Interleukin-1-independent activation of human T lymphocytes stimulated by anti-CD3 and a Hodgkin's disease cell line with accessory cell activity

Abstract Diminished rosetting capacity of T cells is a well-known phenomenon in Hodgkin's disease, and inhibitors of E rosette formation have been reported to be present in the plasma of patients with Hodgkin's disease. The cell line L428, representing an in vitro counterpart of Hodgkin and Sternberg-Reed cells, could be shown to release a factor capable of suppressing the binding of sheep red blood cells (SRBC) to normal peripheral-blood T lymphocytes or to a T-cell line (L735). At maximally effective concentrations, RIF (rosette inhibiting factor) inhibited T lymphocyte rosetting by approximately 40% (mean from 184 healthy controls). The diminished E rosetting of T lymphocytes from Hodgkin's patients was not further suppressed by added RIF. This factor inhibited binding of SRBC to their target cells at 37 degrees C but not at 4 degrees C. The factor could be stored lyophilized at -20 degrees C and was stable at 56 degrees C (30 minutes). RIF was inactive below pH 6 and above pH 9 or after trypsin digestion. Purification by affinity, ion exchange, and molecular sieve chromatography showed activity peaks at 12.5 Kd, 25 Kd, 50 Kd, and 100 Kd.

Download Full-text

A Hodgkin’s Disease Cell Line, KM-H2, Shows Biphenotypic Features of Dendritic Cells and B Cells

International Journal of Hematology ◽

10.1007/bf02981944 ◽

2001 ◽

Vol 73 (2) ◽

pp. 236-244 ◽

Cited By ~ 13

Author(s):

Kazutaka Uehira ◽

Ryuichi Amakawa ◽

Tomoki Ito ◽

Tomoko Uehira ◽

Yoshio Ozaki ◽

...

Keyword(s):

Dendritic Cells ◽

B Cells ◽

Cell Line ◽

Hodgkin's Disease ◽

Hodgkin’S Disease ◽

Disease Cell

Download Full-text

SUP-HD1: a new Hodgkin's disease-derived cell line with lymphoid features produces interferon-gamma [see comments]

Blood ◽

10.1182/blood.v74.8.2733.bloodjournal7482733 ◽

1989 ◽

Vol 74 (8) ◽

pp. 2733-2742 ◽

Cited By ~ 1

Author(s):

L Naumovski ◽

PJ Utz ◽

SK Bergstrom ◽

R Morgan ◽

A Molina ◽

...

Keyword(s):

T Lymphocytes ◽

Cell Line ◽

Interferon Gamma ◽

Heavy Chain ◽

Light Chain ◽

Hodgkin's Disease ◽

Hodgkin’S Disease ◽

Immunoglobulin Heavy Chain ◽

Kappa Light Chain ◽

Ifn Gamma

A new cell line, SUP-HD1, was established from the pleural effusion of a patient with nodular sclerosing Hodgkin's disease (NSHD). The SUP-HD1 cells had the characteristic morphology of Reed-Sternberg cells and contained acid phosphatase and nonspecific esterase. The cells lacked the Epstein-Barr virus (EBV) genome and reacted with monoclonal antibodies (MoAbs) against CD15 (Leu-M1), CD25 (Tac), CD71 (OKT9), Ki67, and HLA-Dr. However, the SUP-HD1 cells were nonreactive with MoAbs that specifically identify T lymphocytes, B lymphocytes, and macrophage/myeloid cells. Karyotype analysis of the cell line showed clonal abnormalities involving 1p13, 7p15, 8q22, and 11q23, chromosomal locations, at which breakpoints have been reported in HD. Southern blot analysis demonstrated rearrangement of the immunoglobulin heavy chain and kappa light chain genes as well as the gene for the beta chain of the T-cell receptor (TCR). Transcriptional analysis showed expression of RNAs for kappa light chain, interferon-gamma (IFN-gamma), and interleukin-2 receptor (IL-2R) but not IL-2. The SUP-HD1 cells lacked cytoplasmic and surface immunoglobulin heavy chain, but a small amount of cytoplasmic kappa light chain was detected. The presence of nuclear factor kappa B (NF kappa B), a B-lymphocyte-associated transcription factor, was demonstrated in stimulated and unstimulated cells. In addition, the SUP-HD1 cell line, produced IFN-gamma, a T-lymphocyte- associated lymphokine. Based on these data, the SUP-HD1 cells appear to be aberrant lymphocytes with characteristics of both activated B and T lymphocytes. Elaboration of lymphokines such as IFN-gamma by the malignant cells may represent one explanation for the unique clinical and pathologic features of HD.

Download Full-text

SUP-HD1: a new Hodgkin's disease-derived cell line with lymphoid features produces interferon-gamma [see comments]

Blood ◽

10.1182/blood.v74.8.2733.2733 ◽

1989 ◽

Vol 74 (8) ◽

pp. 2733-2742 ◽

Cited By ~ 25

Author(s):

L Naumovski ◽

PJ Utz ◽

SK Bergstrom ◽

R Morgan ◽

A Molina ◽

...

Keyword(s):

T Lymphocytes ◽

Cell Line ◽

Interferon Gamma ◽

Heavy Chain ◽

Light Chain ◽

Hodgkin's Disease ◽

Hodgkin’S Disease ◽

Immunoglobulin Heavy Chain ◽

Kappa Light Chain ◽

Ifn Gamma

Abstract A new cell line, SUP-HD1, was established from the pleural effusion of a patient with nodular sclerosing Hodgkin's disease (NSHD). The SUP-HD1 cells had the characteristic morphology of Reed-Sternberg cells and contained acid phosphatase and nonspecific esterase. The cells lacked the Epstein-Barr virus (EBV) genome and reacted with monoclonal antibodies (MoAbs) against CD15 (Leu-M1), CD25 (Tac), CD71 (OKT9), Ki67, and HLA-Dr. However, the SUP-HD1 cells were nonreactive with MoAbs that specifically identify T lymphocytes, B lymphocytes, and macrophage/myeloid cells. Karyotype analysis of the cell line showed clonal abnormalities involving 1p13, 7p15, 8q22, and 11q23, chromosomal locations, at which breakpoints have been reported in HD. Southern blot analysis demonstrated rearrangement of the immunoglobulin heavy chain and kappa light chain genes as well as the gene for the beta chain of the T-cell receptor (TCR). Transcriptional analysis showed expression of RNAs for kappa light chain, interferon-gamma (IFN-gamma), and interleukin-2 receptor (IL-2R) but not IL-2. The SUP-HD1 cells lacked cytoplasmic and surface immunoglobulin heavy chain, but a small amount of cytoplasmic kappa light chain was detected. The presence of nuclear factor kappa B (NF kappa B), a B-lymphocyte-associated transcription factor, was demonstrated in stimulated and unstimulated cells. In addition, the SUP-HD1 cell line, produced IFN-gamma, a T-lymphocyte- associated lymphokine. Based on these data, the SUP-HD1 cells appear to be aberrant lymphocytes with characteristics of both activated B and T lymphocytes. Elaboration of lymphokines such as IFN-gamma by the malignant cells may represent one explanation for the unique clinical and pathologic features of HD.

Download Full-text

Transfection of caspase-3 in the caspase-3–deficient Hodgkin's disease cell line, KMH2, results in enhanced sensitivity to CD95-, TRAIL-, and ARA-C–induced apoptosis

Experimental Hematology ◽

10.1016/s0301-472x(01)00627-0 ◽

2001 ◽

Vol 29 (5) ◽

pp. 572-581 ◽

Cited By ~ 6

Author(s):

Tamara Wrone-Smith ◽

Keith F Izban ◽

Melek Ergin ◽

Ediz F Cosar ◽

Eric D Hsi ◽

...

Keyword(s):

Cell Line ◽

Hodgkin's Disease ◽

Caspase 3 ◽

Hodgkin’S Disease ◽

Enhanced Sensitivity ◽

Induced Apoptosis ◽

Disease Cell

Download Full-text

L428 cells derived from Hodgkin's disease produce E rosette-inhibiting factor

Blood ◽

10.1182/blood.v76.4.791.bloodjournal764791 ◽

1990 ◽

Vol 76 (4) ◽

pp. 791-796 ◽

Cited By ~ 1

Author(s):

I Katay ◽

U Wirnitzer ◽

H Burrichter ◽

C von Kalle ◽

E Schell-Frederick ◽

...

Keyword(s):

T Lymphocytes ◽

Cell Line ◽

T Lymphocyte ◽

Hodgkin's Disease ◽

Hodgkin’S Disease ◽

Target Cells ◽

Normal Peripheral Blood ◽

Inhibiting Factor ◽

C 30

Diminished rosetting capacity of T cells is a well-known phenomenon in Hodgkin's disease, and inhibitors of E rosette formation have been reported to be present in the plasma of patients with Hodgkin's disease. The cell line L428, representing an in vitro counterpart of Hodgkin and Sternberg-Reed cells, could be shown to release a factor capable of suppressing the binding of sheep red blood cells (SRBC) to normal peripheral-blood T lymphocytes or to a T-cell line (L735). At maximally effective concentrations, RIF (rosette inhibiting factor) inhibited T lymphocyte rosetting by approximately 40% (mean from 184 healthy controls). The diminished E rosetting of T lymphocytes from Hodgkin's patients was not further suppressed by added RIF. This factor inhibited binding of SRBC to their target cells at 37 degrees C but not at 4 degrees C. The factor could be stored lyophilized at -20 degrees C and was stable at 56 degrees C (30 minutes). RIF was inactive below pH 6 and above pH 9 or after trypsin digestion. Purification by affinity, ion exchange, and molecular sieve chromatography showed activity peaks at 12.5 Kd, 25 Kd, 50 Kd, and 100 Kd.

Download Full-text