Destruction of Lymphoid Organ Architecture and Hepatitis Caused by CD4+ T Cells Immunopathology Induced by CD4+ T cells
2011

CD4+ T Cells and Their Role in Liver Damage and Immune Response

Sample size: 3 publication 10 minutes Evidence: high

Author Information

Author(s): Matter Matthias S., Hilmenyuk Tamara, Claus Christina, Marone Romina, Schürch Christian, Tinguely Marianne, Terracciano Luigi, Luther Sanjiv A., Ochsenbein Adrian F.

Primary Institution: University of Bern, Bern, Switzerland

Hypothesis

The study investigates the role of CD4+ T cells in the destruction of lymphoid organ architecture and liver damage during lymphocytic choriomeningitis virus (LCMV) infection.

Conclusion

CD4+ T cells play a significant role in inducing immunopathology in the liver and spleen during LCMV infection, leading to the destruction of the splenic marginal zone and liver cell damage.

Supporting Evidence

  • CD4+ T cells were shown to selectively destroy the splenic marginal zone.
  • Elevated serum alanine aminotransferase (ALT) levels indicated liver cell damage.
  • The study demonstrated that CD4+ T cells impaired the production of neutralizing antibodies against LCMV.

Takeaway

When mice get infected with a virus, some immune cells called CD4+ T cells can accidentally hurt the body's own organs, like the liver and spleen, instead of just fighting the virus.

Methodology

The study involved adoptive transfer of CD4+ T cells into CD8+ T cell-depleted mice followed by infection with LCMV, with subsequent analysis of immune responses and tissue damage.

Potential Biases

Potential bias may arise from the specific mouse models used and the controlled experimental conditions.

Limitations

The study primarily focuses on the role of CD4+ T cells in a specific viral infection and may not generalize to other infections or immune responses.

Participant Demographics

C57BL/6 mice and various genetically modified mouse strains were used in the experiments.

Statistical Information

P-Value

p<0.05

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1371/journal.pone.0024772

Want to read the original?

Access the complete publication on the publisher's website

View Original Publication