Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1996-8-26
pubmed:abstractText
A comparative study of immune function and marker expression of CD4+ T cells from MHC class 1-restricted 2C TCR-transgenic (2C+) and control transgene-negative littermate (2C-) mice was performed. While 2C+CD4+ T cells resembled memory T cells on the basis of CD44highCD45RBlow expression, the majority of 2C-CD4+ T cells were of the CD44lowCD45RBhigh naive phenotype. Slightly lower levels of TCR-beta and CD3 were found on 2C+CD4+ T cell than 2C-CD4+ T cells. Vigorous proliferation by 2C-CD4+ T cells was observed upon stimulation with 1) anti-CD3 mAb presented through the FcR of macrophages; 2) immobilized (plate-bound) anti-CD3 + anti-CD28 mAbs; and 3) PMA + ionomycin. In marked contrast, all three mitogenic stimuli stimulated highly deficient proliferative responses by 2C+CD4+ T cells. However, significant IL-2 production was detected both in anti-CD3 and in PMA + ionomycin-stimulated cultures of 2C+CD4+ T cells. While intracellular calcium in 2C-CD4+ T cells rapidly increased following anti-CD3 addition, no such increase was observed for similarly stimulated 2C+CD4+ T cells. Anti-CD28, PMA, and coculture with 2C-CD4+ T cells each failed to significantly correct the deficient 2C+CD4+ T cells proliferation as induced by anti-CD3. In addition, IL-2, IL-4, and IL-7 supplements also failed to reverse the deficient proliferation of 2C+CD4+ T cells despite expression of IL-2R component alpha-, beta-chains and the gamma-chain common also to IL-4R and IL-7R. Thymus CD4+8- T cells from the 2C-transgenic mouse were similarly deficient in proliferation as spleen CD4+ T cells. A small subpopulation of CD4+ T cell from the 2C-transgenic mouse expressed the transgenic TCR alpha:beta heterodimer as detected by the 1B2 anti-2C clonotypic mAb; both 1B2+ and 1B2- subpopulations proliferated poorly in response to anti-CD3 and to PMA + ionomycin. These results raise the possibility that TCR engagement with MHC class 1 molecules during early intrathymic development can result in the emergence of CD4+ T cells characterized by unusual marker expression and function.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
156
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2036-44
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:8690890-Animals, pubmed-meshheading:8690890-Antibodies, Monoclonal, pubmed-meshheading:8690890-Antigens, CD28, pubmed-meshheading:8690890-Antigens, CD3, pubmed-meshheading:8690890-CD4-Positive T-Lymphocytes, pubmed-meshheading:8690890-Cell Cycle, pubmed-meshheading:8690890-Cells, Cultured, pubmed-meshheading:8690890-Coculture Techniques, pubmed-meshheading:8690890-Female, pubmed-meshheading:8690890-Gene Expression Regulation, pubmed-meshheading:8690890-H-2 Antigens, pubmed-meshheading:8690890-Immunosorbents, pubmed-meshheading:8690890-Interleukin-2, pubmed-meshheading:8690890-Ionomycin, pubmed-meshheading:8690890-Lymphocyte Activation, pubmed-meshheading:8690890-Lymphopenia, pubmed-meshheading:8690890-Male, pubmed-meshheading:8690890-Mice, pubmed-meshheading:8690890-Mice, Inbred C57BL, pubmed-meshheading:8690890-Mice, Transgenic, pubmed-meshheading:8690890-Receptors, Antigen, T-Cell, alpha-beta, pubmed-meshheading:8690890-Receptors, Interleukin-2, pubmed-meshheading:8690890-Tetradecanoylphorbol Acetate
pubmed:year
1996
pubmed:articleTitle
Deficient CD4+ T cell proliferation in the class 1 MHC-restricted 2C TCR-transgenic mouse.
pubmed:affiliation
Graduate Institute of Immunology, College of Medicine, National Taiwan University, Taipei, Republic of China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't