Component‐resolved analysis of IgA, IgE, and IgG4 during egg OIT identifies markers associated with sustained unresponsiveness
Background In a previously reported CoFAR study, 55 subjects with egg allergy underwent randomized, placebo‐controlled egg oral immunotherapy (eOIT). Active treatment induced desensitization in most and sustained unresponsiveness (SU) in a smaller subset. We hypothesized that component‐resolved anal...
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| Published in | Allergy (Copenhagen) Vol. 71; no. 11; pp. 1552 - 1560 |
|---|---|
| Main Authors | , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Denmark
Blackwell Publishing Ltd
01.11.2016
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| Subjects | |
| Online Access | Get full text |
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| Abstract | Background
In a previously reported CoFAR study, 55 subjects with egg allergy underwent randomized, placebo‐controlled egg oral immunotherapy (eOIT). Active treatment induced desensitization in most and sustained unresponsiveness (SU) in a smaller subset. We hypothesized that component‐resolved analysis of IgE, IgG4, IgA, IgA1, and IgA2 may identify potential biomarkers of SU in OIT subjects.
Methods
Longitudinal samples for 51 egg‐allergic subjects (37 active and 14 placebo) were available. Egg white (EW)‐, ovalbumin (OVA)‐, and ovomucoid (OVM)‐specific levels of IgA, IgA1, and IgA2 were quantified by ELISA. IgE and IgG4 to these antigens were quantified using ImmunoCAP®. Clinical responders achieved SU to egg; all others were considered nonresponders. Between‐group comparisons were made among active and placebo, as well as responders and nonresponders.
Results
No placebo subjects achieved responder status. Through month 48, among the 37 active subjects, baseline IgE‐OVM was lower in responders (median 3.97 kU/l, n = 19) than in nonresponders (10.9 kU/l, n = 18, P = 0.010). Logistic regression analysis revealed that lower baseline IgE‐EW (P = 0.038), IgE‐OVM (P = 0.032), and a higher IgG4/IgE‐OVM ratio (P = 0.013) were associated with clinical response. Relative increases in IgG4‐EW, IgA‐EW, and IgA2‐EW were observed in responders (P = 0.024, 0.024, and 0.029, respectively). IgG4/IgE, IgA/IgE, and IgA2/IgE ratios for EW and IgA/IgE ratio for OVA were found to be significantly elevated among responders (P = 0.004, 0.009, 0.028, and 0.008, respectively).
Conclusions
Increased IgG4‐EW, IgA‐EW, and IgA2‐EW during eOIT are associated with clinical response to eOIT. Lower pretreatment IgE‐EW and IgE‐OVM are also associated with SU. Future studies are needed to evaluate and validate these potential biomarkers. |
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| AbstractList | Background
In a previously reported CoFAR study, 55 subjects with egg allergy underwent randomized, placebo‐controlled egg oral immunotherapy (eOIT). Active treatment induced desensitization in most and sustained unresponsiveness (SU) in a smaller subset. We hypothesized that component‐resolved analysis of IgE, IgG4, IgA, IgA1, and IgA2 may identify potential biomarkers of SU in OIT subjects.
Methods
Longitudinal samples for 51 egg‐allergic subjects (37 active and 14 placebo) were available. Egg white (EW)‐, ovalbumin (OVA)‐, and ovomucoid (OVM)‐specific levels of IgA, IgA1, and IgA2 were quantified by ELISA. IgE and IgG4 to these antigens were quantified using ImmunoCAP®. Clinical responders achieved SU to egg; all others were considered nonresponders. Between‐group comparisons were made among active and placebo, as well as responders and nonresponders.
Results
No placebo subjects achieved responder status. Through month 48, among the 37 active subjects, baseline IgE‐OVM was lower in responders (median 3.97 kU/l, n = 19) than in nonresponders (10.9 kU/l, n = 18, P = 0.010). Logistic regression analysis revealed that lower baseline IgE‐EW (P = 0.038), IgE‐OVM (P = 0.032), and a higher IgG4/IgE‐OVM ratio (P = 0.013) were associated with clinical response. Relative increases in IgG4‐EW, IgA‐EW, and IgA2‐EW were observed in responders (P = 0.024, 0.024, and 0.029, respectively). IgG4/IgE, IgA/IgE, and IgA2/IgE ratios for EW and IgA/IgE ratio for OVA were found to be significantly elevated among responders (P = 0.004, 0.009, 0.028, and 0.008, respectively).
Conclusions
Increased IgG4‐EW, IgA‐EW, and IgA2‐EW during eOIT are associated with clinical response to eOIT. Lower pretreatment IgE‐EW and IgE‐OVM are also associated with SU. Future studies are needed to evaluate and validate these potential biomarkers. Background In a previously reported CoFAR study, 55 subjects with egg allergy underwent randomized, placebo-controlled egg oral immunotherapy (eOIT). Active treatment induced desensitization in most and sustained unresponsiveness (SU) in a smaller subset. We hypothesized that component-resolved analysis of IgE, IgG4, IgA, IgA1, and IgA2 may identify potential biomarkers of SU in OIT subjects. Methods Longitudinal samples for 51 egg-allergic subjects (37 active and 14 placebo) were available. Egg white (EW)-, ovalbumin (OVA)-, and ovomucoid (OVM)-specific levels of IgA, IgA1, and IgA2 were quantified by ELISA. IgE and IgG4 to these antigens were quantified using ImmunoCAP super( registered ). Clinical responders achieved SU to egg; all others were considered nonresponders. Between-group comparisons were made among active and placebo, as well as responders and nonresponders. Results No placebo subjects achieved responder status. Through month 48, among the 37 active subjects, baseline IgE-OVM was lower in responders (median 3.97 kU/l, n = 19) than in nonresponders (10.9 kU/l, n = 18, P = 0.010). Logistic regression analysis revealed that lower baseline IgE-EW (P = 0.038), IgE-OVM (P = 0.032), and a higher IgG4/IgE-OVM ratio (P = 0.013) were associated with clinical response. Relative increases in IgG4-EW, IgA-EW, and IgA2-EW were observed in responders (P = 0.024, 0.024, and 0.029, respectively). IgG4/IgE, IgA/IgE, and IgA2/IgE ratios for EW and IgA/IgE ratio for OVA were found to be significantly elevated among responders (P = 0.004, 0.009, 0.028, and 0.008, respectively). Conclusions Increased IgG4-EW, IgA-EW, and IgA2-EW during eOIT are associated with clinical response to eOIT. Lower pretreatment IgE-EW and IgE-OVM are also associated with SU. Future studies are needed to evaluate and validate these potential biomarkers. In a previously reported CoFAR study, 55 subjects with egg allergy underwent randomized, placebo-controlled egg oral immunotherapy (eOIT). Active treatment induced desensitization in most and sustained unresponsiveness (SU) in a smaller subset. We hypothesized that component-resolved analysis of IgE, IgG4, IgA, IgA1, and IgA2 may identify potential biomarkers of SU in OIT subjects.BACKGROUNDIn a previously reported CoFAR study, 55 subjects with egg allergy underwent randomized, placebo-controlled egg oral immunotherapy (eOIT). Active treatment induced desensitization in most and sustained unresponsiveness (SU) in a smaller subset. We hypothesized that component-resolved analysis of IgE, IgG4, IgA, IgA1, and IgA2 may identify potential biomarkers of SU in OIT subjects.Longitudinal samples for 51 egg-allergic subjects (37 active and 14 placebo) were available. Egg white (EW)-, ovalbumin (OVA)-, and ovomucoid (OVM)-specific levels of IgA, IgA1, and IgA2 were quantified by ELISA. IgE and IgG4 to these antigens were quantified using ImmunoCAP® . Clinical responders achieved SU to egg; all others were considered nonresponders. Between-group comparisons were made among active and placebo, as well as responders and nonresponders.METHODSLongitudinal samples for 51 egg-allergic subjects (37 active and 14 placebo) were available. Egg white (EW)-, ovalbumin (OVA)-, and ovomucoid (OVM)-specific levels of IgA, IgA1, and IgA2 were quantified by ELISA. IgE and IgG4 to these antigens were quantified using ImmunoCAP® . Clinical responders achieved SU to egg; all others were considered nonresponders. Between-group comparisons were made among active and placebo, as well as responders and nonresponders.No placebo subjects achieved responder status. Through month 48, among the 37 active subjects, baseline IgE-OVM was lower in responders (median 3.97 kU/l, n = 19) than in nonresponders (10.9 kU/l, n = 18, P = 0.010). Logistic regression analysis revealed that lower baseline IgE-EW (P = 0.038), IgE-OVM (P = 0.032), and a higher IgG4/IgE-OVM ratio (P = 0.013) were associated with clinical response. Relative increases in IgG4-EW, IgA-EW, and IgA2-EW were observed in responders (P = 0.024, 0.024, and 0.029, respectively). IgG4/IgE, IgA/IgE, and IgA2/IgE ratios for EW and IgA/IgE ratio for OVA were found to be significantly elevated among responders (P = 0.004, 0.009, 0.028, and 0.008, respectively).RESULTSNo placebo subjects achieved responder status. Through month 48, among the 37 active subjects, baseline IgE-OVM was lower in responders (median 3.97 kU/l, n = 19) than in nonresponders (10.9 kU/l, n = 18, P = 0.010). Logistic regression analysis revealed that lower baseline IgE-EW (P = 0.038), IgE-OVM (P = 0.032), and a higher IgG4/IgE-OVM ratio (P = 0.013) were associated with clinical response. Relative increases in IgG4-EW, IgA-EW, and IgA2-EW were observed in responders (P = 0.024, 0.024, and 0.029, respectively). IgG4/IgE, IgA/IgE, and IgA2/IgE ratios for EW and IgA/IgE ratio for OVA were found to be significantly elevated among responders (P = 0.004, 0.009, 0.028, and 0.008, respectively).Increased IgG4-EW, IgA-EW, and IgA2-EW during eOIT are associated with clinical response to eOIT. Lower pretreatment IgE-EW and IgE-OVM are also associated with SU. Future studies are needed to evaluate and validate these potential biomarkers.CONCLUSIONSIncreased IgG4-EW, IgA-EW, and IgA2-EW during eOIT are associated with clinical response to eOIT. Lower pretreatment IgE-EW and IgE-OVM are also associated with SU. Future studies are needed to evaluate and validate these potential biomarkers. Background In a previously reported CoFAR study, 55 subjects with egg allergy underwent randomized, placebo-controlled egg oral immunotherapy (eOIT). Active treatment induced desensitization in most and sustained unresponsiveness (SU) in a smaller subset. We hypothesized that component-resolved analysis of IgE, IgG4, IgA, IgA1, and IgA2 may identify potential biomarkers of SU in OIT subjects. Methods Longitudinal samples for 51 egg-allergic subjects (37 active and 14 placebo) were available. Egg white (EW)-, ovalbumin (OVA)-, and ovomucoid (OVM)-specific levels of IgA, IgA1, and IgA2 were quantified by ELISA. IgE and IgG4 to these antigens were quantified using ImmunoCAP. Clinical responders achieved SU to egg; all others were considered nonresponders. Between-group comparisons were made among active and placebo, as well as responders and nonresponders. Results No placebo subjects achieved responder status. Through month 48, among the 37 active subjects, baseline IgE-OVM was lower in responders (median 3.97 kU/l, n = 19) than in nonresponders (10.9 kU/l, n = 18, P = 0.010). Logistic regression analysis revealed that lower baseline IgE-EW (P = 0.038), IgE-OVM (P = 0.032), and a higher IgG4/IgE-OVM ratio (P = 0.013) were associated with clinical response. Relative increases in IgG4-EW, IgA-EW, and IgA2-EW were observed in responders (P = 0.024, 0.024, and 0.029, respectively). IgG4/IgE, IgA/IgE, and IgA2/IgE ratios for EW and IgA/IgE ratio for OVA were found to be significantly elevated among responders (P = 0.004, 0.009, 0.028, and 0.008, respectively). Conclusions Increased IgG4-EW, IgA-EW, and IgA2-EW during eOIT are associated with clinical response to eOIT. Lower pretreatment IgE-EW and IgE-OVM are also associated with SU. Future studies are needed to evaluate and validate these potential biomarkers. In a previously reported CoFAR study, 55 subjects with egg allergy underwent randomized, placebo-controlled egg oral immunotherapy (eOIT). Active treatment induced desensitization in most and sustained unresponsiveness (SU) in a smaller subset. We hypothesized that component-resolved analysis of IgE, IgG4, IgA, IgA1, and IgA2 may identify potential biomarkers of SU in OIT subjects. Longitudinal samples for 51 egg-allergic subjects (37 active and 14 placebo) were available. Egg white (EW)-, ovalbumin (OVA)-, and ovomucoid (OVM)-specific levels of IgA, IgA1, and IgA2 were quantified by ELISA. IgE and IgG4 to these antigens were quantified using ImmunoCAP . Clinical responders achieved SU to egg; all others were considered nonresponders. Between-group comparisons were made among active and placebo, as well as responders and nonresponders. No placebo subjects achieved responder status. Through month 48, among the 37 active subjects, baseline IgE-OVM was lower in responders (median 3.97 kU/l, n = 19) than in nonresponders (10.9 kU/l, n = 18, P = 0.010). Logistic regression analysis revealed that lower baseline IgE-EW (P = 0.038), IgE-OVM (P = 0.032), and a higher IgG4/IgE-OVM ratio (P = 0.013) were associated with clinical response. Relative increases in IgG4-EW, IgA-EW, and IgA2-EW were observed in responders (P = 0.024, 0.024, and 0.029, respectively). IgG4/IgE, IgA/IgE, and IgA2/IgE ratios for EW and IgA/IgE ratio for OVA were found to be significantly elevated among responders (P = 0.004, 0.009, 0.028, and 0.008, respectively). Increased IgG4-EW, IgA-EW, and IgA2-EW during eOIT are associated with clinical response to eOIT. Lower pretreatment IgE-EW and IgE-OVM are also associated with SU. Future studies are needed to evaluate and validate these potential biomarkers. |
| Author | Vickery, B. P. Wood, R. A. Wright, B. L. Kulis, M. Leung, D. Y. M. Burks, A. W. Sampson, H. A. Orgel, K. A. Jones, S. M. Sicherer, S. H. Lindblad, R. W. Stablein, D. Dawson, P. Henning, A. K. |
| AuthorAffiliation | 2 Duke University Medical Center, Durham, NC 4 University of Arkansas for Medical Sciences and Arkansas Children's Hospital, Little Rock, AR 1 University of North Carolina School of Medicine, Chapel Hill, NC 6 Icahn School of Medicine at Mt. Sinai, New York, NY 5 Johns Hopkins University School of Medicine, Baltimore, MD 7 National Jewish Health, Denver, CO 3 The EMMES Corporation, Rockville, MD |
| AuthorAffiliation_xml | – name: 6 Icahn School of Medicine at Mt. Sinai, New York, NY – name: 2 Duke University Medical Center, Durham, NC – name: 3 The EMMES Corporation, Rockville, MD – name: 5 Johns Hopkins University School of Medicine, Baltimore, MD – name: 1 University of North Carolina School of Medicine, Chapel Hill, NC – name: 4 University of Arkansas for Medical Sciences and Arkansas Children's Hospital, Little Rock, AR – name: 7 National Jewish Health, Denver, CO |
| Author_xml | – sequence: 1 givenname: B. L. surname: Wright fullname: Wright, B. L. organization: Duke University Medical Center – sequence: 2 givenname: M. surname: Kulis fullname: Kulis, M. email: mike.kulis@unc.edu organization: University of North Carolina School of Medicine – sequence: 3 givenname: K. A. surname: Orgel fullname: Orgel, K. A. organization: University of North Carolina School of Medicine – sequence: 4 givenname: A. W. surname: Burks fullname: Burks, A. W. organization: University of North Carolina School of Medicine – sequence: 5 givenname: P. surname: Dawson fullname: Dawson, P. organization: The EMMES Corporation – sequence: 6 givenname: A. K. surname: Henning fullname: Henning, A. K. organization: The EMMES Corporation – sequence: 7 givenname: S. M. surname: Jones fullname: Jones, S. M. organization: University of Arkansas for Medical Sciences and Arkansas Children's Hospital – sequence: 8 givenname: R. A. surname: Wood fullname: Wood, R. A. organization: Johns Hopkins University School of Medicine – sequence: 9 givenname: S. H. surname: Sicherer fullname: Sicherer, S. H. organization: Icahn School of Medicine at Mt. Sinai – sequence: 10 givenname: R. W. surname: Lindblad fullname: Lindblad, R. W. organization: The EMMES Corporation – sequence: 11 givenname: D. surname: Stablein fullname: Stablein, D. organization: The EMMES Corporation – sequence: 12 givenname: D. Y. M. surname: Leung fullname: Leung, D. Y. M. organization: National Jewish Health – sequence: 13 givenname: B. P. surname: Vickery fullname: Vickery, B. P. organization: University of North Carolina School of Medicine – sequence: 14 givenname: H. A. surname: Sampson fullname: Sampson, H. A. organization: Icahn School of Medicine at Mt. Sinai |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27015954$$D View this record in MEDLINE/PubMed |
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| Copyright | 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. Copyright © 2016 John Wiley & Sons A/S |
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| Issue | 11 |
| Keywords | IgA oral immunotherapy egg allergy component testing food allergy |
| Language | English |
| License | http://doi.wiley.com/10.1002/tdm_license_1.1 2016 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd. |
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| PublicationDate | November 2016 |
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| PublicationPlace | Denmark |
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| Publisher | Blackwell Publishing Ltd |
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| Snippet | Background
In a previously reported CoFAR study, 55 subjects with egg allergy underwent randomized, placebo‐controlled egg oral immunotherapy (eOIT). Active... In a previously reported CoFAR study, 55 subjects with egg allergy underwent randomized, placebo-controlled egg oral immunotherapy (eOIT). Active treatment... Background In a previously reported CoFAR study, 55 subjects with egg allergy underwent randomized, placebo-controlled egg oral immunotherapy (eOIT). Active... |
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| SubjectTerms | Administration, Oral Allergens - administration & dosage Allergens - immunology Biomarkers component testing Desensitization, Immunologic - methods egg allergy Egg Hypersensitivity - immunology Egg Hypersensitivity - therapy Eggs - adverse effects Female food allergy Humans IgA Immunoglobulin A - blood Immunoglobulin A - immunology Immunoglobulin E - blood Immunoglobulin E - immunology Immunoglobulin G - blood Immunoglobulin G - immunology Male oral immunotherapy Treatment Failure Treatment Outcome |
| Title | Component‐resolved analysis of IgA, IgE, and IgG4 during egg OIT identifies markers associated with sustained unresponsiveness |
| URI | https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fall.12895 https://www.ncbi.nlm.nih.gov/pubmed/27015954 https://www.proquest.com/docview/1826415941 https://www.proquest.com/docview/1826672552 https://www.proquest.com/docview/1837317266 https://pubmed.ncbi.nlm.nih.gov/PMC5035709 |
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