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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0704385

Received for publication July 5, 2004.
Revised August 12, 2004.
Accepted for publication August 17, 2004.

Article

Differential macrophage expression of IL-12 and IL-23 upon innate immune activation defines rat autoimmune susceptibility

Åsa Andersson *@, Riikka Kokkola {dagger}, Judit Wefer *, Helena Erlandsson-Harris {dagger}, and Robert A. Harris *

Departments of *Clinical Neurosciences, Applied Immunology, Karolinska Hospital, and {dagger}Medicine, Rheumatology Unit, Karolinska Institutet at Karolinska Hospital, Stockholm, Sweden

@ To whom correspondence should be addressed. E-mail: Asa.Andersson{at}cmm.ki.se.


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Abstract

Rodents typically demonstrate strain-specific susceptibilities to induced autoimmune models such as experimental arthritis and encephalomyelitis. A common feature of the local pathology of these diseases is an extensive infiltration of activated macrophages (M{Phi}). Different functional activation states can be induced in M{Phi} during innate immune activation, and it is this differential activation that might be important in susceptibility/resistance to induction or perpetuation of autoimmunity. In this study, we present an extensive, comparative analysis of the activation phenotypes of M{Phi} derived from autoimmune-susceptible and autoimmune-resistant rat strains to describe a cellular phenotype that defines the disease phenotype. We included investigation of receptor function, intracellular signaling pathways, cytokines, and other soluble mediators released after activation of cells using a panel of stimuli embracing many activation routes. We report that activation of M{Phi} from the autoimmune-susceptible strain was associated with alternative activation indicated by induction of arginase activity, a lower production of classical proinflammatory mediators, and a high production of interleukin (IL)-23, and M{Phi} from the autoimmune-resistant strains were associated with a higher production of proinflammatory mediators, a classical activation phenotype, and preferential induction of IL-12. These M{Phi} phenotypes thus reflect disparate, genetic cellular programs that define autoimmune susceptibility.

Key Words: cytokine • macrophage activation • autoimmunity




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