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*
Institut National de la Santé et de la Recherche Médicale, Unit 28, Institut Fédératif de Recherche 30, and Université Paul Sabatier, Hôpital Purpan, Toulouse, France; Departments of
Immunology and
Neurology, University of Maastricht, Maastricht, The Netherlands; and
§
Unité de Neurobiologie Moléculaire, Institut Pasteur, Paris, France
Experimental autoimmune myasthenia gravis (EAMG) is a T
cell-dependent, Ab-mediated autoimmune disease induced in rats by a
single immunization with acetylcholine receptor (AChR). Although
polarized Th1 responses have been shown to be crucial for the
development of mouse EAMG, the role of Th cell subsets in rat EAMG is
not well established. In the present work we show that while the
incidence and severity of EAMG are similar in Lewis (LEW) and
Brown-Norway (BN) rats, strong differences are revealed in the immune
response generated. Ag-specific lymph node cells from LEW rats produced
higher amounts of IL-2 and IFN-
than BN lymph node cells, but
expressed less IL-4 mRNA. IgG1 and IgG2b anti-AChR isotype
predominated in BN and LEW rats, respectively, confirming the dichotomy
of the immune response observed between the two strains. Furthermore,
although IL-12 administration or IFN- neutralization strongly
influenced the Th1/Th2 balance in BN rats, it did not affect the
disease outcome. These data demonstrate that a Th1-dominated immune
response is not necessarily associated with disease severity in EAMG,
not only in rats with disparate MHC haplotype but also in the same rat
strain, and suggest that in a situation where complement-fixing Ab can
be generated as a consequence of either Th1- or Th2-mediated T cell
help, deviation of the immune response will not be an adequate strategy
to prevent this Ab-mediated autoimmune disease.
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