The first publication of this article as accepted was a prior version of the manuscript. The publisher apologizes for their error in publishing the previous version of this article without prior approval from the authors.
Minor language revision took place throughout the article in response to reviewer comments. Additionally, several previously missing points and back matter sections have been added to this article. The conclusions of this article have not been affected by the changes made to this article. Please see the complete list of additions below:
Abstract:
Neither binding nor blocking was observed in TB negative samples. Indeterminate QuantiFERON results, commonly attributable to technical or immunologic factors, may reflect blocking anti-IFNγ autoantibodies.
Results, paragraph 3, last sentence of subsection (Presence of anti-IFNγ auto-Abs in QFN specimens):
This finding indicates that even under conditions favoring detection of weaker inhibitory effects, non-blocking, high-binding samples did not demonstrate functional interference with IFNγ activity.
Discussion, immediately before sentence ending paragraph 1:
Several samples showed high binding without blocking activity. Such antibodies are generally considered non-pathogenic, but because patient histories were unavailable, potential clinical implications cannot be entirely excluded (2, 3, 7).
Discussion, paragraph 2, beginning with sentence 4:
Additionally, we remain blinded to the IFNγ levels in the individual tubes of the QFN assay for each individual in our sample cohort. our analysis was limited by the absence of subject-level information, including measured IFNγ levels, medical comorbidities, and ancestry/ethnicity as this data was not collected at the time of sample acquisition. As a result, the prevalence estimates reported here cannot be directly applied to specific patient groups or to populations with different baseline risks for anti-IFNγ auto-Abs. These limitations constrain the generalizability of our findings and highlight the need for future studies incorporating more detailed demographic and clinical data.
Disclaimer
This research was supported in part by the Intramural Research Program of the National Institutes of Health (NIH). The contributions of the NIH authors were made as part of their official duties as NIH federal employees, are in compliance with agency policy requirements, and are considered Works of the United States Government. However, the findings and conclusions presented in this paper are those of the authors and do not necessarily reflect the views of the NIH or the U.S. Department of Health and Human Services. All logos, trademarks, and brand names are the property of their respective owners.
Acknowledgements
All authors contributed to the study conception and design. Material preparation, data collection and analysis were performed by SL, AJH, and LBR. The first draft of the manuscript was written by SL, AJH, and LBR, and all authors commented on previous versions of the manuscript. The authors would like to acknowledge the editorial suggestions provided by the NIH Fellows Editorial Board in the preparation of the final draft of this manuscript. All authors read and approved the final manuscript.