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Untitled - D Ank Unlimited

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skin autoantibodies 657 skin immunity<br />

Sjögren’s syndrome.<br />

(LE) cell test is positive in 25% of patients. Numerous<br />

antibodies are produced, including autoantibodies against<br />

salivary duct cells, gastric parietal cells, thyroid antigens,<br />

and smooth muscle mitochondria. Antibodies against<br />

ribonucleoprotein antigens are termed Ro/SSA and La/SSB.<br />

Approximately 90% of the patients have these antibodies.<br />

Anti-SSB shows greater specificity for Sjögren’s syndrome<br />

than do anti-SSA antibodies that also occur in SLE. Patients<br />

who have Sjögren’s syndrome with rheumatoid arthritis may<br />

have antibodies to rheumatoid-associated nuclear antigen<br />

(RANA). A positive correlation exists between HLA-DR3<br />

and primary Sjögren’s syndrome and between HLA-DR4<br />

and secondary Sjögren’s syndrome associated with rheumatoid<br />

arthritis. Genetic predisposition, viruses, and disordered<br />

immunoregulation may play a role in pathogenesis.<br />

About 90% of the patients are 40- to 60-year old females.<br />

In addition to dry eyes and mouth and associated visual or<br />

swallowing difficulties, 50% of the patients show parotid<br />

gland enlargement. Drying of the nasal mucosa is accompanied<br />

by bleeding, pneumonitis, and bronchitis. A lip biopsy<br />

to examine minor salivary glands is needed to diagnose<br />

Sjögren’s syndrome. Inflammation of the salivary and<br />

lacrimal glands was previously called Mikulicz’s disease.<br />

Mikulicz’s syndrome is enlargement of the salivary and lacrimal<br />

glands due to any cause. Enlarged lymph nodes that<br />

reveal a pleomorphic cellular infiltrate with many mitoses<br />

are typical of Sjögren’s syndrome and have been referred<br />

to as pseudolymphoma. Patients have a 40-fold greater risk<br />

than others for lymphoid neoplasms.<br />

skin autoantibodies<br />

Autoantibodies detectable by immunofluorescence associated<br />

with selected bullous skin diseases and useful for<br />

categorizing them. The three principal categories of bullous<br />

skin diseases are intraepidermal bullae with an immunological<br />

etiology, subepidermal bullae with immunological<br />

pathogenesis, and nonimmune bullous disorders.<br />

skin-associated lymphoid tissue (SALT)<br />

Diffuse epidermal T cells, including αβ and γδ T cells and<br />

dendritic (Langerhans) cells together with dermal αβ T<br />

cells, fibroblasts, macrophages, and lymphatic vessels.<br />

skin-fixing antibody<br />

An antibody such as immunoglobulin E (IgE) retained in<br />

the skin following local injection as in passive cutaneous<br />

anaphylaxis. Antibody with this property was referred to<br />

previously as reagin before IgE was described.<br />

Early depiction of skin grafts from forehead, neck, and cheek used to restore<br />

mutilation of the nose, ear, and lip.<br />

skin graft<br />

Skin from an individual (autologous graft) or donor skin<br />

applied to areas of the body surface that have undergone<br />

third-degree burns. A patient’s keratinocytes may be<br />

cultured into confluent sheets that can be applied to the<br />

affected areas, although these may not “take” because of<br />

the absence of type IV collagen 7S basement membrane<br />

sites for binding and fibrils to anchor the graft.<br />

skin immunity<br />

The skin, the largest organ of the body, shields the interior<br />

environment from a hostile exterior. The skin defends the<br />

host through stimulation of inflammatory and local immune<br />

responses. Antigen applied to or injected into the skin<br />

drains to the regional lymph nodes through the skin’s extensive<br />

lymphatic network. Cells of the epidermis and papillary<br />

and reticular dermis play critical roles in the skin’s<br />

immune function. Keratinocytes (epidermal epithelial cells)<br />

secrete various cytokines such as granulocyte–macrophage<br />

colony-stimulating factor (GM-CSF), interleukin-1 (IL1),<br />

IL3, IL6, and tumor necrosis factor (TNF). T lymphocytes<br />

in the skin may secrete interferon-γ (IFN-γ) and other<br />

cytokines that cause these epithelial cells to synthesize<br />

chemokines that lead to leukocyte chemotaxis and activation.<br />

Stimulation by IFN-γ may also lead to expression of<br />

major histocompatibility complex (MHC) class II molecules.<br />

Other epidermal cells include Langerhans’ cells that<br />

form an extensive network in the epidermis that permits<br />

their interaction with any antigen entering the skin. The<br />

few lymphocytes in the epidermis are principally CD8 + T<br />

S

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