Production of Humanized Antibody against Human High-affinity IgE Receptor in a Serum-free Culture of CHO Cells, and Purification of the Fab Fragments

Takai, Toshiro; Takahashi, Kyôko; Akagawa-Chihara, Midori; Fukada, Minako; Yuuki, Toshihumi; Shibuya, Ichiro; Okumura, Ko; Ra, Chisei; Yokota, Toyokazu; Okumura, Yasushi

doi:10.1271/bbb.65.1082

Cited by 4 publications

(4 citation statements)

References 30 publications

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“…As has already been shown, CRA1 reacts with a region other than the IgE binding site, whereas CRA2 reacts directly with the IgE binding site. ( 18 ) We were thus able to confirm the successful dissociation of IgE by confirming that acid treatment increased CRA2 staining levels (Fig. 2 a).…”

Section: Resultssupporting

confidence: 67%

Carboplatin‐induced severe hypersensitivity reaction: Role of IgE‐dependent basophil activation and FcεRI

et al. 2014

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Basophil activation was observed in patients with a history of carboplatin-induced severe hypersensitivity reaction (HR). However, the precise mechanism by which carboplatin induces basophil activation and the associated surrogate markers remains to be elucidated. To investigate whether IgE-dependent mechanisms, including the overexpression of FcεRI, participate in carboplatin-induced basophil activation, 13 ovarian cancer patients were enrolled: 5 with a history of carboplatin-induced severe hypersensitivity reaction within the past 2 years, and 8 with no such history. The expression levels of FcεRI, IgE, and CD203c on basophils were measured using a flow cytometer. Immunoglobulin E-dependent basophil activation was evaluated by testing for IgE passive sensitization using lactic acid, and by testing for phosphatidylinositol 3-kinase inhibition, using wortmannin. In three patients positive for carboplatin hypersensitivity, pretreatment with wortmannin almost completely inhibited carboplatin-induced basophil activation (P < 0.05). In a healthy control subject, whose own IgE showed no response to carboplatin, acquired reactivity to carboplatin when exposed to plasma from patients positive for carboplatin hypersensitivity. This did not occur when the same experiment was carried out using plasma from the patients negative for carboplatin hypersensitivity. Moreover, pretreatment with omalizumab, a monoclonal anti-IgE antibody, almost completely blocked carboplatin-induced basophil activation in the plasma of patients positive for carboplatin hypersensitivity. On further investigation, the HR-positive group had significantly higher levels of FcεRI compared with the negative group (P < 0.05). In conclusion, an IgE-dependent mechanism incorporating FcεRI overexpression participates in carboplatin-induced severe HR. These results establish the relevance of monitoring the pharmacodynamic changes of basophils to prevent carboplatin-induced severe HR.

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Section: Resultssupporting

confidence: 67%

Carboplatin‐induced severe hypersensitivity reaction: Role of IgE‐dependent basophil activation and FcεRI

et al. 2014

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“…This dissociation of IgE from basophils was confirmed by staining either with the anti‐FcεRI antibodies, CRA1 and CRA2, or with an anti‐IgE antibody. As already discussed, CRA1 does not bind directly with the IgE‐binding site, whereas CRA2 does . We were thus able to confirm the successful dissociation of IgE by confirming that lactic acid treatment increased the staining levels of CRA2 ( P < 0.001) (Fig.…”

Section: Resultssupporting

confidence: 79%

“…As already discussed, CRA1 does not bind directly with the IgE-binding site, whereas CRA2 does. [24] We were thus able to confirm the successful dissociation of IgE by confirming that lactic acid treatment increased the staining levels of CRA2 (P < 0.001) ( Fig. 3C and D) and decreased the staining levels of anti-IgE antibody (P < 0.001) ( Fig.…”

Section: Evaluation Of Ige-cetuximab Binding On Basophilssupporting

confidence: 62%

A novel approach to predict cetuximab‐induced hypersensitivity reaction: detection of drug‐specific IgE on basophils

et al. 2016

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Cetuximab is remarkable for the relatively high rate and severity of hypersensitivity reactions (HR) being reported in the literature. Screening for cetuximab‐specific IgE in serum via immunoassay has been found to be useful in preventing HR; however, these tests are known to have a low positive predictive rate. In an attempt to remedy this, we evaluated the interaction between cetuximab and IgE on basophils for predicting severe cetuximab‐induced HR. Twelve head and neck cancer patients were enrolled in this single‐institution study: four with a history of cetuximab‐induced HR and eight with no such history. Cetuximab‐specific and galactose‐α‐1,3‐galactose (α‐gal) specific IgEs in serum were measured in vitro using an enzyme‐linked immunosorbent assay (ELISA). IgE‐cetuximab binding on basophils was also analyzed to evaluate the decrease in cetuximab molecules on basophils after dissociation of IgE from FcεRI. The positive predictive value associated with the presence of cetuximab‐ or α‐gal‐specific IgE in serum was found to be only 0.67, whereas the negative predictive value was 1.00. On the other hand, in all four patients who developed HR, the cetuximab molecules on basophils were decreased significantly due to the dissociation of IgE from basophils (P < 0.05). However, this was not the case in patients who did not develop HR. In conclusion, our results strongly imply that the IgE‐cetuximab interaction on basophils may be key to developing improved methods for predicting severe cetuximab‐induced HR.

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“…In the IgE measurement system developed by our research group, we used antigens obtained through technology to purify human FcεRI recombinant proteins from the CHO transfectant cells expressing human FcεRI (CHO/αβγ) that secreted rsFcεRIα ( Yanagihara et al, 1994 ; Takai et al, 2000 ; Takai et al, 2001 ). To evaluate the accuracy of our assay, we used a spike recovery assay.…”

Section: Methods Of Measuring Free Ige In the Presence Of Omalizumab ...mentioning

confidence: 99%

Omalizumab and IgE in the Control of Severe Allergic Asthma

2022

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Omalizumab, a human immunoglobulin (Ig)G1 antibody against IgE, is a therapeutic agent for bronchial asthma. The Global Initiative for Asthma guidelines indicate that the use of omalizumab should be considered as an option in step 5 of treatment for patients with the most severe type of bronchial asthma. In patients with atopic asthma who are at a high risk of exacerbation, and in whom symptoms are poorly controlled despite treatment with inhaled corticosteroids, omalizumab is one of the few drugs that improves symptoms, reduces the risk of exacerbation, and improves the quality of life while offering a high level of safety. On the other hand, the associated treatment costs are high, and there are no clear methods to identify responders. A recent study suggested that evaluating the therapeutic effects and monitoring the pharmacokinetics of omalizumab could improve the success of omalizumab therapy. This review outlines the relationship between IgE-targeted therapy and the serum level of IgE to enhance the current understanding of the mechanism of omalizumab therapy. It also describes the clinical significance of measuring serum free IgE levels and monitoring omalizumab therapy.

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Production of Humanized Antibody against Human High-affinity IgE Receptor in a Serum-free Culture of CHO Cells, and Purification of the Fab Fragments

Cited by 4 publications

References 30 publications

Carboplatin‐induced severe hypersensitivity reaction: Role of IgE‐dependent basophil activation and FcεRI

Carboplatin‐induced severe hypersensitivity reaction: Role of IgE‐dependent basophil activation and FcεRI

A novel approach to predict cetuximab‐induced hypersensitivity reaction: detection of drug‐specific IgE on basophils

Omalizumab and IgE in the Control of Severe Allergic Asthma

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