The CD4+CD26− T-cell population in classical Hodgkin's lymphoma displays a distinctive regulatory T-cell profile
CYTOKINE GENE-EXPRESSION
Adult
CD4-Positive T-Lymphocytes
Male
IMMUNOLOGICAL SELF-TOLERANCE
Adolescent
HUMAN TH2 CELLS
Dipeptidyl Peptidase 4
Gene Expression
PERIPHERAL-BLOOD
03 medical and health sciences
CC-CHEMOKINE
T-Lymphocyte Subsets
Humans
RNA, Messenger
REED-STERNBERG CELLS
Child
DIFFERENTIAL CHEMOKINE EXPRESSION
0303 health sciences
RECEPTOR CCR4
Sclerosis
Staining and Labeling
Reverse Transcriptase Polymerase Chain Reaction
Ionomycin
Reproducibility of Results
Flow Cytometry
Hodgkin Disease
Immunohistochemistry
TRANSCRIPTION FACTORS
Female
Lymph Nodes
TUMOR MICROENVIRONMENT
DOI:
10.1038/labinvest.2008.24
Publication Date:
2008-03-24T15:30:45Z
AUTHORS (7)
ABSTRACT
Little is known about the gene expression profile and significance of rosetting CD4+CD26− T cells in classical Hodgkin's lymphoma (cHL). To characterize these cells, CD4+CD26+ T-cell populations were sorted from lymph node (LN) cell suspensions nodular sclerosis HL (NSHL) reactive LNs. mRNA profiles stimulated resting subsets evaluated with quantitative RT-PCR for 46 genes. We observed a higher percentage NSHL than The showed levels CD25, CTLA4, OX40 CCR4 compared LNs, supporting regulatory (Treg) type, this was validated by immunohistochemistry. Moreover, low or no Th1- Th2-related cytokines IL-2, IFN-γ, IL-13, IL-12B, IL-4, IL-5, chemoattractant receptor CRTH2. Besides Tregs, Th17 may exist based on significantly IL-17 level both NSHL. Upon stimulation vitro, lack upregulation most cytokine genes indicated an anergic character subset. Anergy fits Treg probably explaining immunosuppressive mechanism involved
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CITATIONS (56)
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