Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1998-10-2
pubmed:abstractText
Reported frequencies of peripheral blood autoantigen-specific cells in autoimmune diseases are typically low, which could be due to true scarcity or to limitations of in vitro assays. In the present study, antigens were targeted to the antigen-presenting cell (APC) to enhance T cell proliferation, using an antigen delivery system (ADS), consisting of biotinylated anti-IgG, streptavidin and biotinylated antigen. This was able to bind B cells and monocytes and was internalized within 24 hours. T cell proliferation to tetanus toxoid was at least doubled using the ADS compared to conventional assay with antigen in simple solution. To evaluate the ADS in an autoimmune disease, we determined T cell responses to the insulin-dependent diabetes mellitus (IDDM)-associated autoantigen IA-2ic in patients with recent-onset IDDM. When IA-2ic was available conventionally in solution, proliferation was poor, but significantly higher in IDDM patients than control subjects. However, the ADS significantly enhanced proliferation by a mean 3-fold for all subjects, while maintaining the significant difference between IDDM patients and healthy controls. Increases in T cell proliferation via the ADS were due to the recruitment of approximately 3 times the number of CD4 + T cells stimulated in conventional assays. B cell depletion abolished enhancement suggesting that the ADS operates through recruitment of B cells as APCs. This flexible modification of the T cell assay offers greatly enhanced sensitivity for determining the frequency of antigen and autoantigen-reactive T cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0022-1759
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
215
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
59-70
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:9744748-Adult, pubmed-meshheading:9744748-Animals, pubmed-meshheading:9744748-Antigen Presentation, pubmed-meshheading:9744748-Antigen-Presenting Cells, pubmed-meshheading:9744748-Antigens, pubmed-meshheading:9744748-Autoimmunity, pubmed-meshheading:9744748-Avidin, pubmed-meshheading:9744748-B-Lymphocytes, pubmed-meshheading:9744748-Biotin, pubmed-meshheading:9744748-CD4-Positive T-Lymphocytes, pubmed-meshheading:9744748-Diabetes Mellitus, Type 1, pubmed-meshheading:9744748-Epitopes, pubmed-meshheading:9744748-Female, pubmed-meshheading:9744748-Humans, pubmed-meshheading:9744748-Immunoglobulin G, pubmed-meshheading:9744748-Leukocytes, Mononuclear, pubmed-meshheading:9744748-Lymphocyte Activation, pubmed-meshheading:9744748-Male, pubmed-meshheading:9744748-Sheep, pubmed-meshheading:9744748-Streptavidin, pubmed-meshheading:9744748-T-Lymphocytes
pubmed:year
1998
pubmed:articleTitle
Enhanced T cell proliferation and increased responder frequency following delivery of antigen to the antigen-presenting cell; B cell dependency and use in detection of autoreactive T cells.
pubmed:affiliation
Department of Immunology, King's College School of Medicine and Dentistry, London, UK.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't