Linked Life Data

12239170

Source:http://linkedlifedata.com/resource/pubmed/id/12239170

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2002-9-19
pubmed:abstractText
Granulocyte colony-stimulating factor (G-CSF) may affect T-cell homeostasis by multiple mechanisms, inducing polarization of cytokine secretion, inhibition of T-cell proliferation, and enhancement of T-cell apoptosis. We analyzed the production of interleukin-10 (IL-10) and transforming growth factor-beta1 (TGF-beta1) by T cells from healthy volunteer donors treated with recombinant human G-CSF. Highly purified CD4(+) T cells obtained before and after G-CSF administration (pre-G and post-G, respectively) were activated using the allogeneic mixed leukocyte reaction. Post-G CD4(+) T cells produced high levels of IL-10 but undetectable levels of IL-2 and IL-4, whereas the level of TGF-beta1 release was comparable to that of pre-G CD4(+) T cells. Notably, post-G CD4(+) T cells proliferated poorly in response to alloantigens and to recall antigens and suppressed the proliferation of autologous CD4(+) T cells in a cell contact-independent and an antigen-nonspecific manner. TGF-beta1 and IL-10 were not dispensable for post-G CD4(+) T cells to mediate suppression, as shown by neutralization studies. Compared with pre-G CD4(+) T cells, alloantigen-activated post-G CD4(+) T cells preferentially expressed markers associated with memory T cells, in conjunction with reduced levels of CD28 and CD62L. Collectively, these data demonstrate that CD4(+) T cells exposed to G-CSF in vivo acquire the properties of T regulatory (Tr) cells once triggered in vitro through the T-cell receptor, including a peculiar cytokine production profile (IL-10(++)TGF-beta1(+)IL-2(low/-)IL-4(low/-)), an intrinsic low proliferative capacity, and a contact-independent suppression of antigen-driven proliferation. Tr cells generated ex vivo after exposure to G-CSF might be clinically relevant for transplantation medicine and for the treatment of human immune-mediated diseases.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
100
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2562-71
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:12239170-Adult, pubmed-meshheading:12239170-Antigens, CD, pubmed-meshheading:12239170-Base Sequence, pubmed-meshheading:12239170-CD4-Positive T-Lymphocytes, pubmed-meshheading:12239170-Cell Cycle, pubmed-meshheading:12239170-Cytokines, pubmed-meshheading:12239170-DNA Primers, pubmed-meshheading:12239170-Female, pubmed-meshheading:12239170-Granulocyte Colony-Stimulating Factor, pubmed-meshheading:12239170-Hematopoietic Stem Cells, pubmed-meshheading:12239170-Humans, pubmed-meshheading:12239170-Interleukin-10, pubmed-meshheading:12239170-Lymphocyte Activation, pubmed-meshheading:12239170-Male, pubmed-meshheading:12239170-Receptors, Chemokine, pubmed-meshheading:12239170-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:12239170-T-Lymphocytes, pubmed-meshheading:12239170-Transforming Growth Factor beta
pubmed:year
2002
pubmed:articleTitle
Role for granulocyte colony-stimulating factor in the generation of human T regulatory type 1 cells.
pubmed:affiliation
Departments of Hematology and Gynecology, Catholic University Medical School, Rome, and the Laboratory of Clinical Pathology and Microbiology, IRCCS San Gallicano, Rome, Italy. sergiorutella@tin.it
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't