Reed-Sternberg-Cell/Lymphocyte Interaction

Payne, S V; Jones, David B.; Wright, D. H.

doi:10.1016/s0140-6736(77)90281-1

Cited by 43 publications

(23 citation statements)

References 11 publications

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“…In tissue sections HRS and L&H cells are usually found entirely surrounded by these T cells. This "rosetting phenomenon" has also been observed in cell suspensions prepared from tumor tissue: autologous T cells spontaneously adhere to HRS cells [6][7][8][9]. The rosetting of CD4 + T cells around these malignant B cells may reflect a cellular response against the tumor.…”

Section: Introductionmentioning

confidence: 80%

Amplification of TCRβ gene rearrangements from micromanipulated single cells: T cells rosetting around Hodgkin and Reed-Sternberg cells in Hodgkin's disease are polyclonal

et al. 1998

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Despite accounting for only a minor fraction of all cells in Hodgkin's lymphoma tissue, the Hodgkin and Reed-Sternberg (HRS) cells represent the malignant tumor cell clone in Hodgkin's disease (HD). By far the most abundant cell type in the tumor tissue are CD4+ T cells. Some of them intimately associate with HRS cells forming rosettes around them. This study addresses the question whether the rosetting phenomenon reflects a specific interaction between T and HRS cells by asking whether the rosettes are composed of T cells expressing a restricted TCR repertoire. Single rosetting T cells were micromanipulated from frozen sections of tumor tissue in two cases of nodular sclerosing HD and one case of lymphocyte predominant HD. TCR Vbeta gene rearrangements were amplified from these single cells by PCR. Of 83 potentially functional Vbeta gene rearrangements obtained altogether from the three cases, 81 were found to be clonally unrelated. Furthermore, they did not show signs of selection of the receptor chains for recognition of common epitopes: The usage of Vbeta and Jbeta gene segments as well as the distribution of complementarity-determining region (CDR) 3 lengths was similar to what was seen in a collection of 60 Vbeta gene rearrangements from blood of healthy donors and no recurrent CDR3 amino acid motifs were found. These data suggest that the HRS cells attract CD4+ T cells nonspecifically.

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Section: Introductionmentioning

confidence: 80%

Amplification of TCRβ gene rearrangements from micromanipulated single cells: T cells rosetting around Hodgkin and Reed-Sternberg cells in Hodgkin's disease are polyclonal

et al. 1998

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“…[6][7][8] The presence of multiple tumor-infiltrating T cells "rosetting," but failing to eliminate, malignant RS cells has been well-described in CHL and is highly suggestive of an ineffectual T cell response in this disease. 9,10 This has been complemented by the demonstration of impaired proliferative responses to mitogenic stimuli in peripheral blood lymphocytes isolated from CHL patients. 11 What explains the impaired T cell responses seen in CHL?…”

Section: T Cells In Chl: Friends or Foes?mentioning

confidence: 99%

The immune microenvironment in Hodgkin lymphoma: T cells, B cells, and immune checkpoints

2016

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“…Some lymphoid cells in S.H. contained increased amounts of Gal, GlcNAc and Man, but Archibald & Frenster (1973) suggested that these T cells had cytotoxic activity, Payne et al (1977) reported that Reed-Sternberg cells at the centre of such clusters remained viable in culture for several days. They suggested that such clusters represented an aberrant attempt at cell cooperation rather than immunological attack.…”

Section: Galnac Neunacmentioning

confidence: 99%

Studies of lectin binding to normal and neoplastic lymphoid tissues. I. Normal nodes and Hodgkin's disease

Bramwell¹,

Crowther²,

Gallagher³

et al. 1982

Br J Cancer

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Lectins are proteins which have the ability to interact specifically with carbohydrate residues of glycoproteins and other glycoconjugates. The staining patterns of 10 fluorescein conjugated lectins (F-Con A, F-LCA, F-RCA, F-WGA, F-PHA, F-PWM, F-LTA, F-SBA, F-PNA, F-DB) and a protease inhibitor (F-LA) have been studied in histological sections of 11 normal or reactive lymph nodes and 6 nodes and one skin biopsy involved by Hodgkin's disease. On the basis of the patterns of lectin binding, and current knowledge of their saccharide specificities, we found that within germinal centres there is an orderly carbohydrate rich extracellular matrix which contains a higher concentration of GlcNAc and terminal Gal residues than the surface membranes of component cells. This suggests active secretion rather than simple membrane shedding, and it is possible that this pericellular domain plays a part in the regulation of the proliferative response, or controls migration of lymphocytes in and out of the germinal centre. Lectin binding in Reed-Sternberg cells suggests that the huge nucleoli contain glycoconjugates of diverse structure, which may be linked with their failure to undergo cytokinesis. Images Fig. 1 Fig. 2 Fig. 3 Fig. 4 Fig. 5

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Reed-Sternberg-Cell/Lymphocyte Interaction

Cited by 43 publications

References 11 publications

Amplification of TCRβ gene rearrangements from micromanipulated single cells: T cells rosetting around Hodgkin and Reed-Sternberg cells in Hodgkin's disease are polyclonal

Amplification of TCRβ gene rearrangements from micromanipulated single cells: T cells rosetting around Hodgkin and Reed-Sternberg cells in Hodgkin's disease are polyclonal

The immune microenvironment in Hodgkin lymphoma: T cells, B cells, and immune checkpoints

Studies of lectin binding to normal and neoplastic lymphoid tissues. I. Normal nodes and Hodgkin's disease

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