Abstract | BACKGROUND: AIM: To determine whether CD23 plays a role in the inflammatory process in severe uncontrolled asthma and whether anti-IgE therapy modulates fc epsilon RII/CD23 expression in these patients. METHODS: RESULTS: Treatment with omalizumab (for 24 weeks) improved disease control and pulmonary function (forced expiratory volume in the first second of expiration, 64.5 versus 74%; p = 0.021). Mean ± SE expression of fc epsilon RI on monocytes was higher in the patients with asthma versus the controls (45.7 ± 12.2% versus 18.6 ± 5.8%; p = 0.04) and was reduced after omalizumab treatment (45.7 ± 12.2% versus 15.6 ± 4.4%; p = 0.027). Mean ± SE TGF-beta levels in supernatants from monocytes were reduced in the patients treated with omalizumab (211 ± 6 pg/mL versus 184 ± 9 pg/mL; p = 0.036). CONCLUSION: Modulation of the low affinity IgE receptor CD23 in severe asthma is complex, and sCD23 may inversely reflect disease activity. Treatment with omalizumab was associated with reduced monocyte activation.
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Authors | Miri Assayag, Shabtai Moshel, Martin Kohan, Neville Berkman |
Journal | Allergy and asthma proceedings
(Allergy Asthma Proc)
Vol. 39
Issue 1
Pg. 36-42
(Jan 01 2018)
ISSN: 1539-6304 [Electronic] United States |
PMID | 29279058
(Publication Type: Journal Article)
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Chemical References |
- Anti-Asthmatic Agents
- Cytokines
- Receptors, IgE
- Transforming Growth Factor beta
- Omalizumab
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Topics |
- Anti-Asthmatic Agents
(therapeutic use)
- Asthma
(drug therapy, immunology)
- Case-Control Studies
- Cytokines
(drug effects, metabolism)
- Humans
- Monocytes
(metabolism)
- Omalizumab
(pharmacology, therapeutic use)
- Receptors, IgE
(drug effects)
- Transforming Growth Factor beta
(drug effects)
- Treatment Outcome
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