Mast cells and basophils

Current Opinion in Hematology

Volumn 7, Issue 1, 2000, Pages 32-39

  Galli, Stephen J ^a  

^a STANFORD UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

IMMUNOGLOBULIN E;

BASOPHIL; CELL DIFFERENTIATION; CELL FUNCTION; CELL MATURATION; EFFECTOR CELL; IMMUNE RESPONSE; IMMUNOGLOBULIN PRODUCTION; MAST CELL; MEDIATOR RELEASE; NONHUMAN; PRIORITY JOURNAL; REVIEW;

ANIMALS; BASOPHILS; HUMANS; IMMUNITY, NATURAL; IMMUNOGLOBULIN E; MAST CELLS;

EID: 0033989686     PISSN: 10656251     EISSN: None     Source Type: Journal    
DOI: 10.1097/00062752-200001000-00007     Document Type: Review

References (84)

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36. 36 Lantz CS, Song CH, Dranoff G, Galli SJ: Interleukin-3 (IL-3) is required for blood basophilia, but not for increased IL-4 production, in response to parasite infection in mice [abstract]. FASEBJ 1999, 13:A325.
37. v mice and their increase by bone marrow transplantation. Blood 1978, 52:447-452.
38. 38 Yuan Q, Gurish MF, Friend DS, Austen KF, Boyce JA: Generation of a novel stem cell factor-dependent mast cell progenitor. J Immunol 1998, 161:5143-5146. This study provides further clarification of the sequential effects of SCF and interleukin-3 in mouse mast cell development in vitro and reports the ability of a mixture of SCF, interleukin-6, and interleukin-10 to induce the development of a subpopulation of cells with features of promastocytes from mouse bone marrow cells in vitro,
39. + cells under conditions optimal for the development of mast cells, basophils, eosinophils, and macrophages indicated that committed progenitors of human mast cells develop from multipotent hematopoietic cells through a pathway distinct from that of other myeloid lineages, including basophils.
40. 40 Wastling JM, Knight P, Ure J, Wright S, Thornton EM, Scudamore CL, et al.: Histochemical and ultrastructural modification of mucosal mast cell granules in parasitized mice lacking the β-chymase, mouse mast cell protease-1. Am J Pathol 1998, 153:491-504. Using gene targeting, the authors produced mice that lacked expression of the β-chymase, mMCP-1, which is expressed mainly by intestinal mucosal mast cells. In these mice intestinal mucosal mast cells transcribed mMCP-2, -4, and -5 apparently normally but expressed striking histochemical and ultrastructural abnormalities of their cytoplasmic granules. This is the first report of a knockout of an apparently mast cell-specific mediator.
41. -/- mice appear to be confined to connective tissue-type and "serosal" mast cell populations that ordinarily contain heparin but apparently do not affect intestinal mucosal mast cells. Thus, the affected cells have morphologically and biochemically abnormal cytoplasmic granules, which contain no detectable mMCP-4, mMCP-5, or mouse mast cell CPA, as well as diminished quantities of mMCP-6 and histamine.
42. -/- mice appear to be confined to connective tissue-type and "serosal" mast cell populations that ordinarily contain heparin but apparently do not affect intestinal mucosal mast cells. Thus, the affected cells have morphologically and biochemically abnormal cytoplasmic granules, which contain no detectable mMCP-4, mMCP-5, or mouse mast cell CPA, as well as diminished quantities of mMCP-6 and histamine.
43. 43 Miller HR, Wright SH, Knight PA, Thornton EM: A novel function for transforming growth factor-beta 1: up-regulation of the expression and the IgE-independent extracellular release of a mucosal mast cell granule-specific beta-chymase, mouse mast cell protease-1. Blood 1999, 93:3473-3486. Using BMCMCs generated in medium supplemented with SCF, interleukin-3, and interleukin-9, the authors found that TGF-β1 markedly upregulated the cells' ability to both produce and store the intestinal mucosal mast cell-specific protease, mMCP-1, and also to release the protease. Interleukin-9-induced enhancement of mMCP-1 expression may reflect endogenous TGF-β1 production, because this enhancement can be inhibited in vitro by anti-TGF-β1 antibodies.
44. 44 Gordon JR, Galli SJ: Promotion of mouse fibroblast collagen gene expression by mast cells stimulated via the FcεRI: role for mast cell-derived transforming growth factor β and tumor necrosis factor α. J Exp Med 1994, 180:2027-2037.
45. 45 Fang KC, Wolters PJ, Steinhoff M, Bidgel A, Blount JL, Caughey GH: Mast cell expression of gelatinases A and B is regulated by kit ligand and TGF-beta. J Immunol 1999, 162:5528-5535.
46. 46 Zhang S, Anderson DF, Bradding P, Coward WR, Baddeley SM, MacLeod JD, et al.: Human mast cells express stem cell factor. J Pathol 1998, 186:59-66.
47. 47 de Paulis A, Minopoli G, Dal Piaz F, Pucci P, Russo T, Marone G: Novel autocrine and paracrine loops of the stem cell factor/chymase network. Int Arch Allergy Immunol 1999, 118:422-425.
48. 48 Welker P, Grabbe J, Gibbs B, Zuberbier T, Henz BM: Human mast cells produce and differentially express both soluble and membrane-bound stem cell factor. Scand J Immunol 1999, 49:495-500.
49. 49 Longley BJ, Tyrrell L, Ma Y, Williams DA, Halaban R, Langley K, et al.: Chymase cleavage of stem celt factor yields a bioactive, soluble product. Proc Natl Acad Sci U S A 1997, 94:9017-9021.
50. 50 Kunisada T, Lu S-Z, Yoshida H, Nishikawa S, Nishikawa S, Mizoguchi M, et al.: Murine cutaneous mastocytosis and epidermal melanocytosis induced by keratinocyte expression of transgenic stem cell factor. J Exp Med 1998, 187:1565-1573. Transgenic mice were produced that targeted expression of two forms of SCF to epidermal keratinocytes. Expression of the membrane-associated form of SCF from which soluble SCF could readily be generated reproduced aspects of the phenotype of human cutaneous mastocytosis (including increases in numbers of dermal mast cells and epidermal hyperpigmentation, as well as epidermal melanocytosis). By contrast, expression of a more membrane-associated form of SCF (tacking both the primary and alternate proteolytic cleavage sites, encoded by exons 6 and 7, through which soluble SCF can be generated) resulted in cutaneous melanocytosis and hyperpigmentation, but not in an increase in dermal mast cells. These findings indicate that mast cell development and survival in mice may be especially dependent on the presence of soluble forms of SCF.
51. 51 Tajima V, Moore MA, Seares V, Ono M, Kissel H, Besmer P: Consequences of exclusive expression in vivo of Kit-ligand lacking the major proteolytic cleavage site. Proc Natl Acad Sci U S A 1998, 95:1903-1908. Transgenic mice were produced that exclusively expressed only one of the two forms of the kit ligand (also known as SCF)-the kit ligand-2 form, which lacks the major proteolytic cleavage site for generating the soluble, but still biologically active, form of kit ligand. Although the mice had only slightly reduced levels of soluble kit ligand in the serum (pointing to alternative routes for producing soluble kit ligand) and the animals were not anemic, they had reduced numbers of skin and peritoneal mast cells. These findings suggest that mast cell development and survival may be particularly dependent on kit ligand-2 that can be processed normally for generation of soluble kit ligand-2.
52. + and contained substantial amounts of tryptase, chymase, and CPA by immunocytochemistry. One interpretation of these findings is that basophils can exhibit alterations in their phenotype in the context of certain immunologic responses.
53. 53 Furitsu T, Tsujimura T, Tono T, Ikeda H, Kitayama H, Koshimizu U, et al.: Identification of mutations in the coding sequences of the proto-oncogene c-kit in a human mast cell leukemia cell line causing ligand independent activation of c-kit product. J Clin Invest 1993, 92:1736-1744.
54. 54 Buttner C, Henz BM, Welker P, Sepp NT, Grabbe J: Identification of activating c-kit mutations in adult-, but not in childhood-onset indolent mastocytosis: a possible explanation for divergent clinical behavior. J Invest Dermatol 1998, 111:1227-1 233. The authors searched for codon 560 or 816 c-kit mutations in skin biopsies of lesions in adult or pediatric subjects with indolent mastocytosis. Codon 816 or 560 mutations were identified in six of six and two of four adult specimens analyzed, respectively, but in none of 11 and none of two pediatric patients analyzed, respectively. These findings offer an important clue to the molecular basis for the different clinical features of adult-versus pediatric-onset indolent mastocytosis.
55. 55 Longley BJ Jr, Metcalfe DD, Tharp M, Wang X, Tyrrell L, Lu SZ, et al.: Activating and dominant inactivating c-KIT catalytic domain mutations in distinct clinical forms of human mastocytosis. Proc Natl Acad Sci U S A 1999, 96:1609-1614. All adult subjects with sporadic mastocytosis who were analyzed had Asp816Val c-kit mutations, and codon 816 mutations were also found in four pediatric-onset cases. Although typical pediatric patients lacked codon 816 mutations, three of six had a dominant inactivating mutation (Glu839Lys) at the site of a potential salt bridge. Sequencing of the entire coding region detected no c-kit mutations in three patients with familial mastocytosis. These findings suggest that codon 816 mutations are characteristic of adult patients with sporadic mastocytosis and of children at risk for extensive or persistent disease but that typical pediatric mastocytosis subjects lack codon 816 mutations and may express other, inactivating, mutations of c-kit.
56. 56 Ma Y, Longley BJ, Wang X, Blount JL, Langley K, Caughey GH: Clustering of activating mutations in c-KIT's juxtamembrane coding region in canine mast cell neoplasms. J Invest Dermatol 1999, 112:165-170.
57. 57 London CA, Galli SJ, Yuuki T, Hu Z-Q, Helfand SC, Geissler EN: Spontaneous canine mast cell tumors express tandem duplications in the proto-oncogene c-kit. Exp Hematol 1999, 27:689-697.
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65. 65 Lantz CS, Yamaguchi M, Oettgen HC, Katona IM, Miyajima I, Kinet J-P, Galli SJ: IgE regulates mouse basophil FcεRI expression in vivo. J Immunol 1997, 158:2517-2521.
66. 66 Yano K, Yamaguchi M, de Mora F, Lantz CS, Butterfield JH, Costa JJ, Galli SJ: Production of macrophage inflammatory protein-1α by human mast cells: increased anti-IgE-dependent secretion after IgE-dependent enhancement of mast cell IgE-binding ability. Lab Invest 1997, 77:185-193.
67. 67 Boesiger J, Tsai M, Maurer M, Yamaguchi M, Brown LF, Claffey KP, et al.: Mast cells can secrete VPF/VEGF and exhibit enhanced release after IgE-dependent upregulation of FcεRI expression. J Exp Med 1998, 188:1135-1145. In vitro derived mouse and human mast cells, as well as purified mouse and rat peritoneal mast cells and the HMC-1 cell line derived from a patient with mast cell leukemia, were identified as potential sources of VPF/VEGF. Secretion of VPF/VEGF was induced in mouse or human mast cells that had been stimulated via FcεRI, and such secretion was markedly upregulated in mast cells that had first undergone IgE-dependent upregulation of surface FcεRI expression; some of the secreted VPF/VEGF appeared to be derived from preformed stores. SCF also enhanced VPF/VEGF secretion from mouse mast cells. Although VPF/VEGF can be produced by many different cell types, this is the first demonstration that the secretion of this factor can be induced in an immunologically specific fashion by stimulating cells via a member of the multichain immune recognition receptor family (ie, FcεRI). Mast cell production of VPF/VEGF represents one mechanism by which mast cells can augment venular permeability and angiogenesis during diverse biologic responses, including those associated with IgE or mastocytosis.
68. 2 on subsequent passive sensitization with IgE and challenge with anti-IgE. Preincubaiion with interleukin-4 enhanced IgE-dependent mediator secretion even in the absence of significant effects on FcεRI surface expression, and different batches of cord blood-derived mast cells (from different donors of cord blood) varied greatly in the magnitude and pattern of histamine and lipid mediator release in response to anti-IgE challenge, both under baseline conditions and after preincubation with IgE or interleukin-4.
69. 206. Mol Biol Cell 1998,9:875-884. The HMC-1 cell line (from a patient with mast cell leukemia) was identified as a source of VPF/VEGF mRNA and protein, and immunoelectron microscopy was used to identify VPF/VEGF protein in some of the mast cells present in partially purified populations of mast cells in human dermis.
70. 70 Coussens LM, Raymond WW, Bergers G, Laig-Webster M, Behrendtsen O, Werb Z, et al.: Inflammatory mast cells up-regulate angiogenesis during squamous epithelial carcinogenesis. Genes Dev 1999,13:1382-1397. Several lines of evidence, derived from both in vitro and in vivo studies, are presented indicating that neoplastic progression in transgenic mice that develop squamous carcinomas due to expression of human papilloma virus-16 early region genes in basal keratinocytes involves the participation of mast cells. In this model, mast cells may promote stromal tissue remodeling and angiogenesis, in part via the activities of mMCP-4 and mMCP-6.
71. 71 Iikura M, Yamaguchi M, Fujisawa T, Miyamasu M, Takaishi T, Morita V, et al.: Secretory IgA induces degranulation of IL-3-primed basophils. J Immunol 1998, 161:1510-1515. Immobilized sIgA, but not monomeric IgA, induced up to approximately 15% histamine release from human basophils in vitro, but only if the cells had first been pretreated with interleukin-3, interleukin-5, or GM-CSF. These findings raise the possibility that, in certain immune responses associated with sIgA production, sIgA may mediate antigen-specific basophil function. The findings also suggest that the phenotype and immunologic function of human basophils can be altered significantly during immune responses associated with production of interleukin-3, interleukin-5, or GM-CSF.
72. 1+ cells such as basophils and mast cells.
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75. + E. coli to BMCMCs and induce BMCMCs to secrete TNF-α. This work defines one mechanism by which bacteria can directly induce mast cell TNF-α release during innate immune responses.
76. +/+ mice, we found thai SCF-treated mice did not appear to be at substantially increased risk (versus vehicle-treated mice) for death when IgE-dependent systemic anaphylaxis was induced by intraperitoneal challenge with specific antigen. The beneficial effects of SCF treatment in CLP may reflect actions on mast cell phenotype and function, as well as expansion of mast cell numbers. This is the first demonstration that normal animals that have been treated to develop higher than baseline levels of mast cells can exhibit enhanced resistance to bacterial infection.
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