Related Experiment Videos
T cell subsets in experimental lupus nephritis: modulation by bacterial superantigen
E De Heer1, L Aaldering, S Florquin
1Leiden University Medical Center, Department of Pathology, The Netherlands.
Summary
Bacterial superantigen staphylococcal enterotoxin B (SEB) modulated chronic graft-versus-host disease (GvH) in mice. SEB delayed proteinuria and shifted kidney pathology toward a proliferative nephropathy.
Area of Science:
- Immunology
- Nephrology
- Microbiology
Background:
- Chronic graft-versus-host disease (GvH) in mice models lupus nephritis.
- This GvH model involves Th2-dependent B cell activation and T cell infiltration in glomeruli.
- Bacterial superantigens, like staphylococcal enterotoxin B (SEB), activate specific T cells.
Purpose of the Study:
- To investigate if SEB exposure modulates the autoimmune syndrome in the murine GvH model.
- To examine the effects of SEB on cytokine profiles, immunoglobulin production, proteinuria, and renal pathology.
Main Methods:
- DBA/2 lymphocytes were injected into (C57BL/6 x DBA/2)F1 hybrid mice to induce chronic GvH.
- Mice received two injections of 20 microg SEB within 2 weeks after GvH induction.
- Cytokine levels (IFN-gamma, IL-10, IL-2), Ig profile, proteinuria, and kidney pathology were analyzed.
Main Results:
- SEB injection increased interferon-gamma (IFN-gamma) and interleukin-10 (IL-10) release in GvH mice.
- SEB-treated GvH mice showed a delayed onset of proteinuria.
- Histological analysis revealed increased interstitial inflammation, mesangial proliferation, and IgG2a deposits in SEB-treated GvH mice.
Conclusions:
- Mice with chronic GvH are more responsive to SEB regarding cytokine production.
- Bacterial superantigen exposure can alter the course of GvH-induced renal disease, shifting it towards a proliferative nephropathy.