Autologous mixed lymphocyte responses in experimentally-induced arthritis of the Lewis rat
| Autor: | Norman A. Staines, A.S. Hamblin, Brian Catchpole |
|---|---|
| Rok vydání: | 2002 |
| Předmět: |
T-Lymphocytes
Immunology Antigen presentation Arthritis Antigen-Presenting Cells Autoimmunity Major histocompatibility complex medicine.disease_cause chemistry.chemical_compound Antigen Adjuvants Immunologic Immunology and Allergy Medicine Animals Antigens Antigen-presenting cell Cells Cultured Cell Proliferation biology business.industry T lymphocyte Mycobacterium tuberculosis medicine.disease Coculture Techniques Rats Phenotype chemistry Rats Inbred Lew biology.protein Immunization Lymphocyte Culture Test Mixed business Muramyl dipeptide |
| Zdroj: | Autoimmunity. 35(2) |
| ISSN: | 0891-6934 |
| Popis: | Lewis rats develop immune-mediated arthritis following injection with a variety of agents including bovine type II collagen (bCII), mycobacteria, muramyl dipeptide and CP20961. Since susceptibility to experimentally-induced arthritis has been linked to the genes encoding the major histocompatibility complex, it is hypothesized that antigen presentation to autoreactive T-cells is a critical event in the pathogenesis of disease. T-cells, isolated from Lewis rats immunized with bCII or mycobacteria, were co-cultured with splenic or thymic antigen presenting cells (APC) and proliferative responses to antigen were assessed by 3H-thymidine incorporation. T-cell proliferation was observed upon culture with APC without requiring the addition of antigen. T-cells from rats injected with non-immunogenic adjuvants also demonstrated an increased autologous MLR compared to T-cells from non-injected animals. In contrast, T-cells from animals immunized with non-arthritogenic antigens, including ovalbumin or tetanus toxoid, proliferated only when co-cultured with specific antigen-pulsed APC. These results suggest that immunization with arthritogens activates a population of self-reactive T-cells, which respond in an autologous MLR. We propose that these autoreactive T-cells recognize endogenously-derived self peptides rather than peptides derived from a joint autoantigen. |
| Databáze: | OpenAIRE |
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