Mast cells (MC) are major participants in the allergic reaction. In addition they possess immunomodulatory roles in the innate and adaptive immune reactions. Their functions are modulated through a number of activating and inhibitory receptors expressed on their surface. This review deals with some of the most recently described receptors, their expression patterns, ligand(s), signal transduction mechanisms, possible cross-talk with other receptors and, last but not least, regulatory functions that the MC can perform based on their receptor expression in health or in disease. Where the receptor role on MC is still not clear, evidences from other hematopoietic cells expressing them is provided as a possible insight for their function on MC. Suggested strategies to modulate these receptors’ activity for the purpose of therapeutic intervention are also discussed.
The study examined how student control over metacognitive prompts in a multimedia environment affects students' ability to solve mathematical problems in immediate comprehension tasks using a multimedia program and a delayed-transfer test. It also examined the effect on metacognitive discourse, mental effort, and engagement with multimedia-based tasks. Participants were 90 8th-grade students, randomly assigned to three groups working in pairs: (a) "solicited prompts" group, with free access to multimedia-based metacognitive prompts; (b) "unsolicited prompts" group, consistently and regularly exposed to on-screen metacognitive prompts; and (c) a control group with no multimedia metacognitive prompts. Mixed method analysis showed that of the three groups the unsolicited prompts group had the highest effects in the immediate comprehension tasks (d = 1.23; 1.92 respectively for the solicited prompts group and the control group) and the delayed-transfer problem solving test (d = 0.55; 0.93, respectively). The level of this group's metacognitive discourse was higher, particularly in the planning phase. Group members displayed less cognitive load on the complex tasks and were more engaged in the multimedia activities. In contrast, the solicited prompts group felt they were under a heavier cognitive load than the other two groups. Finding implications and future directions for study are discussed.
Cell-cell interactions, comprising the ones between inflammatory cells and nerve cells mediated by physical contact and released mediators, have been proven to be crucial both in health and in disease. The neuropeptide substance P (SP) is one major component of these interactions via its high-affinity receptor neurokinin-1 (NK1R) and low-affinity receptors NK2R and NK3R, all expressed on neurons and immune cells such as macrophages, lymphocytes, neutrophils, dendritic cells, mast cells (MCs) and eosinophils (1-3, S1). In this context, SP is considered to have pro-inflammatory properties due to its ability to induce the release of inflammatory mediators, such as cytokines and histamine, and to cause vasodilatation (3).Eosinophils are granulocytes mostly known for their role in parasitic diseases and allergic conditions, although their number increases in several other conditions (4). Eosinophils can be proinflammatory by the release of their distinctive granule-stored basic mediators, a number of cytokines, chemokines, growth factors and lipid mediators (4). Nevertheless, they take part also in the resolution of the inflammation process (S2).In their article, 'Substance P activates human eosinophils', Raap et al. (5) investigated the functional effects of SP on eosinophils, through their known receptors, in atopic and non-atopic patients. SP-induced activation and chemotaxis of eosinophils were demonstrated in earlier works, but the mechanism was not fully described. The novelty of this paper is that it examines both the functionality of SP receptors on primary eosinophils and compares cells from atopic and non-atopic individuals, thus addressing the clinical relevance.The authors show that eosinophils from atopic patients express higher levels of the NK2R and are more responsive to SP stimulation. They found that eosinophil apoptosis from atopic patients, but not from non-atopic ones, was delayed by SP, suggesting that eosinophil accumulation in atopic tissues may be regulated in part by SP. Chemotaxis and Ca 2+ influx were enhanced following SP stimulation, again only in atopic eosinophils. These findings brought them to the conclusion that the functional effects of SP on eosinophils are probably mediated by NK2R, although no inhibiting experiments were performed to confirm this hypothesis (5).On the other hand, even though it seems that eosinophils display very modest expression of NK1R, following their incubation with NK1R antagonist a significant inhibition of Ca 2+ flux was observed (5). This data is therefore puzzling but might indicate that complex mechanisms regulate SP-induced Ca 2+ flux and/or that the antagonist is not fully specific to NK1R.Interestingly, SP was shown to also affect MC chemotaxis and activate them to degranulate and release histamine, tryptase and various cytokines (6). MCs are major effector cells in atopic diseases together with the eosinophils. We have previously shown that eosinophils and MCs can interact (the Allergic Effector Unit) affecting one another's survival and activatio...
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