The Role of LFA-1 in T cell Trafficking and Functions in Demyelinating Disease (99.5)
| Autor: | Kari J Dugger, Kurt R Zinn, Daniel C Bullard, Scott R Barnum |
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| Rok vydání: | 2007 |
| Předmět: | |
| Zdroj: | The Journal of Immunology. 178:S195-S195 |
| ISSN: | 1550-6606 0022-1767 |
| Popis: | Multiple sclerosis (MS) is characterized by autoimmune damage to central nervous system (CNS) myelin, resulting in impaired nerve function. Integrins such as lymphocyte function-associated antigen-1 (LFA-1) are thought to be important in leukocyte trafficking to the CNS and disease development. Studies using monoclonal antibodies to LFA-1 in experimental autoimmune encephalomyelitis (EAE), the animal model for MS, have provided conflicting results regarding the role of LFA-1 in EAE. To overcome the limitations of the antibody-based approach, we used LFA-1-deficient mice and a transgenic mouse (T-lux) with a hCD2 promoter that drives expression of the luciferase gene specifically in T cells thereby providing a novel method of a real-time depiction of T cell trafficking patterns. We found that both LFA-1-deficient and LFA-1 hemizygous mice do not develop clinically significant EAE and have markedly reduced leukocyte infiltration into the CNS. Encephalogenic LFA-1-deficient T-lux cells adoptively transferred into wild type recipients do not localize to the CNS, whereas MOG-specific wildtype T-lux cells transferred to wildtype or LFA-1-deficient recipients, readily migrate to the CNS and draining lymph nodes and proliferate. These data demonstrate that LFA-1 on T cells is necessary for myelin-specific T cells to enter into the CNS and initiate disease. Supported by NIH grant NS46032. |
| Databáze: | OpenAIRE |
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