Oral administration of type I interferon modulates the course of experimental allergic neuritis

TY - JOUR

T1 - Oral administration of type I interferon modulates the course of experimental allergic neuritis

AU - Vriesendorp, Francine J.

AU - Flynn, Robyn E.

AU - Khan, Mohammad

AU - Pappolla, Miguel A.

AU - Brod, Staley A.

N1 - Funding Information: the immune system is unknown but may include secondarily reduced IFN-y production. The effects on Peyer's patches in the gut-associated inability to decrease inflammation in later stages lymphoid tissue (GALT) where requlatory cells of disease may be due to partial suppression of can be generated.30-32 IFN-a may induce im-IFN-y production or the influence of other cyto-munoregulatory factors derived from CD8 + T kines and inflammatory mediators. cells that are responsible for disease modifi-In summary, oral interferon is a biological ~ a t i o n .T~he r-ed~uced IFN-y production asso-response modifier effective in modifying disease ciated with oral IFN-a@ administration suggests in another experimental autoimmune disease, a possible functional inhibition of systemic Thl-EAN. The results of our study in EAN showing like T helper cells found in EAE that produce reduced disease severity in rats fed IFN-alp sugI F N - Y .T~his results in a diminution of T cell gest that oral IFN-do administration may possi-encephalitogenicity of actively or passively in-bly be useful in the treatment of human immune-duced disease. Although we found decreased bo-mediated inflammatory neuropathies such as vine peripheral nerve myelin-induced prolifera-chronic inflammatory demyelinating polyradicu-tion in the spleen, and decreased bovine loneuropathy (CIDP) and other chronic autoim-peripheral nerve myelin-induced IFN-y secretion mune diseases. in the lymph node, thus in two immune compart-Supported by NIH Grant 5 KO8 NS01530 to ments, the immunosuppressive effect of oral IFN-F.J. Vriesendorp and a grant from the Clayton alp was directed against antigen-specific reactiv-Foundation to S.A. Brod. ity and antigen-induced inflammatory cytokine production, suggesting that oral IFN can prefer- entially act on preactivated antigen-specific cells. Parenteral IFN-y administration has been shown to augment both myelin-induced and T-cell mediated EAN with increased clinical signs and histological abnormalities and enhanced oxi- dative burst by macrophages, while the opposite effect was obtained by parenteral administration of anti-IFN-y antibody.36 IFN-y also induces MHC class I and I1 expression on Schwann cells in ~ i t r oI.FÑ-~y, an inflammatory cytokine re- leased by Thl CD4 + T-cells, can upregulate MHC Class I1 expression on macrophages and endothelial cells and activate macrophages that play an important role in myelin phagocyto~is.~~ In our experiments reduced IFN-y expression and reduced inflammation was seen at the onset of clinical disease in IFN-a/P fed animals. Histolog- ical evaluation at the end of the disease process, when recovery had started, showed reduced de- myelination but not inflammation in IFN-a@ fed animals. The findings of early decreased IFN-y and inflammation may reflect reduced IFN-y pro- duction by infiltrating inflammatory cells or a treatment-induced delay of inflammation with

PY - 1996

Y1 - 1996

KW - EAN

KW - IRN-α

KW - IRN-γ

KW - Oral feeding

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U2 - 10.3109/08916939608995361

DO - 10.3109/08916939608995361

M3 - Article

C2 - 9020408

AN - SCOPUS:0030454489

SN - 0891-6934

VL - 24

SP - 157

EP - 165

JO - Autoimmunity

JF - Autoimmunity

IS - 3

ER -