Induction of IL-2 receptor expression in vivo: Response to concanavalin A

Black, Christopher D. V.; Kroczek, Richard A.; Barbet, Jacques; Weinstein, John N.; Shevach, Ethan M.

doi:10.1016/0008-8749(88)90105-0

Cited by 21 publications

(14 citation statements)

References 40 publications

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“…3). CD25 comprises the a chain of the IL-2 receptor, and its expression has also been demonstrated to be up-regulated in T lymphocytes upon stimulation with ConA (Black et al 1988). Cultivation in medium for 24 h in the absence of in vitro stimulus (Fig.…”

Section: Resultsmentioning

confidence: 99%

In vivo lymphocyte activation and apoptosis by lectins of the Diocleinae subtribe

Bessa

Arruda

Cavada

et al. 2001

Mem. Inst. Oswaldo Cruz

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Section: Resultsmentioning

confidence: 99%

In vivo lymphocyte activation and apoptosis by lectins of the Diocleinae subtribe

Bessa

Arruda

Cavada

et al. 2001

Mem. Inst. Oswaldo Cruz

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“…Resting T cells from freshly isolated PBMC do not express CD25, the ® -chain of the IL-2 receptor [19,20], but upon cellular activation in the presence of clone-specific conventional antigen or superantigen, CD25 is up-regulated [21][22][23]. To examine whether NK cells could present superantigen to T cells, we assessed T cell activation by quantifying the expression of up-regulation of CD25 on T cells by flow cytometry.…”

Section: Presentation Of Seb To T Cells By Nk Cellsmentioning

confidence: 99%

Human natural killer (NK) cells present staphylococcal enterotoxin B (SEB) to T lymphocytes

D’Orazio¹,

Stein‐Streilein

1996

Clinical and Experimental Immunology

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SUMMARY Superantigen-mediated T cell activation requires the participation of antigen-presenting cells (APC).Once superantigen has bound class II MHC molecules on the surface of APC, it then can interact with the T cell receptor to induce T cell activation. Superantigen-mediated T lymphocyte activation, along with its consequent cytokine production is thought to be the basis for the pathophysiology of conditions such as toxic shock syndrome, Kawasaki's disease and possibly rheumatoid arthritis. We examined the role of CD56 NK lymphocytes in the interaction between superantigens and T lymphocytes. First, we found that a subpopulation of CD56 cells freshly isolated from human peripheral blood expressed class II MHC molecules. The amount of HLA-DR expression varied between individuals, ranging from 9 . 3% to 37 . 7%. CD56 (NK) cells were purified from the peripheral blood by cell sorting and were tested for their ability to support SEB-mediated T cell activation as assessed by surface expression of IL-2 receptor ® -chain (CD25) on CD3 lymphocytes. We observed that when enriched T cells were incubated with SEB in the presence of NK cells, there was a significant up-regulation of CD25 expression on the T cells. When HLA-DR + cells were removed from sorted CD56 populations, the remaining HLA-DR ÿ NK cells were unable to support SEB-mediated T cell activation. Also, SEB upregulated the expression of HLA-DR on CD56 cells in peripheral blood mononuclear cell (PBMC) populations after 24 h of incubation, implying that the ability of NK cells to function as superantigenpresenting cells is up-regulated by superantigens themselves. Together, these data demonstrate for the first time that human CD56 HLA-DR NK cells can function as superantigen-presenting cells, and imply that NK cells may be involved in the activation of non-specific T cell reactivity during early host defences against superantigen-elaborating microorganisms in vivo. Furthermore, the physical linkage of NK cells and T cells by the interaction of superantigen with HLA class II molecules and T cell receptors, respectively, may lead to NK cell activation and augmented lytic potential, helping to clear the body of superantigen-elaborating microorganisms.

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“…This may be related to the down regulation of IL2R expression by ConA-induced suppressor cells, or that the function of ConA-induced suppressor cells in AsC is higher than that in normal individuals. It was reported that the administration of ConA can result in enhanced activity of the T suppressor cells in mice (1). In this report, however, it is found that the level of IL2R expression of PBMC induced by ConA or HBsAg is too low to initiate an intracellular signal, which may lead to the disability to promote differentiation and proliferation of immune cells.…”

Section: Discussionmentioning

confidence: 58%

Immunohistochemical expression of interleukin 2 receptor (IL2R) and formation of IL2R positive cell rosette in peripheral blood mononuclear cells in asymptomatic hepatitis B surface antigen carriers.

Guo¹,

Luo²,

Ding³

et al. 1991

Acta Histochem. Cytochem

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Induction of IL-2 receptor expression in vivo: Response to concanavalin A

Cited by 21 publications

References 40 publications

In vivo lymphocyte activation and apoptosis by lectins of the Diocleinae subtribe

In vivo lymphocyte activation and apoptosis by lectins of the Diocleinae subtribe

Human natural killer (NK) cells present staphylococcal enterotoxin B (SEB) to T lymphocytes

Immunohistochemical expression of interleukin 2 receptor (IL2R) and formation of IL2R positive cell rosette in peripheral blood mononuclear cells in asymptomatic hepatitis B surface antigen carriers.

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