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Lymphocytic choriomeningitis virus induces a chronic wasting disease in mice lacking class I major histocompatibility
P C Doherty1, S Hou, P J Southern
1Department of Immunology, St. Jude Children's Research Hospital, Memphis, TN 38101.
Abstract:
Lymphocytic choriomeningitis virus (LCMV) induces a chronic, wasting syndrome when injected intracerebrally into H-2b mice homozygous for a beta 2-microglobulin (beta 2-m (-/-)) gene disruption. These mice have very few CD8+ T cells and express little class I MHC glycoprotein, though minimal levels of the H-2Db molecule have been detected on in vitro cultured beta 2-m (-/-) cells. The underlying immunopathological process in these beta 2-m (-/-) mice is mediated by virus immune CD4+ effectors. However, adoptively transferred CD8+ T cells from normal, LCMV-infected H-2Db compatible donors induce significant (but low level) meningitis in beta 2-m (-/-) recipients. Such mice develop neither the neurological disease characteristic of LCM nor the persistent, though generally non-fatal, debility that occurs when only the CD4+ T cell subset is involved.
Insights
Lymphocytic choriomeningitis virus (LCMV) causes wasting in mice lacking beta 2-microglobulin (beta 2-m). CD8+ T cells, though few, can induce meningitis, but not severe LCMV disease.
Area of Science:
- Immunology
- Virology
- Neuroscience
Background:
- Lymphocytic choriomeningitis virus (LCMV) infection in H-2b mice with beta 2-microglobulin (beta 2-m) gene disruption leads to a chronic wasting syndrome.
- These mice exhibit a severe deficiency in CD8+ T cells and class I MHC glycoprotein expression, crucial for immune responses.
Purpose of the Study:
- To investigate the role of CD8+ T cells in the immunopathology of LCMV infection in beta 2-m (-/-) mice.
- To determine if adoptively transferred CD8+ T cells can induce or prevent LCMV-induced neurological disease in this model.
Main Methods:
- Intracerebral injection of LCMV into beta 2-m (-/-) mice.
- Assessment of immune cell populations (CD4+ and CD8+ T cells) and MHC class I expression.
- Adoptive transfer of CD8+ T cells from LCMV-infected donors into beta 2-m (-/-) recipients.
Main Results:
- LCMV infection in beta 2-m (-/-) mice is primarily mediated by CD4+ T cell effectors, causing wasting.
- Adoptive transfer of CD8+ T cells into beta 2-m (-/-) mice induced low-level meningitis.
- Mice receiving CD8+ T cells did not develop characteristic LCMV neurological disease or persistent debility.
Conclusions:
- CD8+ T cells play a limited but specific role in LCMV pathogenesis in beta 2-m deficient mice, primarily causing meningitis.
- The absence of functional CD8+ T cells and MHC class I in beta 2-m (-/-) mice alters the immunopathology of LCMV infection, preventing severe neurological outcomes.
