Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0014070 (encephalomyelitis)
 13,017 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estrogen results in the suppression of experimental allergic encephalomyelitis (EAE), a frequently used experimental animal model of multiple sclerosis (MS). The mechanism by which estrogen acts in diseases with an autoimmune background is less clear. Here, we used splenic dendritic cells (DC) from the Lewis rats EAE model as target cells, and explored the pathway of estrogen in immune modulation. Estrogen did not affect the expression of MHC class II, CD80 and CD86 by DC, but inhibited the ability of DC to stimulate T cell proliferation and production of both Th1 and Th2 cytokines. This was accompanied by increased T cell apoptosis. Estrogen up-regulated DC to express indoleamine 2,3-dioxygenase (IDO) which can limit T cell responses. The effects of estrogen-exposed DC on T cell proliferation and apoptosis were partly abolished by addition of an IDO inhibitor (1-methyl-dl-tryptophan, 1-MT), indicating that estrogen-exposed DC induced IDO-dependent T cell suppression. Our data support the hypothesis that the estrogen-induced suppression of EAE, as well as the reduction in number of MS relapses observed during pregnancy, may be related to the estrogen-DC-IDO axis. This observation could open up a novel therapeutic target for influencing the course of MS and other diseases with an autoimmune diseases background.
Steroids 2004 Sep
PMID:Antigen-specific T cell functions are suppressed over the estrogen-dendritic cell-indoleamine 2,3-dioxygenase axis. 1546 10

Few diseases blur the margins between their childhood and adult-onset varieties as much as optic neuritis. This report will review our state of knowledge of pediatric optic neuritis, as well as its relationship to the latest consensus definitions of neuroinflammatory disease. Current diagnostic and treatment options will be explored, as well as our potential to uncover an understanding of pediatric optic neuritis through systematic prospective studies. The risk of evolving multiple sclerosis is probably less than in adults, but pediatric optic neuritis is more likely to be an initial manifestation of acute disseminated encephalomyelitis. Steroids may hasten visual recovery, but they do not change visual outcome except in cases because of neuromyelitis optica. The role of puberty in modifying the presentation and risk associations is unknown. Prospective studies are required to resolve these diagnostic and management issues.
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PMID:Pediatric Optic Neuritis: What Is New. 2880 45

Familial hemophagocytic lymphohistiocytosis (HLH) is a rare autosomal recessive life-threatening multisystem inflammatory disorder. It is characterized by excessive production of cytokines and uncontrolled activation of lymphocytes and macrophages leading to widespread organ infiltration and tissue destruction. Central nervous system involvement is common occurring in approximately 75% of patients. The neurological symptoms often develop during the course of the disease. However, they can be the initial presenting manifestation. In this article, we describe a patient with adult-onset familial HLH who presented solely with neurological involvement with lack of the initial classical presentation of HLH. He was initially misdiagnosed as acute disseminated encephalomyelitis and later on as multiple sclerosis. This paper indicates that familial HLH may present with pure neurological involvement. A high index of suspicion should be practiced with patients who present with vague recurrent neurological symptoms associated with abnormal non-specific neuroradiological findings. Genetic testing should be included in the investigations of such cases. Steroids and plasma exchange are non-specific therapies that may mask certain conditions including HLH or may be part of the treatment regimen. This may cause a delay in the diagnosis of the underlying causative disease.
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PMID:Adult-onset hemophagocytic lymphohistiocytosis type 2 presenting as a demyelinating disease. 3005 52