Dark Agouti (DA) rats are highly susceptible to induction of Th-l-mediated autoimmunity
disease, including experimental allergic encephalomyelitis (EAE). In contrast to other susceptible
rat strains in which disease is induced only with encephalitogen emulsified in complete
Freund's adjuvants (CFA), in DA rats EAE develops after injection of encephalitogen in
incomplete Freund's adjuvants (IFA) or Titermax, putative Th-2 directed adjuvant. Lymph
node cells derived from immunized DA rats and stimulated invitro produce significantly
more Interferon-γ (IFN-γ) than resistant Albino Oxford (AO) rats. However, cells derived
from both strains produce large amounts of IL-10 but not IL-4. Immunized lymph node cells
derived from EAE susceptible (AO × DA) F1rats induce clinical signs of disease in sublethally
irradiated parental DA but not AO rats. The pathohistology of the target tissue in these
recipients clearly demonstrated infiltration of mononuclear cells in both parental strains.
However, the number of CD4+ cells was significantly higher and number of apoptotic cells
significantly lower in DA rats sacrificed 8 days after passive transfer. We postulate that in
addition to higher IFN-γ and TNF-α production, resistance to early apoptosis of the invading
cells in the target tissue possibly due to lack of downregulation by TGF-β leads to exceptional
susceptibility to EAE in DA rats.
