Conditions enhancing the percentage and size of E rosettes formed by T lymphocytes

Moore, Ann L.; Zusman, Jaime

doi:10.1016/0022-1759(78)90202-8

Cited by 21 publications

(2 citation statements)

References 30 publications

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“…fw/zmp/o^/oHo/77i»)/7/ior)7c.v. T cells were enumerated by rosetiing wiih 2-aniinoelhylisothiouronitjm bromide (AET)-treated sheep erythrocyles and maintaining the cell pellet at 4°C overnight before resuspension [7].…”

Section: Methodsmentioning

confidence: 99%

The Generation of Specific Cytotoxic Responses by Human Lymphocytes Requires Antigen and Activities Provided by a Lymphokine Supernatant‐

Warren¹

1981

Scand J Immunol

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The requirements for the generation of specific cytotoxic responses by human lymphocytes have been investigated using as a model system the response to the ultraviolet light-killed mouse tumour P815. These requirements are antigen (P815UV) and activities provided by a human lymphokine (LK) supernatant. Cells that give rise to non-specific cytotoxicity can be separated on discontinuous Percoll density gradients after a 3-day incubation of peripheral blood leucocytes with the lymphokine supernatant. Cells from which specific cytotoxic responses can subsequently be generated in the presence of P815UV and LK sediment at a higher density.

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Section: Methodsmentioning

confidence: 99%

The Generation of Specific Cytotoxic Responses by Human Lymphocytes Requires Antigen and Activities Provided by a Lymphokine Supernatant‐

Warren¹

1981

Scand J Immunol

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“…The T cell rosette assay used aminoethylisothiouronium bromide hydrobromide (AET)-treated SRBC (23) and rosettes were enumerated al 20 h. MoAb inhibition of T cell rosette formation was tested following incubation of T cells with optimum MoAb concentrations for 30 min on ice.…”

Section: Rosette Assaysmentioning

confidence: 99%

Mapping the dextran sulfate binding site on CD2

Warren¹,

Parish²

1990

Immunology & Cell Biology

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Summary This study has analysed the binding of a series of anti-CD2 monoclonal anlibodies (MoAbs) to T cells in the presence of the suUated polysaccharide dextran sulfatc (2 3 sulfates/ monosaccharide, 500 kDa) (DXS) to define Ihe DXS binding site on CD2. The results show that DXS interacts primarily at theTl 11 epitope. Thus fiveanti-CD2 MoAbs which bound tothcTI 12 epitope were inhibited in their binding by DXS. In contrast, seven anti-CD2 MoAbs that totally inhibited sheep red blood cells (SRBC) rosetting (identifying the Til I epitope) were unaReeted in their binding to T cells in the presenee oI'DXS. Three MoAbs which partially inhibited SRBC rosetting and thereby definingonly part of theTl 1 [ epitope. were also inhibited in their binding by DXS. Consistent with the conelusion that (he DXS binding site on CD2 is associated with the Tl 12 epitope was the observation that interaetion of DXS with CD2 resulted in augmented binding of the four MoAbs defining theTl 13 epitope, possibly reflecting an increased expression of the TI li (activation. CD2R) epitope of CD2. Collectively, the data presented support the notion that a natural ligand for theTl 12 epitope of CD2 will be identified as a sulphated carbohydrate structure.

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T cells and erythroid burst forming units in chronic lymphocytic leukemia

Socinski

Ershler

1984

American J Hematol

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Substantial evidence exists indicating T cell abnormalities in chronic lymphocytic leukemia (CLL). There is also evidence that the T cell is an important source of burst promoting activity (BPA) for the peripheral blood (PB) erythroid burst forming unit (BFU-e). We studied the BPA of T cells and response of BFU-e in normals and untreated early stage B cell CLL patients in a methylcellulose colony assay. Normal null cell cultures grew significantly more BFU-e than CLL null cell cultures. Addition of autologous T cells to normal or CLL null cells significantly increased BFU-e only in normals. Allogeneic coculture of T cells from CLL patients with null cells from normals yielded normal responses of BFU-e in five of six cases. In contrast, allogeneic coculture of normal T cells with CLL null cells yielded a normal response in only one of six studies. Furthermore, adding increasing quantities of autologous or normal allogeneic T cells to CLL null cells did not augment the BFU-e response. Accounting for the expanded lymphocyte pool in CLL, BFU-e are decreased in concentration but the absolute number is normal or increased. The decrease in concentration could be secondary to expansion of the null cell fraction in CLL by pre-B cells. CLL T cells appeared to augment normal allogeneic PB BFU-e in a normal fashion, whereas, in several cases, CLL BFU-e were hyporesponsive to autologous or normal allogeneic T cells. It is therefore apparent that in untreated early stage B cell CLL, erythroid progenitor cells are present in the peripheral blood but are diluted in an expanded null cell compartment and may, in some cases, be hyporesponsive to T cell BPA. T cell BPA of CLL T cells in this early stage of disease is preserved.

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Conditions enhancing the percentage and size of E rosettes formed by T lymphocytes

Cited by 21 publications

References 30 publications

The Generation of Specific Cytotoxic Responses by Human Lymphocytes Requires Antigen and Activities Provided by a Lymphokine Supernatant‐

The Generation of Specific Cytotoxic Responses by Human Lymphocytes Requires Antigen and Activities Provided by a Lymphokine Supernatant‐

Mapping the dextran sulfate binding site on CD2

T cells and erythroid burst forming units in chronic lymphocytic leukemia

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