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Interferons and autoimmunity.

¹Department of Virology, Weizmann Institute of Science, Rehovot, Israel.

The American Journal of the Medical Sciences

|June 1, 1988

Summary

This summary is machine-generated.

Interferon (IFN) can accelerate autoimmune disease in mice and humans. Aberrant expression of MHC class II antigens, induced by IFN-gamma, plays a key role in autoimmune disease development.

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Area of Science:

Immunology
Virology
Genetics

Background:

Autoimmunity can be accelerated in genetically susceptible murine models.
Interferon (IFN) or IFN-inducers can trigger autoimmune disease.
IFN plays a role in mediating or enhancing autoimmune disease manifestations and immunological aberrations.

Purpose of the Study:

To investigate the role of interferon in the induction and exacerbation of autoimmune diseases.
To explore the significance of circulating IFN levels and specific IFN types in autoimmune patients.
To understand the mechanism by which IFN-gamma induces MHC class II antigen expression and its implication in autoimmunity.

Main Methods:

Studies in genetically prone murine models.
Treatment of normal mice with interferon or interferon-inducers.

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Clinical observation of human cases with IFN-induced autoimmune disease.

Analysis of circulating IFN levels and types in patients.

Investigation of IFN-gamma's effect on MHC class II antigen expression.

Main Results:

Interferon (IFN) can accelerate or induce autoimmunity in mice.
Autoimmune disease cases linked to IFN treatment have been observed in humans.
High levels of circulating IFN, particularly acid-labile IFN-alpha (often associated with viral infections), are found in many patients.
IFN-gamma induces MHC class II antigens on cells that are normally negative for these markers.
Aberrant HLA-DR expression on nonlymphoid cells is an early indicator in various autoimmune conditions.

Conclusions:

Interferon is implicated in the pathogenesis of autoimmune diseases.
The presence of specific IFN types, like acid-labile IFN-alpha, may suggest an infectious etiology for autoimmunity.
IFN-gamma-induced MHC class II expression on nonlymphoid cells is a critical factor in initiating autoimmune responses.