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Myelin proteolipid protein-induced experimental allergic encephalomyelitis. Variations of disease expression in
Abstract:
Strains of mice with diverse genetic backgrounds were tested for susceptibility to experimental allergic encephalomyelitis (EAE) induced by myelin proteolipid protein. EAE was elicited in all strains of mice tested, but the clinical and histologic features varied. SJL (H-2s) mice had a high incidence of both clinical and histologic disease characterized by early onset of clinical signs. Inguinal lymph node T cells from diseased animals responded specifically [( 3H]thymidine incorporation) to proteolipid protein and not to myelin basic protein. In contrast, BALB/c (H-2d), DBA/1 (H-2q), C57BL/6 (H-2b), AKR (H-2k), CBA (H-2k), C3H (H-2k), B10.BR (H-2k), and C57BR (H-2k) mice showed a later onset of clinical signs and typically a lower disease incidence. However, the most marked variations in disease incidence occurred among BALB/c (H-2d) substrains in which the incidence of EAE ranged from eight of nine (BALB/cPt) to complete resistance (BALB/cWt and BALB/cORNL). Because these BALB/c substrains were initially derived from the same inbred genetic source and are serologically identical at H-2, these results suggest that expression of proteolipid protein-induced EAE in the mouse involves additional loci outside the MHC.
Insights
Genetic background influences experimental allergic encephalomyelitis (EAE) susceptibility in mice. Non-MHC loci outside the major histocompatibility complex (MHC) play a role in proteolipid protein-induced EAE.
Area of Science:
- Immunology
- Neuroscience
- Genetics
Background:
- Experimental allergic encephalomyelitis (EAE) is a model for demyelinating diseases.
- Myelin proteolipid protein (PLP) is a key autoantigen in EAE.
- Genetic factors influence EAE susceptibility.
Purpose of the Study:
- To investigate the role of genetic background in PLP-induced EAE.
- To identify genetic loci controlling EAE susceptibility.
Main Methods:
- Induction of EAE in various mouse strains using PLP.
- Clinical and histological assessment of disease severity.
- T cell proliferation assays to assess antigen specificity.
Main Results:
- EAE was elicited in all tested mouse strains, but with varying clinical and histological features.
- SJL (H-2s) mice exhibited high incidence and early onset of EAE.
- BALB/c substrains showed significant variation in EAE incidence, suggesting non-MHC genetic control.
Conclusions:
- Mouse genetic background significantly impacts PLP-induced EAE.
- Genetic loci outside the MHC are involved in regulating EAE susceptibility.
- Further research is needed to identify specific genes controlling EAE.