Macrophage inflammatory protein-1 alpha activates basophils and mast cells.

Alam, Rafeul; Forsythe, P.; Stafford, Susan; Lett-Brown, Michael A.

doi:10.1084/jem.176.3.781

Cited by 181 publications

(83 citation statements)

References 24 publications

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“…CCL3 was reported to stimulate human mast cell degranulation in vitro (16) and murine mast cell degranulation in vitro and in vivo (7,17). We found that treatment of mast cells with CCL3 and Ag results in greater degranulation than does cross-linking of FcεRI alone (8,17).…”

mentioning

confidence: 55%

Role of CCL7 in Type I Hypersensitivity Reactions in Murine Experimental Allergic Conjunctivitis

Kuo

Collins

Boettner

et al. 2017

The Journal of Immunology

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Molecules that are necessary for ocular hypersensitivity reactions include the receptors CCR1 and CCR3; CCL7 is a ligand for these receptors. Therefore, we explored the role of CCL7 in mast cell activity and motility in vitro and investigated the requirement for CCL7 in a murine model of IgE-mediated allergic conjunctivitis. For mast cells treated with IgE and Ag, the presence of CCL7 synergistically enhanced degranulation and calcium influx. CCL7 also induced chemotaxis in mast cells. CCL7-deficient bone marrow–derived mast cells showed decreased degranulation following IgE and Ag treatment compared with wild-type bone marrow–derived mast cells, but there was no difference in degranulation when cells were activated via an IgE-independent pathway. In vivo, CCL7 was upregulated in conjunctival tissue during an OVA-induced allergic response. Notably, the early-phase clinical symptoms in the conjunctiva after OVA challenge were significantly higher in OVA-sensitized wild-type mice than in control challenged wild-type mice; the increase was suppressed in CCL7-deficient mice. In the OVA-induced allergic response, the numbers of conjunctival mast cells were lower in CCL7-deficient mice than in wild-type mice. Our results demonstrate that CCL7 is required for maximal OVA-induced ocular anaphylaxis, mast cell recruitment in vivo, and maximal FcεRI-mediated mast cell activation in vitro. A better understanding of the role of CCL7 in mediating ocular hypersensitivity reactions will provide insights into mast cell function and novel treatments for allergic ocular diseases.

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mentioning

confidence: 55%

Role of CCL7 in Type I Hypersensitivity Reactions in Murine Experimental Allergic Conjunctivitis

Kuo

Collins

Boettner

et al. 2017

The Journal of Immunology

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“…CCL3, a C-C chemokine, can chemoattract neutrophils, monocytes, eosinophils, basophils, and lymphocytes, and is a ligand for both CCR1 and CCR5 [44][45][46][47][48]. CCL3 caused a dose-dependent increase in neutrophil recruitment in a dinitrofluorobenzene-induced contact hypersensitivity model [49].…”

Section: Discussionmentioning

confidence: 99%

Role of C‐C chemokine receptors 1 and 5 and CCL3/macrophage inflammatory protein‐1α in the cutaneous Arthus reaction: possible attenuation of their inhibitory effects by compensatory chemokine production

et al. 2004

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The deposition of immune complexes induces an acute inflammatory response with tissue injury. Immune complex-induced tissue injury is mediated by inflammatory cell infiltration that is highly regulated by multiple chemokines. To assess the role of the chemokine receptors CCR1 and CCR5, and a ligand for these receptors CCL3/macrophage inflammatory protein1a, in this pathogenic process, the reverse passive cutaneous Arthus reaction was induced in mice lacking CCR1, CCR5, or CCL3. Edema was significantly attenuated in CCR1-deficient (CCR1 -/-) and CCL3 -/-mice but not CCR5 -/-mice, compared with wild-type mice. Numbers of infiltrating neutrophils and mast cells were reduced in CCL3 -/-and CCR1 -/-mice, respectively, compared with wild-type mice. CCR1 and CCR5 were expressed on neutrophils and mast cells. Remarkably, the intradermal mRNA expression of CCL5/RANTES, another ligand for CCR1 and CCR5, was increased in CCR5 -/-and CCL3 -/-mice, compared with wild-type mice, while the cutaneous CCL3 mRNA expression was augmented in CCR1 -/-and CCR5 -/-mice. These results indicate that CCR1, CCR5, and CCL3 cooperatively contribute to the cutaneous Arthus reaction, and also suggest that enhanced expression of CCL3 and CCL5 compensates for the loss of CCR1, CCR5, and CCL3 in the reaction.

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“…Such influences have primarily been attributed to the biological effects of T cellderived soluble mediators on mast cell function (38,39). However, recent investigations of mast cell-T cell interactions have revealed a novel intercellular communication exclusively involving the binding of cell surface molecules.…”

Section: Discussionmentioning

confidence: 99%

Human Mast Cells Release Metalloproteinase-9 on Contact with Activated T Cells: Juxtacrine Regulation by TNF-α

Baram

Vaday

Salamon

et al. 2001

The Journal of Immunology

214

177

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Mast cells, essential effector cells in allergic inflammation, have been found to be activated in T cell-mediated inflammatory processes in accordance with their residence in close physical proximity to T cells. We have recently reported that mast cells release granule-associated mediators and TNF-α upon direct contact with activated T cells. This data suggested an unrecognized activation pathway, where mast cells may be activated during T cell-mediated inflammation. Herein, we show that this cell-cell contact results in the release of matrix metalloproteinase (MMP)-9 and the MMP inhibitor tissue inhibitor of metalloproteinase 1 from HMC-1 human mast cells or from mature peripheral blood-derived human mast cells. The expression and release of these mediators, as well as of β-hexosaminidase and several cytokines, were also induced when mast cells were incubated with cell membranes isolated from activated, but not resting, T cells. Subcellular fractionation revealed that the mature form of MMP-9 cofractionated with histamine and tryptase, indicating its localization within the secretory granules. MMP-9 release was first detected at 6 h and peaked at 22 h of incubation with activated T cell membranes, while TNF-α release peaked after only 6 h. Anti-TNF-α mAb inhibited the T cell membrane-induced MMP-9 release, indicating a possible autocrine regulation of MMP release by mast cell TNF-α. This cascade of events, whereby mast cells are activated by T cells to release cytokines and MMP-9, which are known to be essential for leukocyte extravasation and recruitment to affected sites, points to an important immunoregulatory function of mast cells within the context of T cell-mediated inflammatory processes.

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Macrophage inflammatory protein-1 alpha activates basophils and mast cells.

Cited by 181 publications

References 24 publications

Role of CCL7 in Type I Hypersensitivity Reactions in Murine Experimental Allergic Conjunctivitis

Role of CCL7 in Type I Hypersensitivity Reactions in Murine Experimental Allergic Conjunctivitis

Role of C‐C chemokine receptors 1 and 5 and CCL3/macrophage inflammatory protein‐1α in the cutaneous Arthus reaction: possible attenuation of their inhibitory effects by compensatory chemokine production

Human Mast Cells Release Metalloproteinase-9 on Contact with Activated T Cells: Juxtacrine Regulation by TNF-α

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