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1

Epitope spreading: a mechanism for progression of autoimmune disease

100%

Tuohy V. K., Kinkel P.

Archivum Immunologiae et Therapiae Experimentalis

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2000

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vol. 48

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issue 5

347-352

EN

Autoimmune diseases are typically characterized by a persistent inflammatory self-recognition process that ultimately leads to chronic progressive disability. Over the past several years we have addressed the fundamental question of why autoimmune diseases are chronic. Our working hypothesis in these studies has been that autoimmunity involves a continuous acquisition of new self-recognition events, thereby providing an inflammatory steady-state that leads to chronicity. This acquired T cell neoautoreactivity is commonly referred to as epitope spreading. By studying mulitple sclerosis (MS) and its related animal model, experimental autoimmune encephalomyelitis (EAE), we have found that chronic progression of autoimmune disease is invariably linked to the development of any epitope-spreading process that manifests as a cascade of inflammatory T cell neoautoreactivities to a sequential series of predictable new target self-antigens. However, our most recent observations indicated that the emergence of epitope spreading is accompanied by a concurrent regression of the established primary autoreactivity associated with disease onset. Thus, our studies indicate that progression of autoimmune disease involves a shifting of T cell autoreactivity from primary initiating self-determinants to defined cascades of secondary determinants that sustain the inflammatory self-recognition process during progression to chronicity. Our data support the view that the natural development of self-recognition during autoimmune disease may best be understood when considered in the temporal context of an ?epitope du jour? and ?moving target? perspective.

2

Influence of aging on the protein profile of myelin isolated from human brain white matter

100%

Niebroj-Dobosz I., Rafalowska J., Lukasiuk M., Wisniewska W., Dziewulska D.

Neuropatologia Polska

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1992

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vol. 30

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issue 2

147-154

EN

Myelin proteins composition was examined in material of 20 autoptic cases at ages from 20 to 97 years. The technique of polyacrylamide gel electrophoresis and isotachophoresis was applied. In polyacrylamide gel electrophoresis a progressive increase starting at the age of 60 years of Wolfgram protein at the expense of Folch-Less proteolipid protein and DM-20 protein was observed. The myelin-associated protein started to increase in the 4th and 5th decade of life, returning therafter to values observed in younger cases. The isotachophoretic technique did not differentiate the changes observed in myelin protein in the course of aging.

3

The role of cytokines in experimental autoimmune encephalomyelitis

88%

Bettelli E., Nicholson L. B.

Archivum Immunologiae et Therapiae Experimentalis

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2000

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vol. 48

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issue 5

389-398

EN

Experimental autoimmune encephalomyelitis (EAE) is an animal model of the demyelinating disease multiple sclerosis. In EAE cytokines play a critical role in defining the Th1 or Th2 nature of the autoantigen directed immune response, and in propagating and regulating inflammation within the central nervous system. In this review we summarize some of the recent developments in the field of cytokine research that relate to this model of human disease, focusing principally on disease induced with the autoantigens myelin proteolipid protein and myelin oligodendrocyte protein.

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2 Archivum Immunologiae et Therapiae Experimentalis

1 Neuropatologia Polska

2 2000

1 1992

1 Bettelli E.

1 Dziewulska D.

1 Kinkel P.

1 Lukasiuk M.

1 Nicholson L. B.

1 Niebroj-Dobosz I.

1 Rafalowska J.

1 Tuohy V. K.

1 Wisniewska W.

Epitope spreading: a mechanism for progression of autoimmune disease

Influence of aging on the protein profile of myelin isolated from human brain white matter

The role of cytokines in experimental autoimmune encephalomyelitis