0000000000121567
AUTHOR
Ina Haasler
Free Serum IgE In Patients With Severe Allergic Asthma Treated With Omalizumab
Monitoring free serum IgE in severe asthma patients treated with omalizumab
SummaryBackgroundBenefit of treatment with the monoclonal anti-IgE-antibody omalizumab in severe IgE-dependent asthma requires a significant reduction of serum free IgE concentrations. It is unclear if monitoring free serum IgE is clinically meaningful once omalizumab treatment is initiated.MethodsFree IgE and omalizumab serum concentrations were quantified in 22 patients with severe asthma (68% female, 47 ± 11 yrs, mean (±SD) pre-bronchodilator FEV1 62 ± 13%, baseline mean (±SEM) free serum IgE 652 ± 136 ng/ml) treated with omalizumab for 4 months using a Recovery-ELISA.ResultsOmalizumab treatment reduced free serum IgE prior to the second omalizumab injection by 73%, after 16 weeks by 81%…
Cytokine Production Profile Of T-lymphocytes In Patients With Allergic Asthma Receiving Anti-IgE Therapy
Reduction Of Pulmonary Inflammation Through HIV-1 Envelope Protein GP120 In A Humanized Mouse Model Of Allergic Asthma Depends On Regulatory T Cells
Quantification Of Total Serum IgE In Patients With Asthma Using 3 Different Methods
Asthma bronchiale: neue Erkenntnisse und Entwicklungen
In mild asthma low-dose steroid inhalation treatment reduces severe exacerbations and exacerbation associated loss of lung function. In patients with mild asthma, symptom-driven use of a combination of inhaled steroid and short-acting beta-2-sympathomimetics in a single inhaler is feasible. In moderate and severe asthma the fixed combination of formoterol and budesonide can be used a maintenance therapy but also as treatment of acute symptoms. Monotherapy with long-acting beta 2-sympathomimetics should be completely avoided. Long-acting anticholinergic drugs are equally efficacious as long-acting beta-2-sympathomimetics, but have not yet been approved for use in patients with asthma. The co…
CD4-mediated regulatory T-cell activation inhibits the development of disease in a humanized mouse model of allergic airway disease
Background Based on their potency to control allergic diseases, regulatory T (Treg) cells represent a promising target for novel strategies to interfere with allergic airway inflammation. We have previously demonstrated that stimulation of the CD4 molecule on human Treg cells activates their suppressive activity in vitro and in vivo . Objective We sought to determine the effect of CD4-mediated Treg-cell activation on pulmonary inflammation in a humanized mouse model of allergic airway inflammation. Methods PBMCs obtained from donors allergic to birch pollen or from healthy donors were injected into NOD-severe combined immunodeficiency γc −/− mice, followed by allergen airway challenges and …