Macrophage-inactivating IL-13 suppresses experimental autoimmune encephalomyelitis in rats.

Authors: Cash, E  Minty, A  Ferrara, P  Caput, D  Fradelizi, D  Rott, O 
Citation: Cash E, etal., J Immunol. 1994 Nov 1;153(9):4258-67.
Pubmed: (View Article at PubMed) PMID:7523520

Experimental autoimmune encephalomyelitis (EAE) is initiated by myelin basic protein (MBP)-specific CD4+ T cells of the Th1 phenotype that subsequently trigger the invasion of monocytes/macrophages into the brain. In this study, we evaluated the potential of human recombinant (hr) IL-13 to exert a protective effect on the development of EAE in Lewis rats. hrIL-13 is found to be a potent in vitro modulator of various rat macrophage functions, including an inhibition of the production of the proinflammatory cytokines IL-1 beta and TNF, and a simultaneous enhancement of MHC class II and CD4 receptor expression. Furthermore, hrIL-13 displayed a slight, but highly reproducible, inhibitory effect on the in vitro proliferative responses of encephalitogenic MBP-specific T cells stimulated in the presence of thymic APCs. Upon in vivo application of hrIL-13-secreting vector cells into MBP-immunized animals, the cytokine was capable of markedly suppressing the development of EAE, as assessed by a reduction of the mean duration, severity, and incidence of disease. This suppression of disease coincided with an only minimal reduction of MBP-directed T cell autoreactivity and no alteration in MBP-specific autoantibody production. We infer from these results that a strictly Th1-initiated immune disease can be attenuated efficiently by the administration of a cytokine that primarily targets cells of the macrophage/monocyte lineage and seems to exert no undesirable general suppression on either T cell or B cell immunoreactivity in vivo.

Annotation

Disease Annotations
Objects Annotated

Additional Information

 
CRRD Object Information
CRRD ID: 5684367
Created: 2011-12-16
Species: All species
Last Modified: 2011-12-16
Status: ACTIVE



NHLBI Logo

RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.