CD62L Is Required on Effector Cells for Local Interactions in the CNS to Cause Myelin Damage in Experimental Allergic Encephalomyelitis
| Autor: | Harald G. Foellmer, Iqbal S. Grewal, Hua Wang, Wyne P. Lee, Charles A. Janeway, Daniel Tumas, Richard A. Flavell, Kate D. Grewal |
|---|---|
| Rok vydání: | 2001 |
| Předmět: |
CD4-Positive T-Lymphocytes
Central Nervous System Genetically modified mouse Adoptive cell transfer Encephalomyelitis Autoimmune Experimental Recombinant Fusion Proteins Encephalomyelitis Immunology Receptors Antigen T-Cell Antigen-Presenting Cells Autoimmunity Mice Transgenic chemical and pharmacologic phenomena Biology Lymphocyte Activation Mice 03 medical and health sciences Myelin 0302 clinical medicine Cell Adhesion medicine Animals Immunology and Allergy L-Selectin Myelin Sheath 030304 developmental biology Mice Knockout B-Lymphocytes 0303 health sciences Cell adhesion molecule Effector Macrophages T-cell receptor Myelin Basic Protein hemic and immune systems medicine.disease Adoptive Transfer Immunohistochemistry 3. Good health Mice Inbred C57BL Chemotaxis Leukocyte Infectious Diseases medicine.anatomical_structure Infiltration (medical) Gene Deletion 030217 neurology & neurosurgery |
| Zdroj: | Immunity. 14:291-302 |
| ISSN: | 1074-7613 |
| Popis: | Adhesion molecules are believed to facilitate infiltration of leukocytes into the CNS of mice with experimental allergic encephalomyelitis (EAE). The role of the adhesion molecule CD62L (L-selectin) in the immunopathology of EAE is not known. To study this, we crossed CD62L-deficient mice with myelin basic protein–specific TCR (MBP-TCR) transgenic mice. CD62L-deficient MBP-TCR transgenic mice failed to develop antigen-induced EAE, and, despite the presence of leukocyte infiltration, damage to myelin in the CNS was not seen. EAE could, however, be induced in CD62L-deficient mice upon adoptive transfer of wild-type macrophages. Our results suggest that CD62L is not required for activation of autoimmune CD4 T cells but is important for the final destructive function of effector cells in the CNS and support a novel mechanism whereby CD62L expressed on effector cells is important in mediating myelin damage. |
| Databáze: | OpenAIRE |
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