hypersensitivity/phosphatase

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Phosphatase wild-type p53-induced phosphatase 1 controls the development of TH9 cells and allergic airway inflammation.

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BACKGROUND Allergic asthma is one of the most common diseases worldwide, resulting in a burden of diseases. No available therapeutic regimens can cure asthma thus far. OBJECTIVE We sought to identify new molecular targets for TH9 cell-mediated allergic airway inflammation. METHODS Wild-type

Salmeterol attenuates chemotactic responses in rhinovirus-induced exacerbation of allergic airways disease by modulating protein phosphatase 2A.

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BACKGROUND β-Agonists are used for relief and control of asthma symptoms by reversing bronchoconstriction. They might also have anti-inflammatory properties, but the underpinning mechanisms remain poorly understood. Recently, a direct interaction between formoterol and protein phosphatase 2A (PP2A)

[Differential diagnosis of allergic and non-allergic dermatitis by measuring the levels of acid phosphatase in neutrophils and peripheral blood lymphocytes].

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Using the cytoenzymatic method acid phosphatase was determined in peripheral blood neutrophils and lymphocytes in 25 patients with allergic eczema, 31 patients with eczema due to irritants and 18 clinically healthy subjects. In patients with allergic eczema the percent of neutrophils and lymphocytes

Acid phosphatase locus 1 genetic polymorphism, endometriosis, and allergy.

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Recent studies suggest that acid phosphatase locus 1 (ACP1) could be involved in T-cell antigen receptor signaling and in immune disorders. The present study shows that the ACP1( *)C allele, which is associated with elevated enzymatic activity, is significantly more common in women with

Mucosal and serum alkaline phosphatase activities in milk allergy.

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The effect of cow's milk protein (CMP) challenge on the levels of alkaline phosphatase (ALP) in the upper jejunal mucosa and the serum were studied in 25 infants clinically suspected to have cow's milk allergy. Following CMP provocation 3 groups were identified. Group 1 consisted of 10 infants who

Novel function of DUSP14/MKP6 (dual specific phosphatase 14) as a nonspecific regulatory molecule for delayed-type hypersensitivity.

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BACKGROUND Nonspecific unresponsive states of delayed-type hypersensitivity (DTH) to unrelated antigens are induced in mice by a single administration of hapten. In these studies, we found a unique regulatory mechanism of contact hypersensitivity (CHS) mediated by nonspecific suppressor factor (NSF)

Loss-of-function of inositol polyphosphate-4-phosphatase reversibly increases the severity of allergic airway inflammation.

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Inositol polyphosphate phosphatases regulate the magnitude of phosphoinositide-3 kinase signalling output. Although inositol polyphosphate-4-phosphatase is known to regulate phosphoinositide-3 kinase signalling, little is known regarding its role in asthma pathogenesis. Here we show that modulation

Tyrosine phosphatase SHP-1 in allergic and anaphylactic inflammation.

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Protein tyrosine phosphatase SHP-1 is an essential regulatory molecule in many different signaling pathways. The biological importance of SHP-1 is underscored by the motheaten mutant mouse strains with immunological disorders involving multiple organs and by the close association of aberrant SHP-1

The role of protein tyrosine phosphatases in the regulation of allergic asthma: implication of TC-PTP and PTP-1B in the modulation of disease development.

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Protein tyrosine phosphorylation is an important early event in the signal transduction of numerous cell receptors involved in the immune response. The implication of protein tyrosine kinases in allergic asthma is well recognized, but the role of protein tyrosine phosphatases (PTPs) remains poorly

Ultracytochemical localization of alkaline phosphatase activity in endothelial cells in chronic relapsing experimental allergic encephalomyelitis.

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To investigate the functions of endothelial cells (ECs) in chronic relapsing experimental allergic encephalomyelitis (EAE), we examined ECs ultracytochemically in various stages of EAE, in conjunction with the localization of alkaline phosphatase (AP) activity. We also studied the relation between

src homology 2 domain-containing tyrosine phosphatase SHP-1 controls the development of allergic airway inflammation.

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Th2 cells are generated from naive CD4 T cells upon T cell receptor (TCR) recognition of antigen and IL-4 stimulation and play crucial roles in humoral immunity against infectious microorganisms and the pathogenesis of allergic and autoimmune diseases. A tyrosine phosphatase, SHP-1, that contains

Lineage-specific regulation of allergic airway inflammation by the lipid phosphatase Src homology 2 domain-containing inositol 5-phosphatase (SHIP-1).

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BACKGROUND Inpp5d (Src homology 2 domain-containing inositol-5-phosphatase [Ship1])-deficient mice experience spontaneous airway inflammation and have enhanced sensitivity to allergen-induced airway inflammation. OBJECTIVE We hypothesized that lineage-specific deletion of Ship1 expression in cells

Src homology 2 domain-containing inositol 5-phosphatase 1 deficiency leads to a spontaneous allergic inflammation in the murine lung.

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BACKGROUND Src homology 2 domain-containing inositol 5-phosphatase 1 (SHIP-1) controls the intracellular level of the phosphoinositide 3-kinase product phosphotidylinositol-3,4,5-trisphosphate and functions as a negative regulator of cytokine and immune receptor signaling. Emerging evidence suggests

Protein tyrosine phosphatase 11 acts through RhoA/ROCK to regulate eosinophil accumulation in the allergic airway.

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Src homology domain 2-containing protein tyrosine phosphatase 2 (SHP2) participates in multiple cell functions including cell shape, movement, and differentiation. Therefore, we investigated the potential role of SHP2 in eosinophil recruitment into lungs in allergic airway inflammation and explored

Suppression of Food Allergic Symptoms by Raw Cow's Milk in Mice is Retained after Skimming but Abolished after Heating the Milk-A Promising Contribution of Alkaline Phosphatase.

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Raw cow's milk was previously shown to suppress allergic symptoms in a murine model for food allergy. In the present study, we investigated the contribution of fat content and heat-sensitive milk components to this allergy-protective effect. In addition, we determined the potency of alkaline

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