Related Experiment Videos
Autoimmune myocarditis does not require B cells for antigen presentation.
S Malkiel1, S Factor, B Diamond
1Department of Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Journal of Immunology (Baltimore, Md. : 1950)
|November 24, 1999
Summary
B cells are not critical for initiating autoimmune myocarditis. Macrophages or dendritic cells likely activate the autoreactive T cells responsible for this condition in mice.
Area of Science:
- Immunology
- Autoimmunity
- Cardiovascular Research
Background:
- T cells are the primary drivers of autoimmune myocarditis in BALB/c mice.
- The role of B cells as antigen-presenting cells (APCs) in initiating this autoimmune response remains unclear.
Purpose of the Study:
- To investigate whether B cells are essential APCs for the induction of autoimmune myocarditis.
- To identify the APCs responsible for activating pathogenic T cells in this model.
Main Methods:
- Utilized B cell-deficient mice created through IgM gene disruption or anti-IgM antibody treatment.
- Immunized B cell-deficient and wild-type mice with cardiac myosin.
- Assessed myocarditis incidence and severity in both groups.
Main Results:
- B cell-deficient mice developed myocarditis with comparable incidence and severity to wild-type mice.
- This suggests that B cells are not critical APCs for initiating autoimmune myocarditis.
- Macrophages or dendritic cells are likely responsible for activating autoreactive T cells.
Conclusions:
- B cells do not play a critical role in the induction of autoimmune myocarditis.
- Autoreactive T cells are likely activated by macrophages or dendritic cells.
- Mechanisms such as epitope presentation or sequestration may explain the escape of autoreactive T cells from tolerance.