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Receptor-Deficient Mice Is Conditioned by Mycobacteria in Freund’s Adjuvant and by Increased Expansion of Mac-1+ Myeloid Cells1
*
Rega Institute, University of Leuven, Leuven, Belgium;
Children’s Hospital, Harvard Medical School, Boston, MA 02115; and
Laboratory of Histochemistry, Faculty of Medicine, University of Leuven, Leuven, Belgium
Induction of experimental autoimmune diseases often relies on
immunization with the organ-specific autoantigens in CFA, which
contains heat-killed mycobacteria. In several of these models,
including collagen-induced arthritis, endogenous IFN-
acts as a
disease-limiting factor in the pathogenesis of the disease. Here we
show that in collagen-induced arthritis the protective effect of
IFN- depends on the presence of mycobacteria in the adjuvant.
Omission of mycobacteria inverts the role of endogenous IFN- to a
disease-promoting factor. Thus, the mycobacterial component of CFA
opens a pathway by which endogenous IFN- exerts a protective effect
that supersedes its otherwise disease-promoting effect. Extramedullary
hemopoiesis and expansion of the Mac-1+ cell population
accompanied the accelerated and more severe disease course in the
IFN- receptor knockout mice immunized with CFA. Treatment of such
mice with Abs against the myelopoietic cytokines IL-6 or IL-12
inhibited both disease development and the expansion of the
Mac-1+ population. We postulate that mycobacteria in CFA
stimulate the expansion of the Mac-1+ cell population by a
hemopoietic process that is restrained by endogenous IFN-. These
results have important implications for the validity of animal models
of autoimmunity to study the pathogenesis and to evaluate
cytokine-based therapy of autoimmune diseases.
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