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US28 734 uveitis
Rhus toxicodendron, now commonly called Toxicodendron radicans.
The cutaneous lesion is T cell-mediated and classified as
type IV hypersensitivity. The four Rhus catechols differ
according to pentadecyl side-chain saturation and induce
type IV delayed hypersensitivity. They are present in such
plants as poison oak, poison sumac, and poison ivy.
US28
A member of the G protein-coupled receptor family, the
chemokine receptor branch of the rhodopsin family. It is
expressed in late phases of lytic infections of leukocytes.
Tissue sources include human cytomegalovirus (CMV)
DNA and CMV-infected human fibroblasts. Ligands
include COS-7 cells transfected with US28-bound 125 I-
MCP-1 and 125 I-RANTES. Also called human CMV
G-protein-coupled receptor.
Usual interstitial pneumonitis (UIP). Biopsy reveals idiopathic pulmonary
fibrosis. Histopathology reveals a bronchus with chronic lymphocytic
infiltrate, interstitial inflammation, fibrosis, and edema. Only a few air
spaces are irregularly located.
usual interstitial pneumonia (UIP)
Lung disease associated with interstitial inflammation and
fibrosis that lead to progressive insufficiency. It is the most
frequent type of idiopathic interstitial pneumonitis and is
known by various names including Hamman–Rich syndrome.
It is believed to have an immunologic basis, with
20% of the cases associated with collagen vascular diseases
such as rheumatoid arthritis, progressive systemic sclerosis,
and systemic lupus erythematosus. Autoantibodies include
Usual interstitial pneumonitis (UIP). Histopathology reveals fibrosis and
inflammation, numerous plasma cells, fibroblasts, histiocytes, and vascular
destruction.
Usual interstitial pneumonitis (UIP).
antinuclear antibodies and rheumatoid factor. Immune complexes
may be found in the blood, alveolar walls, and bronchoalveolar
lavage fluid, yet the antigen remains unknown.
Alveolar macrophages are believed to become activated after
phagocytizing immune complexes, possibly followed by the
release of cytokines that attract neutrophils that cause injuries
of alveolar walls, leading to interstitial fibrosis. Pathological
symptoms include chronic inflammation of interstitial spaces
and extensive alveolar damage of normal lung parenchyma.
Areas of diffuse alveolar damage contain infiltrates of lymphocytes
and plasma cells in alveolar walls and hypoplasia
of type II pneumocytes. Fibrosis varies from mild to severe,
leading even to honeycomb lung in severe cases. The distal
acinus shrinks and proximal bronchioles dilate as fibrosis
may be accompanied by pulmonary hypertension. UIP may
occur over a 5- to 10-year period with development of dyspnea
on exertion and dry cough. The disease may follow acute
viral infection of the respiratory tract in one third of patients
or in rare cases involve acute fulminating interstitial inflammation
and fibrosis leading to Hamman–Rich syndrome that
may lead to death. Treatment modalities include corticosteroids
or cytophosphamide in lung transplantation.
uveitis
Uveal tract inflammation involving the uvea, iris, ciliary body,
and choroid of the eye. It may be associated with Behçet’s
disease, sarcoidosis, and juvenile rheumatoid arthritis.