Nonspecific Esterase Activity in T Cells

Mueller, Joachim D.; Keller, H. U.; Re, G. Brun del; Buerki, H.; Hess, M. W.

doi:10.1007/978-1-4613-4355-4_17

Cited by 5 publications

(5 citation statements)

References 5 publications

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“…Glomerular grading was on a 0-4+ basis, with notation of focal or diffuse proliferation. Proliferation was quantitatively assessed using a Zeiss eye-piece micrometer and by measuring the diameter of glomerular tufts in 10-20 glomeruli cut through the stalk (30 (38,40). Deparaffinized sections were washed in deionized water, air dried, and incubated in pararosanilin/alpha-naphthyl acetate/sodium nitrite, pH 6.0, mixed immediately before incubation.…”

Section: Phase Imentioning

confidence: 44%

New avian model of experimental glomerulonephritis consistent with mediation by cellular immunity. Nonhumorally mediated glomerulonephritis in chickens.

Bolton¹,

Tucker²,

Sturgill³

1984

J. Clin. Invest.

113

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Section: Phase Imentioning

confidence: 44%

New avian model of experimental glomerulonephritis consistent with mediation by cellular immunity. Nonhumorally mediated glomerulonephritis in chickens.

Bolton¹,

Tucker²,

Sturgill³

1984

J. Clin. Invest.

113

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“…[19] was modified as described [20]. In short, microscope slides were made with a cytocentrifuge or by using cells grown on coverslips.…”

Section: Demonstration Of Anae Activity In Effector Cellssupporting

confidence: 49%

Identification of the effector cells in human blood displaying spontaneous cytotoxicity to chicken erythrocytes

1977

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By combining velocity and linear density fractionations as well as target cell rosetting techniques we have isolated and morphologically identified the human effector cell type responsible for spontaneous, trypsin-augmentable cytotoxicity against chicken red cells and human myeloma cell line targets. This cell is a large lymphoid cell with strong alpha-naphthyl esterase activity concentrated in a limited area in the cytoplasm usually at the indentation site of a slightly reniform nucleus. Cells with this morphology also formed plaques on chicken erythrocyte monolayers. The cell is nonphagocytic and nonadherent, it carries Fc receptors but no complement receptors on its surface, and shows a weak affinity to sheep red blood cells (SRBC). The frequency of these cells based on morphological analysis is 3 x 10(4)--6 x 10(4)/ml in normal human blood. This cell shows similarities (surface Ig-, Fc+, C3-) with the human natural killer (NK) cells lytic to hematopoetic target cell lines but differs in that the cytotoxicity is augmentable by trypsin and the affinity to SRBC is lower. Therefore, we postulate that these two killer populations represent different subpopulations of human NK cells.

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“…Immunofluorescence staining of membrane immunoglobulin was done to identify B lymphocytes among suspended spleen cells (61. Staining for «-naphtylacetate esterase (ANAL) activity was performed to identify T cells [12], Thymectomy Thymectomy was performed under ether anes thesia through an about 5-mm-long midstcrnal in cision beginning at the jugulum. The wound mar gins were held apart by pincettes to expose the two lobes of the gland which were then suctioned with a Pasteur pipette.…”

Section: Preparation and Characterization Of Lymphoid Cellsmentioning

confidence: 50%

Interaction of Cholera Toxin and Toxin Derivatives with Lymphocytes

Lange¹,

Lindholm²,

Holmgren³

1978

Int Arch Allergy Immunol

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The influence of cholera toxin (CT), and thus probably of cyclic AMP, on the capacity of parental lymphoid cells to elicit a graft-versus-host reaction (GVHR) was studied. Toxin-treated DBA/1 mice were used as cell donors and untreated DBA/1xC57B1/ 6 F1 hybrid mice as recipients, and the GVHR reactivity of the transferred cells was estimated by their ability to induce spleen enlargement or stimulation of antibody formation (‘allogenic effect’) in the recipients. Spleen cells from donors intravenously injected with 1 μg CT 1–3 days earlier, gave a significantly stronger GVHR than did spleen cells of untreated mice. Choleragenoid, a toxin analog devoid of the toxin’s ability to activate plasma membrane adenylate cyclase even though it binds efficiently to cells, had no effect on the GVHR-inducing capacity of the spleen cells. The enhanced GVHR by spleen cells from toxin-treated DBA/1 animals was reduced to the normal level when the donor cells were transferred along with lymphoid cells from untreated animals of the same strain. Spleen was the most powerful source of the suppressive influence. No evidence for a redistribution of suppressor cells following administration of CT was found. Spleen cells from mice syngeneic with the recipients had no suppressive effect. The results suggest that parenterally administered CT, directly or indirectly, can inhibit a cell population in spleen which normally exerts an antigen-specific suppressive regulatory influence on the development of GVHR.

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Nonspecific Esterase Activity in T Cells

Cited by 5 publications

References 5 publications

New avian model of experimental glomerulonephritis consistent with mediation by cellular immunity. Nonhumorally mediated glomerulonephritis in chickens.

New avian model of experimental glomerulonephritis consistent with mediation by cellular immunity. Nonhumorally mediated glomerulonephritis in chickens.

Identification of the effector cells in human blood displaying spontaneous cytotoxicity to chicken erythrocytes

Interaction of Cholera Toxin and Toxin Derivatives with Lymphocytes

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