Mast cells as effector cells: a co-stimulating question

2007 ◽  
Vol 28 (8) ◽  
pp. 360-365 ◽  
Author(s):  
Ido Bachelet ◽  
Francesca Levi-Schaffer
Keyword(s):  
Mast Cells ◽  
Effector Cells

scholarly journals Mast Cells as a Potential Prognostic Marker in Prostate Cancer

2013 ◽  
Vol 35 ◽  
pp. 711-720 ◽  
Author(s):  
Gianluigi Taverna ◽  
Guido Giusti ◽  
Mauro Seveso ◽  
Rodolfo Hurle ◽  
Piergiuseppe Colombo ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Mast Cells ◽  
Immunoglobulin E ◽  
Expression Patterns ◽  
Tumor Biology ◽  
Effector Cells ◽  
Host Interactions ◽  
Adaptive Immune Cells ◽  
Primary Prostate Cancer ◽  
Intensive Investigation

Despite years of intensive investigation that has been made in understanding prostate cancer, it remains one of the major men’s health issues and the leading cause of death worldwide. It is now ascertained that prostate cancer emerges from multiple spontaneous and/or inherited alterations that induce changes in expression patterns of genes and proteins that function in complex networks controlling critical cellular events. It is now accepted that several innate and adaptive immune cells, including T- and B-lymphocytes, macrophages, natural killer cells, dendritic cells, neutrophils, eosinophils, and mast cells (MCs), infiltrate the prostate cancer. All of these cells are irregularly scattered within the tumor and loaded with an assorted array of cytokines, chemokines, and inflammatory and cytotoxic mediators. This complex framework reflects the diversity in tumor biology and tumor-host interactions. MCs are well-established effector cells in Immunoglobulin-E (Ig-E) associated immune responses and potent effector cells of the innate immune system; however, their clinical significance in prostate cancer is still debated. Here, these controversies are summarized, focusing on the implications of these findings in understanding the roles of MCs in primary prostate cancer.

scholarly journals Interleukin-4 (IL-4) enhances and soluble interleukin-4 receptor (sIL-4R) inhibits histamine release from peripheral blood basophils and mast cellsin vitroandin vivo

1997 ◽  
Vol 6 (2) ◽  
pp. 111-118 ◽  
Author(s):  
B. Niggemann ◽  
T. Zuberbier ◽  
U. Herz ◽  
K. Enssle ◽  
U. Wahn ◽  
...  
Keyword(s):  
Mast Cells ◽  
Histamine Release ◽  
Peripheral Blood ◽  
Specific Ige ◽  
Interleukin 4 ◽  
Effector Cells ◽  
Antibody Titres ◽  
Interleukin 4 Receptor

The aim of the study was to analyse the effect of interleukin-4 (IL-4) on allergen and anti-IgE mediated histamine release from basophils and human skin mast cells and to assess whether soluble recombinant interleukin-4 receptor (sIL4R) can inhibit these effects. Anti-IgE stimulated histamine release from peripheral blood basophils and mast cells of atopic donors was enhanced after preincubation with IL-4, whereas after preincubation with sIL-4R it was inhibited. These effects were even more pronounced when samples were stimulated with a clinically relevant allergen. In IL-4 preincubated skin mast cells, there was a similar enhancement of anti-IgE stimulated histamine release, which could again be inhibited by sIL-4R. The effects of IL-4 and sIL4R were dose- and time-dependent. Mice sensitized to ovalbumin and treated with soluble recombinant murine sIL-4R showed significantly reduced immediate-type cutaneous hypersensitivity responses compared with untreated mice. Thesein vivoeffects were IgE independent, since there were no significant differences in total and allergen specific IgE/IgG1 antibody titres between treated and untreated mice. This indicates that IL4 exerts priming effects on histamine release by effector cells of the allergic response and that these effects are potently antagonized by soluble IL-4R bothin vitroandin vivo.

scholarly journals Natural Killer Cells and Mast Cells from gp49B Null Mutant Mice Are Functional

2000 ◽  
Vol 20 (19) ◽  
pp. 7178-7182 ◽  
Author(s):  
Susana Rojo ◽  
Christopher C. Stebbins ◽  
Mary E. Peterson ◽  
David Dombrowicz ◽  
Nicolai Wagtmann ◽  
...  
Keyword(s):  
Mast Cells ◽  
Immune Responses ◽  
Nk Cells ◽  
Natural Killer ◽  
Survival Rates ◽  
Term Survival ◽  
Effector Cells ◽  
Null Mutant Mice

ABSTRACT Immune responses are controlled by a combination of positive and negative cellular signals. Effector cells in the immune system express inhibitory receptors that serve to limit effector cell expansion and to protect the host from autoreactivity. gp49B is a receptor of unknown function that is expressed on activated mast cells and natural killer (NK) cells and whose cytoplasmic tail endows it with inhibitory potential. To gain insight into the function of gp49B in mice, we disrupted the gp49B gene by homologous recombination. gp49B0 mice were born at expected ratios, were healthy and fertile, and displayed normal long-term survival rates. gp49B0 mice showed no defect in NK or mast cell development. Furthermore, NK and mast cells from the gp49B0mice showed activation properties in vitro similar to those of cells isolated from wild-type mice. Therefore, gp49B is not critical for the development, expansion, and maturation of mast cells and NK cells in vivo. The healthy status of gp49B0 mice makes them suitable for testing the role of gp49B in immune responses to infectious agents.

Mast cells are crucial for early inflammation, migration of Langerhans cells, and CTL responses following topical application of TLR7 ligand in mice

Blood ◽  
2007 ◽  
Vol 110 (3) ◽  
pp. 946-953 ◽  
Author(s):  
Valeska Heib ◽  
Marc Becker ◽  
Tobias Warger ◽  
Gerd Rechtsteiner ◽  
Christine Tertilt ◽  
...  
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Topical Application ◽  
Langerhans Cells ◽  
Cytotoxic T Lymphocyte ◽  
Effector Cells ◽  
Tnf Α ◽  
Transcutaneous Immunization ◽  
Antigen Presenting ◽  
Tlr7 Ligand

Abstract Until recently, IgE-activated mast cells have been regarded merely as effector cells of adaptive immune responses, involved in allergic reactions and mucosal immunity to parasites. Herein, we report that murine dermal mast cells, activated by local administration of a cream containing the synthetic TLR7 ligand imiquimod, are essential to initiate an early inflammatory reaction. The mast-cell–derived cytokines TNF-α and IL-1β play an important role in this process. Furthermore, TLR7-activated mast cells are also able to promote the emigration of Langerhans cells, which partly depends on the expression of mast-cell–derived IL-1β. We have previously shown that TLR7 ligation enhances transcutaneous immunization evoked by topical application of vaccine antigens to the skin, a procedure that directly targets skin-resident antigen-presenting cells. Consequently, we now demonstrate here that the capacity to mount a peptide-specific cytotoxic T-lymphocyte response following transcutaneous immunization using imiquimod as adjuvant is severely impaired in mast-cell–deficient mice. Thus, these findings demonstrate the potent versability of alternatively activated mast cells at the interface of innate and adaptive immunity.

Mouse mast cells as anti-tumor effector cells

1980 ◽  
Vol 55 (2) ◽  
pp. 294-301 ◽  
Author(s):  
E. Farram ◽  
D.S. Nelson
Keyword(s):  
Mast Cells ◽  
Effector Cells

Mast cells and eosinophils: the two key effector cells in allergic inflammation

2009 ◽  
Vol 58 (10) ◽  
pp. 631-638 ◽  
Author(s):  
Yael Minai-Fleminger ◽  
Francesca Levi-Schaffer
Keyword(s):  
Mast Cells ◽  
Allergic Inflammation ◽  
Effector Cells

scholarly journals Requirement for vasoactive amines for production of delayed-type hypersensitvity skin reactions.

1975 ◽  
Vol 142 (3) ◽  
pp. 732-747 ◽  
Author(s):  
R K Gershon ◽  
P W Askenase ◽  
M D Gershon
Keyword(s):  
T Cells ◽  
Mast Cells ◽  
Suppressive Effect ◽  
Delayed Type Hypersensitivity ◽  
Postcapillary Venule ◽  
Skin Reactions ◽  
Effector Cells ◽  
Homologous Antigen ◽  
T Cell Regulation ◽  
Pass Through

The skin sites of the mouse where delayed-type hypersensitivity (DTH) reactions are most easily elicited (foot pads and ears) are particularly rich in 5-hydroxytryptamine (5-HT)-containing mast cells. Since mice are deficient in circulating basophils, which play a role in at least some DTH reactions, we investigated the possibility that the mast cells were playing an important role in the evolution of the skin reactions of DTH in mice. We found that reserpine, a drug which depletes mast cells of 5-HT, abolished the ability of the mouse to make DTH reactions in the skin. The suppressive effect of reserpine could be partially blocked by monoamine oxidase inhibitors which prevent the degradation of 5-HT in the cytosol of the mast cell. Spleen cells of immune, reserpine-treated mice transferred DTH reactions to nonimmune mice normally, indicating that the reserpine treatment did not affect immune T cells. DTH reactions could not be transferred into reserpine-treated mice. We suggest that T cells are continually emigrating from the blood, through postcapillary venule endothelium, by a mechanism which does not depend on vasoactive amines. If they are appropriately immune and meet the homologous antigen in the tissue, they induce mast cells to release vasoactive amines which cause postcapillary venule endothelial cells to separate, allowing the egress from the blood of cells which ordinarily do not recirculate. The secondarily arriving vasoactive amine-dependent cells are responsible for the micro- and macroscopic lesions of DTH reactions. Chemotactic factors may also be involved in bringing cells to the DTH reaction sites but we propose that T-cell regulation of vasoactive amine-containing cells allows the effector cells to pass through the endothelial gates after they are called.

scholarly journals Role of Leukotriene B4 Receptor-2 in Mast Cells in Allergic Airway Inflammation

2019 ◽  
Vol 20 (12) ◽  
pp. 2897 ◽  
Author(s):  
Sun-Young Kwon ◽  
Jae-Hong Kim
Keyword(s):  
Mast Cells ◽  
Airway Inflammation ◽  
Allergic Inflammation ◽  
Allergic Airway Inflammation ◽  
Leukotriene B4 ◽  
Vascular Endothelial ◽  
Effector Cells ◽  
Elevated Expression ◽  
Leukotriene B4 Receptor ◽  
Endothelial Growth Factor

Mast cells are effector cells in the immune system that play an important role in the allergic airway inflammation. Recently, it was reported that BLT2, a low-affinity leukotriene (LT) B4 receptor, plays a pivotal role in the pathogenesis of allergic airway inflammation through its action in mast cells. We observed that highly elevated expression levels of BLT2 are critical for the pathogenesis leading to allergic airway inflammation, and that if BLT2 expression is downregulated by siBLT2-mediated knockdown, allergic inflammation is dramatically alleviated. Furthermore, we demonstrated that BLT2 mediates the synthesis of vascular endothelial growth factor (VEGF) and Th2 cytokines, such as interleukin (IL)-13, in mast cells during allergic inflammation. Based on the critical roles of BLT2 in mast cells in allergic inflammation, anti-BLT2 strategies could contribute to the development of new therapies for allergic airway inflammation.

Mast Cells Reduce Gvhd Severity In Allogeneic Transplantation by Reducing the Proliferation of Conventional T Cells

Blood ◽  
2010 ◽  
Vol 116 (21) ◽  
pp. 243-243
Author(s):  
Dennis B Leveson-Gower ◽  
Emanuela I Sega ◽  
Janet Kalesnikoff ◽  
Mareike Florek ◽  
Stephen J Galli ◽  
...  
Keyword(s):  
Bone Marrow ◽  
T Cells ◽  
T Cell ◽  
Mast Cells ◽  
Bone Marrow Cells ◽  
Conflicts Of Interest ◽  
Tissue Injury ◽  
Allogeneic Transplantation ◽  
Treg Cells ◽  
Effector Cells

Abstract Abstract 243 Mast cells are important effector cells in many innate and adaptive immune responses, and can influence the function of several immune cells including granulocytes, monocytes/macrophages, dendritic cells, T cells, B cells, NK cells, and NKT cells. In contrast to their well-know pro-inflammatory roles, in certain models, mast cells have been shown to decrease inflammation and tissue injury. We explored the biological activity of mast cells in a well-established model of mouse graft-versus-host disease (GVHD) by comparing C57BL/6-KitW-sh/W-sh mice (which lack mast cells) to wild-type (WT) C57BL/6 (H-2b) recipients in a major-MHC mismatched model of allogeneic transplantation. After myeloablative irradiation, recipients received 5×106 T-cell depleted bone marrow cells from FVB/N donors (H-2q) on day 0 followed by transfer of 2×106 FVB/N CD4 and CD8 conventional T cells (Tcon) at a 2:1 ratio on day 4. A dramatic decrease in survival was observed in the animals lacking mast cells where 100% of KitW-sh/W-sh recipients died by day 15 following transplantation while over 50% of WT recipients were alive at day 60 (p < 0.0001). The exacerbated GVHD in KitW-sh/W-sh mice correlated with an increase in Tcon proliferation as indicated by bioluminescence imaging (BLI), particularly in lymph node, liver, and gastrointestinal tract tissue sites (p < 0.001). The percentage of Foxp3 positive Treg cells was similar before and after transplantation in KitW-sh/W-sh and WT recipients, and CD4+CD25hi Treg from KitW-sh/W-sh mice were capable of suppressing T cell proliferation in a mixed leukocyte reaction. When KitW-sh/W-sh mice were given 5×106 bone marrow-derived cultured mast cells (BMCMCs) i.p., mast cell re-population of the gut and peritoneal cavity was indicated by both BLI and traditional staining methods. Preliminary experiments with KitW-sh/W-sh recipients engrafted with BMCMCs i.p. 6 weeks before allogenic transplantation demonstrated improved survival in the above GVHD model, but not if the BMCMCs were derived from IL-10-/- C57BL/6 mice. Together, these results support the hypothesis that mast cells can decrease Tcon proliferation and reduce GVHD severity by a mechanism that involves production of IL-10 by mast cells but which is independent of CD4+CD25+ Treg. Disclosures: No relevant conflicts of interest to declare.

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