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
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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