Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1994-4-1
pubmed:abstractText
Patients with myasthenia gravis have a high prevalence of acetylcholine receptor-specific T lymphocytes in the peripheral blood. Our earlier study shows that these T lymphocytes are stimulated to secrete interferon (IFN)-gamma and interleukin (IL)-2 in response to the autoantigen. Such stimulated T cells may be subdivided into different subsets according to the pattern of cytokine production. In the present study we have investigated the subpopulations of cells by analyzing their IL-4, IFN-gamma and IL-2 secretion pattern. Autoantigen-stimulated IL-4 secretion was found in 55% of the patients, IFN-gamma secretion in 86% and IL-2 secretion in 72%. T lymphocytes from all patients who responded with increased IL-2 secretion also showed increased IFN-gamma secretion. Stimulated IL-4 secretion was detected both in the presence and absence of stimulated IFN-gamma secretion. Depletion of monocytes/macrophages from peripheral blood mononuclear cell preparation and treatment of the cells with a mouse anti-human HLA-DR antibody abolished the secretion of IFN-gamma and IL-4. There were positive correlations between the numbers of IFN-gamma- and IL-2-secreting T cells and the numbers of B cells secreting antibodies against the acetylcholine receptor. Our results show that acetylcholine receptor-stimulated T lymphocytes secrete IL-4, IFN-gamma and/or IL-2. This T cell response is major histocompatibility complex (MHC) class II-restricted and monocyte/macrophage-dependent. Our study indicates that both Th1/Th2 or Th0 subpopulations of the T lymphocytes are involved in the autoimmune response in myasthenia gravis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0165-5728
pubmed:author
pubmed:issnType
Print
pubmed:volume
50
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
177-86
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:8120139-Adolescent, pubmed-meshheading:8120139-Adult, pubmed-meshheading:8120139-Aged, pubmed-meshheading:8120139-Antibodies, pubmed-meshheading:8120139-B-Lymphocytes, pubmed-meshheading:8120139-Bungarotoxins, pubmed-meshheading:8120139-Cytokines, pubmed-meshheading:8120139-Female, pubmed-meshheading:8120139-Histocompatibility Antigens Class II, pubmed-meshheading:8120139-Humans, pubmed-meshheading:8120139-Interleukins, pubmed-meshheading:8120139-Macrophages, pubmed-meshheading:8120139-Male, pubmed-meshheading:8120139-Middle Aged, pubmed-meshheading:8120139-Monocytes, pubmed-meshheading:8120139-Myasthenia Gravis, pubmed-meshheading:8120139-Receptors, Cholinergic, pubmed-meshheading:8120139-Recombinant Proteins, pubmed-meshheading:8120139-T-Lymphocytes, pubmed-meshheading:8120139-T-Lymphocytes, Helper-Inducer
pubmed:year
1994
pubmed:articleTitle
Acetylcholine receptor-reactive T cells in myasthenia gravis: evidence for the involvement of different subpopulations of T helper cells.
pubmed:affiliation
Immunological Research Laboratory, Karolinska Hospital, Stockholm, Sweden.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't