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Updated: Jun 14, 2026

Induction of Experimental Autoimmune Encephalomyelitis in Mice and Evaluation of the Disease-dependent Distribution of Immune Cells in Various Tissues
Published on: May 8, 2016
Induction of distinct neurologic disease manifestations during relapsing fever requires T lymphocytes
Hongqi Liu1, Denise Fitzgerald, Bruno Gran
1Department of Microbiology and Immunology, Thomas Jefferson University, Philadelphia, PA 19107, USA.
Abstract:
Relapsing fever borreliosis is a multisystemic infection characterized primarily by bacteremia but can extend to the CNS. The incidence of CNS disease manifestations in humans depends on the infecting relapsing fever Borrelia species. In the murine model of Borrelia hermsii infection we found high incidence of distinct signs of CNS disease that ranged from a flaccid tail to complete paralysis of hind limbs. Infiltration of large number of T cells into the spinal cord of B. hermsii-infected mice and the upregulation of MHC class II and CD80 on infiltrating macrophages and on microglial cells suggested a role for T cell and Ag-presenting cell interactions in this pathogenesis. Indeed, B. hermsii infection did not induce CNS disease manifestations in T cell-deficient mice (TCR-beta x delta(-/-)), although it resulted in bacteremia comparable to wild-type (Wt) level. Moreover, the infiltration of immune cells into the spinal cord of TCR-beta x delta(-/-) mice was reduced and the resident microglial cells were not activated. Histopathological analysis of lumbar sections of the spinal cord confirmed severe inflammation in Wt but not in TCR-beta x delta(-/-) mice. Induction of CNS disease was dependent on the B. hermsii strain as well as on the ability of the host to control bacteremia. Mice that are impaired in controlling B. hermsii, such as CD14(-/-) mice, exhibited more severe CNS disease than Wt mice. This study demonstrates that distinct neurologic disease manifestations develop during relapsing fever and that T cells play a critical role in the induction of neuropathogenesis.
Insights
T cells are critical for causing central nervous system (CNS) disease in relapsing fever borreliosis. Without T cells, mice infected with Borrelia hermsii did not develop neurological symptoms, despite high bacterial levels.
Area of Science:
- Neuroscience
- Immunology
- Infectious Disease
Background:
- Relapsing fever borreliosis is a systemic infection caused by Borrelia species.
- Central nervous system (CNS) involvement varies depending on the Borrelia species.
- Neurological manifestations can range from mild symptoms to severe paralysis.
Purpose of the Study:
- To investigate the role of T cells in the development of CNS disease during Borrelia hermsii infection in a murine model.
- To understand the mechanisms underlying Borrelia-induced neuropathogenesis.
Main Methods:
- Utilized a murine model of Borrelia hermsii infection.
- Compared disease progression in wild-type (Wt) mice and T cell-deficient mice (TCR-beta x delta(-/-)).
- Assessed CNS pathology, immune cell infiltration, and microglial activation via histopathology and flow cytometry.
Main Results:
- Borrelia hermsii infection led to significant CNS disease signs in Wt mice, including paralysis.
- T cell-deficient mice showed no CNS disease, despite comparable bacteremia levels to Wt mice.
- Reduced immune cell infiltration and microglial activation were observed in the spinal cords of T cell-deficient mice.
- CNS disease severity was influenced by the Borrelia strain and the host's ability to control bacteremia (e.g., CD14(-/-) mice showed more severe disease).
Conclusions:
- T cells are essential for the induction of Borrelia-induced neuropathogenesis.
- The study highlights the critical role of T cell-mediated immunity in preventing or mediating CNS complications of relapsing fever borreliosis.
- Distinct neurological diseases arise during relapsing fever, with T cells playing a pivotal role.
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