Simultaneous in situ detection of IgE receptors and cytoplasmic granules in murine cutaneous mast cells

Giorno, Ralph; Choi, Ken Lee; Claman, Henry N.

doi:10.1016/0022-1759(87)90121-9

Cited by 14 publications

(5 citation statements)

References 11 publications

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“…16 In fact, mast cell degranulation may be so complete that these cells are not seen by conventional metachromatic staining and special tech¬ niques are required to reveal them. 17 Following this lead, we also found that mast cells are increased in scleroderma, but only in the involved skin of relatively recent-onset disease.18 Similar findings have been reported recently from Japan.19 In addition, mast cells and fibroblasts interact in vitro (reviewed in references 20 and 21). Thus, there is growing evidence, even if only circumstantial, that mast cells play a role in conditions where fibroblasts are active.…”

supporting

confidence: 59%

New Hope for Neurofibromatosis? The Mast Cell Connection

Claman¹

1987

JAMA

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supporting

confidence: 59%

New Hope for Neurofibromatosis? The Mast Cell Connection

Claman¹

1987

JAMA

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“…Mast cell granules were identified in the same tissue fields with TRITC-labeled avidin (12,17). In normal mouse skin (12) and normal human skin, all cells staining for IgE receptors had avidin-binding granules. We therefore believe that this technique identifies the high-affinity IgE receptor on mast cells and basophils, but not the low-affinity IgE receptor (17).…”

Section: Discussionmentioning

confidence: 99%

“…In the present study, we used a double immunofluorescence technique to simultaneously measure mast cell membranes and mast cell granules in the skin of patients with generalized scleroderma. Mast cell membranes were identified by reagents that stain IgE receptors on cells, specifically by using IgE (to saturate the receptors), anti-IgE (goat origin), and a fluoresceinated swine anti-goat antibody (12). Mast cell granules were identified in the same tissue fields with TRITC-labeled avidin (12,17).…”

Section: Discussionmentioning

confidence: 99%

“…Our method has been well studied in murine chronic graft-versus-host disease, compared with toluidine blue staining of unfixed tissue, electron microscopy. and immunofluorescence of frozen sections, without evidence of artifactual effect (6,12).…”

Section: Discussionmentioning

confidence: 99%

“…Our procedure for detecting mast cell high-affinity Fc receptors for IgE and mast cell granules was analogous to that previously described in murine studies (12). Frozen sections were incubated for 30 minutes with IgE, rinsed in PBS, incubated 30 minutes with goat anti-human IgE, rinsed in PBS, and finally, incubated for 30 minutes in a mixture of FITC-conjugated swine anti-goat IgG and TRITC-labeled avidin or TR-labeled avidin.…”

Section: Methodsmentioning

confidence: 99%

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Dermal mast cell degranulation in systemic sclerosis

Seibold

Giorno

Claman

1990

Arthritis & Rheumatism

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127

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Paired biopsy samples from involved and uninvolved skin were obtained from 19 patients with generalized scleroderma (11 with early, progressive disease and 8 with late, improving disease). Skin biopsy samples were double stained for mast cell granules and for mast cell membrane. The number of mast cells was increased in patients with systemic sclerosis (SSc), in both involved and uninvolved skin and in both early and late disease. There was an increase in the number of degranulated mast cells in the involved skin of patients with both early and late disease and in the not-yet-involved skin of patients with early disease; however, there was no increase in the number of degranulated mast cells in areas of previously involved but now normal skin of patients with late disease. Increases in mast cell number and degranulation precede clinically apparent dermal fibrosis in SSc. These observations and the absence of mast cell degranulation in regressing skin suggest a participatory role of the mast cell in the clinical progression of skin changes in SSc.

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On Scleroderma

Claman¹

1989

JAMA

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An integrated view of the pathogenesis of scleroderma should include vascular, immunologic, and fibrotic processes. This review introduces the mast cell into this picture, emphasizing recent knowledge gained from a study of experimental chronic graft-vs-host disease and scleroderma itself. In both of these situations, increased mast cell activity occurs. A link between the activation of both endothelial cells and fibroblasts may be provided by the family of heparin-binding growth factors. These cytokines are produced by many cells and are bound, protected, and enhanced by heparin, which may be provided by the activated mast cells. These and other growth factors may be responsible for endothelial proliferation and excess collagen production by fibroblasts. This enlarged schema should provide additional points for therapeutic intervention in scleroderma.

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Simultaneous in situ detection of IgE receptors and cytoplasmic granules in murine cutaneous mast cells

Cited by 14 publications

References 11 publications

New Hope for Neurofibromatosis? The Mast Cell Connection

New Hope for Neurofibromatosis? The Mast Cell Connection

Dermal mast cell degranulation in systemic sclerosis

On Scleroderma

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