title: Higher levels of soluble Fas ligand and transforming growth factor-β after omalizumab treatment: a case report.
abstract: A skewed T-helper (T(h))1/T(h)2 immune response is considered to be the major cause of allergic disorders. Overproduction of T(h)2 cytokines, which promote recruitment and activation of mast cells and eosinophils, plays a key part in the pathogenesis of allergic asthma. The mechanisms by which omalizumab is effective in asthma treatment are not yet fully understood. A 16-year-old girl who was experiencing frequent asthma attacks in spite of daily administration of budesonide (640 μg) and montelukast (10mg) was given omalizumab (375 mg) at intervals of 2 weeks, to prevent a visit to the emergency room. Plasma levels of T(h)1 cytokines [interferon (IFN)-γ and interleukin (IL)-12p70], T(h)2 cytokines (IL-4 and IL-13), other proinflammatory and regulatory cytokines [IL-6, IL-10, IL-17, tumor necrosis factor (TNF)-α, and transforming growth factor (TGF)-β], chemokines [monocyte chemotactic protein (MCP)-1, chemokine ligand (CCL)7, and CCL17], and soluble Fas ligand (sFasL) were measured before treatment and after treatment for 8 weeks. She showed a good clinical response to omalizumab: her lung function parameters improved and the use of β2-agonist decreased. No emergency room visits were required after omalizumab treatment for 8 weeks. Plasma levels of sFasL and TGF-β showed obvious increases after omalizumab therapy. IL-12p70 levels were decreased as compared to the corresponding baseline levels. These findings suggest that the effects of omalizumab in asthma treatment are not restricted to the regulation of the skewed T(h)1/T(h)2 cytokine immune response, and sFasL-mediated apoptosis and regulatory T-cell (Treg)-mediated TGF-β seem to have important roles in the therapeutic effects of omalizumab.
authors.affiliation: Department of Respiratory Therapy, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Graduate Institute of Clinical Medical Science, Chang Gung University College of Medicine, Taiwan, ROC.
authors.forename: Shu-Ling
authors.initials: SL
authors.lastname: Kao
authors.forename: Hong-Ren
authors.initials: HR
authors.lastname: Yu
authors.forename: Ho-Chang
authors.initials: HC
authors.lastname: Kuo
authors.forename: Ka-Yin
authors.initials: KY
authors.lastname: Tsui
authors.forename: Chih-Chiang
authors.initials: CC
authors.lastname: Wu
authors.forename: Ling-Sai
authors.initials: LS
authors.lastname: Chang
authors.forename: Chi-Di
authors.initials: CD
authors.lastname: Liang
authors.forename: Yu-Hsiu
authors.initials: YH
authors.lastname: Chung
authors.forename: Kuender D
authors.initials: KD
authors.lastname: Yang
mesh_terms: D000085:Acetates / Q000008:administration & dosage; D000293:Adolescent; D000888:Antibodies, Anti-Idiotypic / Q000008:administration & dosage*; D061067:Antibodies, Monoclonal, Humanized / Q000008:administration & dosage*; D017209:Apoptosis; D001249:Asthma / Q000188:drug therapy*; D019819:Budesonide / Q000008:administration & dosage; D003521:Cyclopropanes; D053222:Fas Ligand Protein / Q000097:blood*; D005260:Female; D006801:Humans; D007155:Immunologic Factors / Q000008:administration & dosage*; D008168:Lung / Q000503:physiopathology; D000069444:Omalizumab; D011804:Quinolines / Q000008:administration & dosage; D012129:Respiratory Function Tests; D013440:Sulfides; D050378:T-Lymphocytes, Regulatory / Q000276:immunology; D016212:Transforming Growth Factor beta / Q000097:blood*; D016896:Treatment Outcome
chemical_list: D000085:Acetates; D000888:Antibodies, Anti-Idiotypic; D061067:Antibodies, Monoclonal, Humanized; D003521:Cyclopropanes; D053222:Fas Ligand Protein; D007155:Immunologic Factors; D011804:Quinolines; D013440:Sulfides; D016212:Transforming Growth Factor beta; D000069444:Omalizumab; D019819:Budesonide; C093875:montelukast