Role of major histocompatibility complex class I molecules in autoimmune myositis.

Abstract:

PURPOSE OF REVIEW:Recent work has continued to clarify the role of major histocompatibility complex class I in the pathogenesis of autoimmune myositis. In the past year, several new observations have been made in this area. This review describes these findings and discusses their relevance to the pathogenesis of autoimmune myositis. RECENT FINDINGS:Recent studies have confirmed earlier observations of the up-regulation of major histocompatibility complex class I antigens in myositis. In particular, a recent study has strengthened the conclusion that major histocompatibility complex class I expression is highly specific to inflammatory myopathies and may be of diagnostic value. Two new studies have indicated that endoplasmic reticulum stress response pathway (the endoplasmic reticulum overload [NF-kB] and unfolded protein response [GRP78]) are highly activated in patients with myositis. One study using transgenic mice has further indicated that abnormal accumulation of major histocompatibility complex class I in the endoplasmic reticulum of muscle may be responsible for the initiation of this endoplasmic reticulum stress response. Furthermore, studies of normal muscle cells have shown that endoplasmic reticulum stress also plays an important role in skeletal muscle development. Investigations of autoantigen expression in myositis biopsies have revealed that regenerating muscle cells express high levels of autoantigens and major histocompatibility complex class I, indicating that these cells are the targets of cytotoxic T-cell attack and may participate in the initiation of a myositis-specific autoimmune response. SUMMARY:Defining the role of major histocompatibility complex class I in autoimmune myositis may be useful not only for diagnosis of this group of diseases but also for therapeutic opportunities for these difficult disorders.

journal_name

Curr Opin Rheumatol

authors

Nagaraju K

doi

10.1097/01.bor.0000179947.58271.9a

keywords:

subject

Has Abstract

pub_date

2005-11-01 00:00:00

pages

725-30

issue

6

eissn

1040-8711

issn

1531-6963

pii

00002281-200511000-00007

journal_volume

17

pub_type

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