Mutual Phenotypic Changes between Connective Tissue Type and Mucosal Mast Cells

1987 ◽  
Vol 82 (3-4) ◽  
pp. 244-248 ◽  
Author(s):  
Yukihiko Kitamura ◽  
Yuzuru Kanakura ◽  
Sanae Sonoda ◽  
Hidekazu Asai ◽  
Toru Nakano
Keyword(s):  
Mast Cells ◽  
Connective Tissue ◽  
Tissue Type ◽  
Phenotypic Changes ◽  
Mucosal Mast Cells

scholarly journals The rat c-kit ligand, stem cell factor, induces the development of connective tissue-type and mucosal mast cells in vivo. Analysis by anatomical distribution, histochemistry, and protease phenotype.

1991 ◽  
Vol 174 (1) ◽  
pp. 125-131 ◽  
Author(s):  
M Tsai ◽  
L S Shih ◽  
G F Newlands ◽  
T Takeishi ◽  
K E Langley ◽  
...  
Keyword(s):  
Mast Cell ◽  
Stem Cell ◽  
Mast Cells ◽  
Connective Tissue ◽  
Stem Cell Factor ◽  
Tissue Type ◽  
Tyrosine Kinase Receptor ◽  
Kit Ligand ◽  
Mucosal Mast Cells

Mast cell development is a complex process that results in the appearance of phenotypically distinct populations of mast cells in different anatomical sites. Mice homozygous for mutations at the W or S1 locus exhibit several phenotypic abnormalities, including a virtual absence of mast cells in all organs and tissues. Recent work indicates that W encodes the c-kit tyrosine kinase receptor, whereas S1 encodes a c-kit ligand that we have designated stem cell factor (SCF). Recombinant or purified natural forms of the c-kit ligand induce proliferation of certain mast cell populations in vitro, and injection of recombinant SCF permits mast cells to develop in mast cell-deficient WCB6F1-S1/S1d mice. However, the effects of SCF on mast cell proliferation, maturation, and phenotype in normal mice in vivo were not investigated. We now report that local administration of SCF in vivo promotes the development of connective tissue-type mast cells (CTMC) in the skin of mice and that systemic administration of SCF induces the development of both CTMC and mucosal mast cells (MMC) in rats. Rats treated with SCF also develop significantly increased tissue levels of specific rat mast cell proteases (RMCP) characteristic of either CTMC (RMCP I) or MMC (RMCP II). These findings demonstrate that SCF can induce the expansion of both CTMC and MMC populations in vivo and show that SCF can regulate at least one cellular lineage that expresses c-kit, the mast cell, through complex effects on proliferation and maturation.

Extensive proliferation of mature connective-tissue type mast cells in vitro

Nature ◽  
1986 ◽  
Vol 324 (6092) ◽  
pp. 65-67 ◽  
Author(s):  
Tatsutoshi Nakahata ◽  
Toshimi Kobayashi ◽  
Akira Ishiguro ◽  
Kohichiro Tsuji ◽  
Kuniaki Naganuma ◽  
...  
Keyword(s):  
Mast Cells ◽  
Connective Tissue ◽  
Tissue Type

Mast cell heterogeneity

1984 ◽  
Vol 62 (6) ◽  
pp. 734-737 ◽  
Author(s):  
F. Shanahan ◽  
J. A. Denburg ◽  
J. Bienenstock ◽  
A. D. Befus
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Connective Tissue ◽  
Regulatory Peptides ◽  
Cell Heterogeneity ◽  
Cell Secretion ◽  
Biochemical Basis ◽  
Mucosal Mast Cells ◽  
Mast Cell Heterogeneity

Increasing evidence for the existence of inter- and intra-species mast cell heterogeneity has expanded the potential biological role of this cell. Early studies suggesting that mast cells at mucosal sites differ morphologically and histochemically from connective tissue mast cells have been confirmed using isolated intestinal mucosal mast cells in the rat and more recently in man. These studies also established that mucosal mast cells are functionally distinct from connective tissue mast cells. Thus, mucosal and connective tissue mast cells differ in their responsiveness to a variety of mast cell secretagogues and antiallergic agents. Speculation about the therapeutic use of antiallergic drugs in disorders involving intestinal mast cells cannot, therefore, be based on extrapolation from studies of their effects on mast cells from other sites. Regulatory mechanisms for mast cell secretion may also be heterogeneous since mucosal mast cells differ from connective tissue mast cells in their response to a variety of physiologically occurring regulatory peptides. The development of techniques to purify isolated mast cell sub-populations will facilitate future analysis of the biochemical basis of the functional heterogeneity of mast cells.

scholarly journals Cell Intrinsic Deregulated ß-Catenin Signaling Promotes Expansion of Bone Marrow Derived Connective Tissue Type Mast Cells, Systemic Inflammation, and Colon Cancer

2019 ◽  
Vol 10 ◽  
Author(s):  
Abdulrahman Saadalla ◽  
Mariana Machado Lima ◽  
Funien Tsai ◽  
Abu Osman ◽  
Mahendra Pal Singh ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Colon Cancer ◽  
Mast Cells ◽  
Connective Tissue ◽  
Systemic Inflammation ◽  
Tissue Type

scholarly journals Mouse connective tissue mast cell proteases tryptase and carboxypeptidase A3 play protective roles in itch induced by endothelin-1

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Elín I. Magnúsdóttir ◽  
Mirjana Grujic ◽  
Jessica Bergman ◽  
Gunnar Pejler ◽  
Malin C. Lagerström
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Connective Tissue ◽  
Treatment Options ◽  
Cell Types ◽  
Tissue Type ◽  
Human Mast Cell ◽  
Knock Out ◽  
Endothelin 1 ◽  
Deficient Mice

Abstract Background Itch is an unpleasant sensation that can be debilitating, especially if it is chronic and of non-histaminergic origin, as treatment options are limited. Endothelin-1 (ET-1) is a potent endogenous vasoconstrictor that also has the ability to induce a burning, non-histaminergic pruritus when exogenously administered, by activating the endothelin A receptor (ETAR) on primary afferents. ET-1 is released endogenously by several cell-types found in the skin, including macrophages and keratinocytes. Mast cells express ETARs and can thereby be degranulated by ET-1, and mast cell proteases chymase and carboxypeptidase A3 (CPA3) are known to either generate or degrade ET-1, respectively, suggesting a role for mast cell proteases in the regulation of ET-1-induced itch. The mouse mast cell proteases (mMCPs) mMCP4 (chymase), mMCP6 (tryptase), and CPA3 are found in connective tissue type mast cells and are the closest functional homologs to human mast cell proteases, but little is known about their role in endothelin-induced itch. Methods In this study, we evaluated the effects of mast cell protease deficiency on scratching behavior induced by ET-1. To investigate this, mMCP knock-out and transgenic mice were injected intradermally with ET-1 and their scratching behavior was recorded and analyzed. Results CPA3-deficient mice and mice lacking all three proteases demonstrated highly elevated levels of scratching behavior compared with wild-type controls. A modest increase in the number of scratching bouts was also seen in mMCP6-deficient mice, while mMCP4-deficiency did not have any effect. Conclusion Altogether, these findings identify a prominent role for the mast cell proteases, in particular CPA3, in the protection against itch induced by ET-1.

scholarly journals Effects of interleukin-3 and interleukin-4 on the development of "connective tissue-type" mast cells: interleukin-3 supports their survival and interleukin-4 triggers and supports their proliferation synergistically with interleukin-3

Blood ◽  
1990 ◽  
Vol 75 (2) ◽  
pp. 421-427 ◽  
Author(s):  
K Tsuji ◽  
T Nakahata ◽  
M Takagi ◽  
T Kobayashi ◽  
A Ishiguro ◽  
...  
Keyword(s):  
Mast Cells ◽  
Connective Tissue ◽  
Colony Formation ◽  
Colony Growth ◽  
Interleukin 4 ◽  
Tissue Type ◽  
Dependent Manner ◽  
Humoral Factors ◽  
Interleukin 3

Abstract We examined the effects of interleukin-3 (IL-3) and interleukin-4 (IL- 4) on connective tissue-type mast cells (CTMC) purified from murine peritoneal cells. Although both factors failed to induce extensive proliferation of CTMC, they stimulated CTMC proliferation synergistically in a dose-dependent manner. Pretreatment of CTMC with IL-3 and/or IL-4 indicated that the sustained presence of both factors was required for the development of type 1 mast cell colonies. The delayed addition of IL-3 to cultures of purified CTMC with IL-4 induced no colony formation, while the delayed addition of IL-4 to cultures with IL-3, even on day 28 of culture, induced type 1 colony formation. In replating type 1 colonies induced by IL-3 and IL-4 to secondary cultures with IL-3 alone, few secondary colonies developed. However, the delayed addition of IL-4 to the secondary culture induced many type 1 colonies. The purified CTMC cultured with IL-3 retained the morphological and cytochemical characteristics of CTMC, as well as proliferative ability. These observations indicate that IL-3 supports the survival of CTMC in methylcellulose culture and that IL-4 triggers and supports CTMC proliferation synergistically with IL-3. The serum- free culture of purified CTMC and the culture of single CTMC demonstrated that the synergistic effect of IL-3 and IL-4 on colony growth and the surviving effect of IL-3 on CTMC require no influence from accessory cells or other humoral factors.

scholarly journals Author Correction: Novel six-week protocol for generating functional human connective tissue-type (MCTC) mast cells from buffy coats

2017 ◽  
Vol 67 (1) ◽  
pp. 105-105
Author(s):  
Issan Yee San Tam ◽  
Chun Wai Ng ◽  
See-Ying Tam ◽  
Hang Yung Alaster Lau
Keyword(s):  
Mast Cells ◽  
Connective Tissue ◽  
Tissue Type ◽  
Generating Functional

Involvement of connective tissue–type mast cells in Th1 immune responses via Stat4 expression

Blood ◽  
2005 ◽  
Vol 105 (3) ◽  
pp. 1016-1020 ◽  
Author(s):  
Tatsuki R. Kataoka ◽  
Nobuyasu Komazawa ◽  
Eiichi Morii ◽  
Keisuke Oboki ◽  
Toru Nakano
Keyword(s):  
Mast Cells ◽  
Connective Tissue ◽  
Immune Responses ◽  
Tissue Type ◽  
Hematopoietic Stem ◽  
Α Subunit ◽  
Enhanced Expression ◽  
Microphthalmia Transcription Factor ◽  
Nitric Oxide Synthase 2 ◽  
Th1 Immune Responses

Abstract Mast cells are the sentinels of immune systems and, like other immuno-competent cells, they are produced by hematopoietic stem cells. We analyzed the expression of signal transducer and activator of transcription 4 (Stat4), and investigated its role in mast cells. Murine mast cells are usually divided into 2 distinct populations by their distribution and contents of their granules: mucosal mast cells (MMCs) and connective tissue–type mast cells (CTMCs). Stat4 protein was detected in CTMCs but not in MMCs. The absence of Stat4 expression in cultured mast cells was due to the presence of Stat6. In T-helper (Th) cells, Stat4 plays an important role in Th1 shift by inducing a set of genes, such as interferon gamma (IFN-γ) and interleukin-18 receptor α subunit (IL-18Rα). As in Th1 shift, we found that Stat4 trans-activated these genes in the Stat4-expressing cultured mast cells, namely, microphthalmia transcription factor (MITF)–deficient cultured MMCs, Stat6-deficient cultured MMCs, and cultured CTMCs. Stat4 also enhanced expression of nitric oxide synthase 2 (NOS2) in CTMCs, which brought about increased levels of NO-dependent cytotoxic activity. These data indicate that expression of Stat4 in CTMCs plays an important role on Th1 immune responses.

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