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[Pterygium and mast cells--mast cell number, phenotype, and localization of stem cell factor].

We examined the number and phenotype of mast cells, and the localization of stem cell factor (SCF) as a growth factor of mast cells in the excised tissue of 38 cases of pterygium. In histopathology with toluidine blue stain and immunohistochemistry with a monoclonal antibody to tryptase, the mean mast cell count in pterygium specimens was twice as high as in normal conjunctiva. In pterygium specimens more than 94% of tryptase-positive mast cells were found to express chymase and c-kit. There was no phenotypic difference between mast cells in pterygium and normal conjunctiva. In all immunohistochemical specimens in which we could examine the head of the pterygium, SCF was expressed in subepithelial fibroblasts at the central edge of pterygium. The results suggest that overexpression of SCF was accompanied with the augmentation of mast cells in the pterygium.

Cell Count↗

Regulation by T cells of delayed hypersensitivity reaction in mouse lung as reflected by mononuclear cells, mast cells and mucus-producing cells.

The appearance of mononuclear cells, mast cells and mucus-producing cells in the lung and their linkage to the development of delayed hypersensitivity (DH) reactions were studied. Adoptive transfer of immune lymph node cells, spleen cells and serum and in vivo treatment with monoclonal antibodies to L3T4-positive T cells in Balb/c mice were performed to investigate the cellular regulation of the number of mononuclear cells, mast cells and mucus-producing cells in the lung. Immune lymph node cells and, to a lesser extent, immune spleen cells from mice sensitized epicutaneously with picrylchloride transferred DH reactions to the recipients as assessed by ear thickness increase after challenge. Serum from sensitized mice was not able to transfer a DH reaction. Cyclophosphamide treatment of donor mice increased the DH reaction in the recipient mice. Adoptive transfer of immune lymph node cells and spleen cells gave a slight increase in the number of mononuclear cells in the lung of recipient mice compared with controls. This weak accumulation of mononuclear cells in the lungs of recipient mice, however, was not accompanied by a consistent increase in the number of mucus-producing cells and mast cells. The number of spleen cells expressing the L3T4 antigen decreased after in vivo treatment with the monoclonal GK1.5 (anti-L3T4) antibody as assessed by immunohistochemistry. This antibody treatment also resulted in an inhibition of the DH reaction and a decrease in the number of mononuclear cells and mucus-producing cells, but not in mast cells in the lung of sensitized and challenged mice.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Immunological suppression of delayed hypersensitivity responses in mouse lungs as reflected by numbers of mononuclear cells, mast cells and mucus-producing cells.

The suppression of delayed hypersensitivity (DH) in the lung as reflected by the appearance of mononuclear cells, mast cells and mucus-producing cells was studied in Balb/c mice. Immunosuppression was induced by intravenous and peroral administration of picrylsulfonic acid (PSA) in mice subsequently sensitized with picrylchloride (PiCl). The animals exhibited a decreased DH reactivity as assessed by ear thickness increase compared with mice sensitized but not exposed to PSA pretreatment. In mice exposed to PSA intravenously (suppressed) and sensitized with PiCl there was a decrease in the number of mononuclear cells in the lung after challenge, compared to mice sensitized and challenged only. Similarly, the mast cell and mucus-producing cell numbers were slightly lower in animals immunosuppressed intravenously with PSA compared with sensitized mice. Such a decrease in the numbers of mononuclear cells, mast cells and mucus-producing cells in the lung was not seen in animals treated with PSA perorally, although these animals exhibited suppressed DH reaction in the ears. The present results indicate that induction of mononuclear cells and to some extent mast cells and mucus-producing cells in the lung relates to the DH reaction and its regulation.

Animals↗

Mononuclear cells, mast cells and mucous cells as part of the delayed hypersensitivity response to aerosolized antigen in mice.

Mice (BALB/c) exposed to picryl chloride (PiCl) on their shaved abdomen and untreated animals were after 7 days exposed to daily aerosolized trinitrophenylated dog serum albumin (TNP-DSA). Mice exposed to PiCl tended to respond earlier and more strongly with both delayed hypersensitivity (DH) and IgG antibodies in serum and bronchial washings than did mice exposed to aerosol only. Picryl chloride sensitization resulted in spontaneously proliferating axillary lymph node cells, which could not be further stimulated with antigen or mitogen. Histological examination of lung tissue of aerosol-sensitized animals revealed an increase in mononuclear cells and mast cells around bronchioli and mucous cells, particularly in those animals exposed for prolonged periods and sensitized with PiCl prior to aerosol. Sensitization of mice with aerosolized TNP-DSA administrated in two 2- and 1-week periods with a 4-week interval responded with DH and IgG antibody in a dose dependent fashion irrespective of presensitization with PiCl. In bronchial washings IgG antibodies were found particularly after two 2-week periods of exposure. The cells taken from the axillary or brachial lymph nodes showed spontaneous proliferation. Culture of the cells to achieve mast cell maturation resulted in no or very low numbers of mast cells in the lymph nodes.

Aerosols↗

Argyrophil cells, mast cells, and histamine in the fundic mucosa of antrectomized patients.

Fasting gastrinemia, fundic argyrophil cell density, mast cell number, basal fundic histamine content and histidine decarboxylase activity were determined in 20 antrectomized patients and 20 control subjects. Fasting gastrinemia and fundic argyrophil cell density were significantly lower in antrectomized patients than in controls, whereas fundic mast cell number, basal histamine content, and histidine decarboxylase activity did not differ significantly between the two groups. In antrectomized patients the basal fundic histamine content appears related to the fundic mast cell number, as a consequence of the reduced effect of gastrin on argyrophil cells.

Aged↗

Linker for activation of T cells (LAT), a novel immunohistochemical marker for T cells, NK cells, mast cells, and megakaryocytes: evaluation in normal and pathological conditions.

LAT (linker for activation of T cells) is an integral membrane protein of 36-38 kd that plays an important role in T cell activation. Using a rabbit polyclonal antibody generated against the cytosolic portion of LAT, we investigated the immunohistochemical expression of LAT in normal and pathological hematolymphoid tissues. LAT reacts with human T cells in paraffin sections, including decalcified bone marrow trephines. LAT appears early in T cells at the thymocyte stage and before TdT expression in embryos, and is expressed in peripheral lymphoid tissues, without restriction to any T cell subpopulations. In addition to T cells, natural killer (NK) cells (evaluated with flow cytometry), megakaryocytes and mast cells are also LAT-positive, whereas B cells and other myeloid and monocytic derived cells are negative. Tested on a total of 264 paraffin-embedded tissue biopsies, LAT reacted with the great majority (96.8%) of T/NK-cell neoplasms, covering the full range of T cell maturation. Although antibodies to both LAT and CD3 had a similarly high sensitivity in the staining of T/NK-cell lymphomas, when used in conjunction, they successfully identified a higher number of cases (98.4%). Atypical megakaryocytes from different hematological disorders, as well as mast cells in mastocytosis were also LAT-positive, but all neoplasms of B cell origin, Hodgkin's lymphomas, and several nonlymphoid malignancies were negative. These data indicate that the anti-LAT antibody may be of value to diagnostic histopathologists for the identification of T cell neoplasms.

Adaptor Proteins, Signal Transducing↗

The mast cell and mast cell disease.

Mast cell disease or mastocytosis is a heterogeneous group of clinical disorders characterized by the proliferation and accumulation of mast cells in a variety of tissues, most often the skin. The signs and symptoms of mast cell disease are varied, dependent on the localization of mast cells in different organs and the local and systemic effects of mediators released from these cells. Although mast cell disease is most commonly identified in the skin, involvement of the skeletal, hematopoietic, gastrointestinal, cardiopulmonary, and central nervous systems may be seen. Clinical management of mastocytosis depends most heavily on knowledge of the diverse effects of mast cell mediators on various tissues and organs, the stimuli that can cause their release, and the different methods available for blocking the effects of these mediators.

Bone Diseases↗