0
Correspondence |

ResponseResponse FREE TO VIEW

Hatice Kaya, MD; Seyfettin Gümüş, MD; Ergun Uçar, MD; Mehmet Aydoğan, MD; Uğur Muşabak, MD; Ergun Tozkoparan, MD; Hayati Bilgiç, MD
Author and Funding Information

Affiliations: From the Turkish Armed Forces Rehabilitation Center (Dr Kaya); and the Department of Pulmonary Medicine (Drs Gümüş, Uçar, Aydoğan, Tozkoparan, and Bilgiç), and the Department of Allergy and Clinical Immunology (Dr Muşabak), Gulhane Military Medical Academy.,  Dr Kaya is currently affiliated with the Department of Pulmonary Medicine, Gulhane Military Medical Academy (Ankara, Turkey) and George Washington University (Washington, DC).

Correspondence to: Hatice Kaya, MD, TSK Rehabilitasyon Merkezi, 06540, Bilkent, Ankara, Turkey; e-mail: drhaticekaya@yahoo.com


Financial/nonfinancial disclosures: The authors have reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2013;143(1):274-275. doi:10.1378/chest.12-2249
Text Size: A A A
Published online
To the Editor:

We read the correspondence by Drs Domingo and Pomares about our case report1 with interest. The case described by the authors, and probably some other unpublished cases, support the potential benefits of omalizumab in chronic eosinophilic pneumonia and other hypereosinophilic states.

The mechanism of the effect of omalizumab on hypereosinophilia is unclear; however, the defective expression of CD23 on B cells, as in our case, might be an explanation.1 The low-affinity receptor for IgE, FcɛRII, also known as CD23, is expressed on the B cells, monocytes, eosinophils, and Langerhans cells and plays an important role in the regulation of IgE production by B cells.2 This molecule is a transmembrane glycoprotein (type 2) of approximately 45 kDa and can be cleaved to yield a range of freely soluble CD23 (sCD23) fragments by the metalloprotease ADAM10. The best characterized ligands of CD23 are IgE and CD21, respectively. It was shown that antigen-IgE complexes are captured and internalized by CD23, which facilitate the antigen processing and presentation with major histocompatibility complex class 2 proteins.3 In addition, CD23 serves as a negative regulator of IgE production, which has been demonstrated through experimental animal studies in vivo. Increased production of IgE and defective antigen presentation were found in mice deficient in CD23.4 Accordingly, our case has defective expression of CD23 on B cells. Because of technical and financial reasons, we could analyze neither mutation of this molecule nor its soluble fragment in serum. We suggest that future studies investigating the role of CD23 (both its soluble fragments and expression on inflammatory cells, including B cells and eosinophils) and its mutation may provide some information about allergic and hypereosinophilic disorders and the mechanism of action of omalizumab on them.

The optimal duration of omalizumab treatment in allergic diseases is not known. It has been reported that lowering the recommended omalizumab dose may likely result in a clinical deterioration.5 On the other hand, however, after the discontinuation of the drug some effect of the therapy may continue up to 3 years.6 In our chronic eosinophilic pneumonia case, we plan to taper and discontinue omalizumab after completing at least 3 years of therapy.

References

Kaya H, Gümüş S, Uçar E, et al. Omalizumab as a steroid-sparing agent in chronic eosinophilic pneumonia. Chest. 2012;142(2):513-516. [CrossRef] [PubMed]
 
Acharya M, Borland G, Edkins AL, et al. CD23/FcɛRII: molecular multi-tasking. Clin Exp Immunol. 2010;162(1):12-23. [CrossRef] [PubMed]
 
Kijimoto-Ochiai S, Noguchi A. Two peptides from CD23, including the inverse RGD sequence and its related peptide, interact with the MHC class II molecule. Biochem Biophys Res Commun. 2000;267(3):686-691. [CrossRef] [PubMed]
 
Ford JW, Sturgill JL, Conrad DH. 129/SvJ mice have mutated CD23 and hyper IgE. Cell Immunol. 2009;254(2):124-134. [CrossRef] [PubMed]
 
Slavin RG, Ferioli C, Tannenbaum SJ, Martin C, Blogg M, Lowe PJ. Asthma symptom re-emergence after omalizumab withdrawal correlates well with increasing IgE and decreasing pharmacokinetic concentrations. J Allergy Clin Immunol. 2009;123(1):107-113.e3. [CrossRef] [PubMed]
 
Nopp A, Johansson SG, Adédoyin J, Ankerst J, Palmqvist M, Oman H. After 6 years with Xolair; a 3-year withdrawal follow-up. Allergy. 2010;65(1):56-60. [CrossRef] [PubMed]
 

Figures

Tables

References

Kaya H, Gümüş S, Uçar E, et al. Omalizumab as a steroid-sparing agent in chronic eosinophilic pneumonia. Chest. 2012;142(2):513-516. [CrossRef] [PubMed]
 
Acharya M, Borland G, Edkins AL, et al. CD23/FcɛRII: molecular multi-tasking. Clin Exp Immunol. 2010;162(1):12-23. [CrossRef] [PubMed]
 
Kijimoto-Ochiai S, Noguchi A. Two peptides from CD23, including the inverse RGD sequence and its related peptide, interact with the MHC class II molecule. Biochem Biophys Res Commun. 2000;267(3):686-691. [CrossRef] [PubMed]
 
Ford JW, Sturgill JL, Conrad DH. 129/SvJ mice have mutated CD23 and hyper IgE. Cell Immunol. 2009;254(2):124-134. [CrossRef] [PubMed]
 
Slavin RG, Ferioli C, Tannenbaum SJ, Martin C, Blogg M, Lowe PJ. Asthma symptom re-emergence after omalizumab withdrawal correlates well with increasing IgE and decreasing pharmacokinetic concentrations. J Allergy Clin Immunol. 2009;123(1):107-113.e3. [CrossRef] [PubMed]
 
Nopp A, Johansson SG, Adédoyin J, Ankerst J, Palmqvist M, Oman H. After 6 years with Xolair; a 3-year withdrawal follow-up. Allergy. 2010;65(1):56-60. [CrossRef] [PubMed]
 
NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.

  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543