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Major histocompatibility complex genes, such as HLA-A1, B8, and DR3 [4], as well as alleles that cause deficiency in complement components—C1q, C2, and C4 [5]—have all been linked to lupus.SLE is a complex disease process demonstrating dysregulation of the immune system at multiple levels.Orbital involvement is a rare manifestation of SLE.Vasculitis, myositis, and panniculitis have all been described.

Orbital myositis is often initially misdiagnosed as bacterial orbital cellulitis, as it usually presents with significant pain, proptosis, periorbital swelling, and globe restriction.

Mass production of autoantibodies relies on multiple factor, which have each independently been targeted as potential immunotherapy in the treatment of lupus.

Important steps include T-cell activation via antigen binding to the T-cell receptor and proper costimulation; T-cell activation of B cells; production of cytokines such as TNF-α, INF-γ, IL-10, and B-lymphocyte stimulator.

Two major theories exist on how these autoantibodies cause tissue damage.

The first model suggests that anti-double-stranded DNA antibodies bind to circulating nucleosomes to form immune complexes that then get deposited in end-organ capillary beds such as the renal glomerulus and activate immune/inflammatory responses [7].

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