Reactivity of HTLV-transformed human T-cell lines to MHC class II antigens

Nature ◽  
1984 ◽  
Vol 312 (5991) ◽  
pp. 275-277 ◽  
Author(s):  
Nicole Suciu-Foca ◽  
Pablo Rubinstein ◽  
Mikulas Popovic ◽  
Robert C. Gallo ◽  
Donald W. King
Keyword(s):  
T Cell ◽  
Cell Lines ◽  
Mhc Class Ii ◽  
Class Ii ◽  
Human T Cell ◽  
Mhc Class Ii Antigens ◽  
T Cell Lines ◽  
Class Ii Antigens

Regulation of MHC class II expression in human T-cell malignancies

Blood ◽  
2004 ◽  
Vol 103 (4) ◽  
pp. 1438-1444 ◽  
Author(s):  
Tjadine M. Holling ◽  
Erik Schooten ◽  
Anton W. Langerak ◽  
Peter J. van den Elsen
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Lines ◽  
Mhc Class Ii ◽  
Lymphoblastic Leukemia ◽  
Class Ii ◽  
Activated T Cells ◽  
Prolymphocytic Leukemia ◽  
Human T Cell ◽  
T Cell Lines

Abstract Expression of major histocompatibility complex (MHC) class II molecules in human activated T cells is under normal circumstances regulated exclusively by the CIITA-PIII subtype of the class II transactivator (CIITA). In this study, we show that the absence of MHC class II expression in leukemic T cells was due to a lack of expression of CIITA, whereas in T-lymphoma cells, expression of CIITA correlated with expression of MHC class II. Interestingly, activation of a CIITA-promoter (P)III–reporter construct was not affected in leukemic T cells. This revealed that the absence of endogenous CIITA expression was not caused by a lack of transcription factors critical for CIITA-PIII activation but suggests the involvement of an epigenetic silencing mechanism. Subsequent analysis showed that the lack of human leukocyte antigen–DR (HLA-DR) expression correlated with hypermethylation of CIITA-PIII in leukemic T-cell lines and in primary T-cell acute lymphoblastic leukemia (T-ALL) and a T-cell prolymphocytic leukemia (T-PLL). Treatment of leukemic T-cell lines with a demethylation agent showed re-expression of CIITA-PIII and HLA-DRA. Furthermore, in vitro methylation of CIITA-PIII and subsequent assessment of CIITA-PIII activity in Jurkat leukemic T cells resulted in reduction of constitutive and CREB-1 (cyclic adenosine monophosphate [cAMP]–response element binding protein 1)–induced promoter activity. Together, these results argue for an important role of DNA hyper-methylation in the control of CIITA expression in leukemic T cells.

scholarly journals Nonmalignant T cells stimulate growth of T-cell lymphoma cells in the presence of bacterial toxins

Blood ◽  
2006 ◽  
Vol 109 (8) ◽  
pp. 3325-3332 ◽  
Author(s):  
Anders Woetmann ◽  
Paola Lovato ◽  
Karsten W. Eriksen ◽  
Thorbjørn Krejsgaard ◽  
Tord Labuda ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Lines ◽  
Mhc Class Ii ◽  
Interleukin 2 ◽  
Class Ii ◽  
Bacterial Toxins ◽  
Dependent Manner ◽  
Malignant Cells ◽  
T Cell Lines

AbstractBacterial toxins including staphylococcal enterotoxins (SEs) have been implicated in the pathogenesis of cutaneous T-cell lymphomas (CTCLs). Here, we investigate SE-mediated interactions between nonmalignant T cells and malignant T-cell lines established from skin and blood of CTCL patients. The malignant CTCL cells express MHC class II molecules that are high-affinity receptors for SE. Although treatment with SE has no direct effect on the growth of the malignant CTCL cells, the SE-treated CTCL cells induce vigorous proliferation of the SE-responsive nonmalignant T cells. In turn, the nonmalignant T cells enhance proliferation of the malignant cells in an SE- and MHC class II–dependent manner. Furthermore, SE and, in addition, alloantigen presentation by malignant CTCL cells to irradiated nonmalignant CD4+ T-cell lines also enhance proliferation of the malignant cells. The growth-promoting effect depends on direct cell-cell contact and soluble factors such as interleukin-2. In conclusion, we demonstrate that SE triggers a bidirectional cross talk between nonmalignant T cells and malignant CTCL cells that promotes growth of the malignant cells. This represents a novel mechanism by which infections with SE-producing bacteria may contribute to pathogenesis of CTCL.

The role of N-linked oligosaccharides of MHC class II antigens in T cell stimulation

1994 ◽  
Vol 172 (1) ◽  
pp. 95-104 ◽  
Author(s):  
Bishwajit Nag ◽  
H. Garrett Wada ◽  
Subhashini Arimilli ◽  
Katherine Fok ◽  
David Passmore ◽  
...  
Keyword(s):  
T Cell ◽  
Mhc Class Ii ◽  
Class Ii ◽  
Cell Stimulation ◽  
T Cell Stimulation ◽  
Mhc Class Ii Antigens ◽  
Class Ii Antigens

Class II determinants recognized by TNP-specific cloned human T cell lines

1985 ◽  
Vol 14 (1) ◽  
pp. 59-76 ◽  
Author(s):  
Jeffrey H. Hanke ◽  
Marion F. Brown ◽  
Marilyn S. Pollack ◽  
Robert R. Rich
Keyword(s):  
T Cell ◽  
Cell Lines ◽  
Class Ii ◽  
Human T Cell ◽  
T Cell Lines

scholarly journals Differential expression of MHC class II antigens in myelomonocytic leukemia cell lines

Blood ◽  
1989 ◽  
Vol 73 (4) ◽  
pp. 931-937 ◽  
Author(s):  
JJ Yunis ◽  
H Band ◽  
F Bonneville ◽  
EJ Yunis
Keyword(s):  
Cell Line ◽  
Cell Lines ◽  
Mhc Class Ii ◽  
Surface Expression ◽  
Class Ii ◽  
Monocytic Cell ◽  
Monocytic Cell Line ◽  
Mhc Class Ii Antigens ◽  
Ifn Treatment ◽  
Class Ii Antigens

Abstract Major histocompatibility complex (MHC) class II antigens are discordantly expressed on hematopoietic progenitor cells. Their expression is linked to differential responsiveness of the cells to growth factors and inhibitors. We examined the expression of different MHC class II antigens in a panel of human myelomonocytic cell lines representing different stages of differentiation, by cytofluorographic analysis with monoclonal antibody (MoAb) and Northern blot analysis with specific cDNA probes. These analyses revealed discordant expression of different MHC class II antigens both in basal state and after gamma-IFN induction. Thus KG-1 myeloblast cells express all class II antigens (DR greater than DP greater than DQ) constitutively and their expression increased after gamma-IFN treatment. KG-1a, an immature blast variant of KG-1, does not express class II antigens, even after gamma-IFN treatment. THP-1, a monocytic cell line expresses DR but not DP or DQ under basal conditions. DP and DQ are, however, gamma-IFN inducible. The class II negative HL-60 promyelocytic cell line, expresses DR and DP but not DQ after gamma-IFN induction. In all the above cell lines, surface expression of class II antigens correlated with the levels of mRNA expression as determined with specific cDNA probes. In U-937, a monocytic cell line, no surface expression of class II MHC antigens was observed either with or without gamma-IFN, however, specific mRNA message was observed under basal conditions and was further increased with gamma-IFN, indicating a possible defect in assembly or transport of class II antigens. The patterns of class II MHC antigens in these leukemic cell lines may be a useful model to delineate molecular basis of discordant MHC class II expression during myelomonocytic differentiation.

scholarly journals Transforming Growth Factor β (TGF-β)-dependent Inhibition of T Helper Cell 2 (Th2)-induced Autoimmunity by Self–Major Histocompatibility Complex (MHC) Class II–specific, Regulatory CD4+ T Cell Lines

1997 ◽  
Vol 185 (10) ◽  
pp. 1769-1775 ◽  
Author(s):  
Frank Bridoux ◽  
Abdallah Badou ◽  
Abdelhadi Saoudi ◽  
Isabelle Bernard ◽  
Elvira Druet ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Lines ◽  
Mhc Class Ii ◽  
Class Ii ◽  
T Helper Cell ◽  
Helper Cell ◽  
T Helper ◽  
Autoreactive T Cells ◽  
T Cell Lines

Autoreactive anti–MHC class II T cells are found in Brown Norway (BN) and Lewis (LEW) rats that receive either HgCl2 or gold salts. These T cells have a T helper cell 2 (Th2) phenotype in the former strain and are responsible for Th2-mediated autoimmunity. In contrast, T cells that expand in LEW rats produce IL-2 and prevent experimental autoimmune encephalomyelitis, a cell-mediated autoimmune disease. The aim of this work was to investigate, using T cell lines derived from HgCl2-injected LEW rats (LEWHg), the effect of these autoreactive T cells on the development of Th2-mediated autoimmunity. The five LEWHg T cell lines obtained protect against Th2-mediated autoimmunity induced by HgCl2 in (LEW × BN)F1 hybrids. The lines produce, in addition to IL-2, IFN-γ and TGF-β, and the protective effect is TGF-β dependent since protection is abrogated by anti-TGF-β treatment. These results identify regulatory, TGF-β–producing, autoreactive T cells that are distinct from classical Th1 or Th2 and inhibit both Th1- and Th2-mediated autoimmune diseases.

Recognition of MHC Class II Antigens by the CD4: T Cell Receptor Complex

H-2 Antigens ◽  
1987 ◽  
pp. 441-449
Author(s):  
Charles A. Janeway ◽  
Pilar Portoles ◽  
John P. Tite ◽  
Jose Rojo ◽  
Kaj Saizawa ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Receptor ◽  
Mhc Class Ii ◽  
Cell Receptor ◽  
Class Ii ◽  
Cd4 T Cell ◽  
Receptor Complex ◽  
Mhc Class Ii Antigens ◽  
Class Ii Antigens

Expression of Lymphocyte Activation Gene 3 (LAG-3/CD223) by Chronic Lymphocytic Leukemia B Cells.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 2952-2952
Author(s):  
Han-Yu Chuang ◽  
Yu-Tsueng Liu ◽  
Laura Z. Rassenti ◽  
Lang Huynh ◽  
Dennis Carson ◽  
...  
Keyword(s):  
Gene Expression ◽  
Flow Cytometry ◽  
T Cell ◽  
B Cells ◽  
Chronic Lymphocytic Leukemia ◽  
Mhc Class Ii ◽  
Class Ii ◽  
Lymphocytic Leukemia ◽  
Mhc Class Ii Antigens ◽  
Class Ii Antigens

Abstract The clinical course of chronic lymphocytic leukemia (CLL) is variable. DNA-microarray studies have shown that the gene-expression patterns of CLL cells with unmutated IgVH genes are similar to those of cells with mutated IgVH genes, but that the patterns of both are distinct from those of other leukemias and lymphomas. Nevertheless, the two subtypes of CLL can be distinguished by the differential expression of a small number of genes, one of which encodes ZAP-70, an intracellular tyrosine kinase with a critical role in T-cell receptor signaling. Further analysis of the mutation status of IgVH genes and ZAP-70 expression revealed that CLL patients with B cells expressing ZAP-70 and unmutated IgVH genes had a more aggressive disease. LAG-3 (CD223) is thought to play a role in immune responses mediated by T and NK cells. LAG-3, a CD4 homolog, is a ligand for MHC class II antigens. Similar to ZAP-70, LAG-3 is selectively expressed on activated T and NK cells and has recently been shown to be expressed on T-cell activated B cells. We compared the gene expression profiles of the B cells purified from 15 CLL patients using the Affymetrix HG-U133 plus 2.0. This analysis revealed LAG-3 and parathymosin differentially expressed at higher levels by the CLL cells expressing ZAP-70 and unmutated IgVH genes. LAG-3 and parathymosin are located on chromosome 12p13 with head-to-tail orientation. To examine for surface expression of LAG-3, we performed flow cytometry on these same 15 CLL samples using an anti LAG-3 mAb (CD223). We found LAG-3 expressed at high levels by the CD5/CD19 B cells of 4/8 (50%) cases that expressed ZAP-70 and unmutated IgVH genes. Conversely, the samples with B cells lacking ZAP-70 and with mutated IgVH genes did not express LAG-3 (0/7). All samples (15/15) expressed high level of MHC class II antigens, as assessed by flow cytometry. LAG-3 may interact with MHC class II molecules expressed by CLL cells to form an autocrine loop that may further enhance the activation of ZAP-70-expressing CLL B cells. Further analysis is needed to delineate the role of LAG-3 in the pathogenesis and/or progression of this disease.

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