Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2002-2-19
pubmed:abstractText
Allergic contact dermatitis ensues from exaggerated T cell responses to haptens. Dendritic cells are required for the initiation of hapten sensitization, but they may not be necessary for disease expression. Here we investigated the antigen-presenting cell requirement of nickel-specific CD4+ lymphocytes isolated from the blood of six allergic individuals. A significant proportion (42 out of 121; 35%) of the T cell clones proliferated in vitro to nickel also in the absence of professional antigen-presenting cells, suggesting a direct T-T hapten presentation. Antigen-presenting-cell-independent T cells showed a predominant T helper 1 phenotype. Nickel recognition by these T cells was major histocompatibility complex class II restricted, not influenced by CD28 triggering, independent from their state of activation, and did not require processing. The capacity of this T cell subset to be directly stimulated by nickel was not due to unique antigen-presenting properties, as both antigen-presenting-cell-dependent and antigen-presenting-cell-independent clones displayed comparable levels of HLA-DR, CD80, and CD86, and were equally capable of presenting nickel to antigen-presenting-cell-independent clones. In contrast, neither T cell types activated antigen-presenting-cell-dependent T lymphocytes. T-T presentation induced T cell receptor downregulation, CD25, CD80, CD86, and HLA-DR upregulation, and interferon-gamma release, although to a lesser extent compared to those induced by dendritic cell-T presentation. Following T-T presentation, the clones did not undergo unresponsiveness and maintained the capacity to respond to dendritic cells pulsed with antigen. In aggregate, our data suggest that antigen-presenting-cell-independent T cell activation can effectively amplify hapten- specific immune responses.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD28, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD80, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD86, http://linkedlifedata.com/resource/pubmed/chemical/CD86 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Haptens, http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class II, http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma, http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins, http://linkedlifedata.com/resource/pubmed/chemical/Nickel, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-2
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0022-202X
pubmed:author
pubmed:issnType
Print
pubmed:volume
118
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
172-9
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:11851891-Adult, pubmed-meshheading:11851891-Antigen-Presenting Cells, pubmed-meshheading:11851891-Antigens, CD, pubmed-meshheading:11851891-Antigens, CD28, pubmed-meshheading:11851891-Antigens, CD80, pubmed-meshheading:11851891-Antigens, CD86, pubmed-meshheading:11851891-CD4-Positive T-Lymphocytes, pubmed-meshheading:11851891-Down-Regulation, pubmed-meshheading:11851891-Female, pubmed-meshheading:11851891-Haptens, pubmed-meshheading:11851891-Histocompatibility Antigens Class II, pubmed-meshheading:11851891-Humans, pubmed-meshheading:11851891-Interferon-gamma, pubmed-meshheading:11851891-Lymphocyte Activation, pubmed-meshheading:11851891-Male, pubmed-meshheading:11851891-Membrane Glycoproteins, pubmed-meshheading:11851891-Nickel, pubmed-meshheading:11851891-Receptors, Antigen, T-Cell, pubmed-meshheading:11851891-Receptors, Interleukin-2, pubmed-meshheading:11851891-Up-Regulation
pubmed:year
2002
pubmed:articleTitle
Activation of nickel-specific CD4+ T lymphocytes in the absence of professional antigen-presenting cells.
pubmed:affiliation
Laboratory of Immunology and Department of Immunodermatology, Istituto Dermopatico dell' Immacolata, IRCCS, Rome, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't