyte proliferation were not different in anti-NKR-P1A mAb-treated rats compared to the control antibody-treated rats. The cytotoxic activity of NKR-P1A+ cells, determined by NK cell-sensitive K562 cells as target cells, decreased markedly in anti-NKR-P1A mAb-treated rats, suggesting that decrease of the cytotoxic activities of NKR-P1A+ cells is not sufficient to alter clinical EAN, although NKR-P1A+ cells may participate in the pathogenesis of T cell-mediated autoimmune diseases, such as EAN, by the mechanisms that involve the release of cytokines. © 2002 Wiley-Liss, Inc. |
| Databáze: | OpenAIRE |
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