The research report should be a detailed narrative explaining the function, biological processes, and localization of the gene product. Citations should be given for all claims.
You should prioritize authoritative reviews and primary scientific literature when conducting research. You can supplement
this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.
We are specifically interested in the primary function of the gene - for enzymes, what reaction is catalyzed, and what is the substrate specificity? For transporters, what is the substrate? For structural proteins or adapters, what is the broader structural role? For signaling molecules, what is the role in the pathway.
We are interested in where in or outside the cell the gene product carries out its function.
We are also interested in the signaling or biochemical pathways in which the gene functions. We are less interested in broad pleiotropic effects, except where these elucidate the precise role.
Include evidence where possible. We are interested in both experimental evidence as well as inference from structure, evolution, or bioinformatic analysis. Precise studies should be prioritized over high-throughput, where available.
The UniProt accession P42224 corresponds to human STAT1 (“signal transducer and activator of transcription 1-alpha/beta”; historically described as ISGF3 component p91/p84), a STAT-family transcription factor central to interferon (IFN) signaling, consistent with STAT-family domain architecture and STAT1’s role in IFN-induced transcriptional complexes. (babadei2024transcriptionalcontrolof pages 2-3, meesilpavikkai2024unravelingtheimmunogenetics pages 1-3)
STAT1 is a signal transducer and transcription factor that is activated downstream of cytokine receptors (classically IFN receptors) via receptor-associated Janus kinases (JAKs), leading to STAT phosphorylation, dimerization, nuclear translocation, and transcriptional regulation of IFN-responsive genes. (ott2023jaksandstats pages 1-2, babadei2024transcriptionalcontrolof pages 2-3)
Recent authoritative reviews summarize canonical STAT-family domain organization present in STAT1: N-terminal domain, coiled-coil domain, DNA-binding domain, linker, SH2 domain, and a C-terminal transactivation domain (TAD); these domains support receptor docking (via SH2), dimerization (via phosphotyrosine–SH2 interactions), DNA binding, and transcriptional activation. (babadei2024transcriptionalcontrolof pages 2-3, meesilpavikkai2024unravelingtheimmunogenetics pages 1-3)
STAT1’s primary biochemical function is sequence-specific transcriptional regulation as part of IFN-activated transcription factor complexes (GAF and ISGF3), controlling expression of interferon-stimulated genes (ISGs). (babadei2024transcriptionalcontrolof pages 2-3, babadei2024transcriptionalcontrolof pages 1-2)
STAT1 exists in unphosphorylated/preassociated states at baseline and, upon tyrosine phosphorylation, forms dimers that translocate to the nucleus, where they bind regulatory DNA elements (GAS/ISRE) and regulate transcription. (babadei2024transcriptionalcontrolof pages 1-2, babadei2024transcriptionalcontrolof pages 2-3)
A 2024 mechanistic virology study illustrates that nuclear entry is a critical control point: respiratory syncytial virus (RSV) NS1 can bind STAT1 and reduce STAT1 nuclear translocation (and reduce interaction with nuclear transport adaptor KPNA1) even when IFNα-induced STAT1 phosphorylation is enhanced, thereby suppressing ISRE/GAS promoter activity and antiviral gene induction. (efstathiou2024respiratorysyncytialvirus pages 1-2)
A 2024 JBC review synthesizes a cross-cell-type analysis that identified 975 ISGs across 11 cell types, including a core set of 166 ISGs robustly induced by type I IFNs. This review also emphasizes that tyrosine-phosphorylated STAT1 can form homodimers or STAT1–STAT2 heterodimers, and that the relative abundance depends on IFN type (more persistent STAT1 homodimers after IFNγ; STAT1–STAT2 heterodimers predominate after type I/III IFNs). (babadei2024transcriptionalcontrolof pages 1-2)
A 2023 time-resolved RNA-seq + ChIP-seq study in Huh7.5 cells integrated transcriptional induction with binding of pSTAT1, pSTAT2, IRF9, and IRF1, identifying 319 IFNα-responsive integrated genes and 286 IFNγ-inducible integrated genes with associated binding profiles. The study reported 108 IFNα-specific and 75 IFNγ-specific integrated genes, and found that GAS genes tend to be early responders while ISRE genes predominate later, with ISRE+GAS composite sites acting as switch-like regulatory elements enabling mechanistic overlap between IFNα and IFNγ programs. (sekrecka2023timedependentrecruitmentof pages 8-9, sekrecka2023timedependentrecruitmentof pages 1-2)
A 2024 EMBO Journal study profiled nascent transcription over 48 hours and concluded that IFNβ and IFNγ programs overlap early but diverge over time, driven by differential deployment of ISGF3 and the “second-tier” transcription factor IRF1. Notably, the study reports a large nuclear interactome for STAT1 and provides quantitative proximity-labeling results: 184 STAT1 interactors vs 37 IRF1 interactors, with 127 STAT1-specific, 30 IRF1-specific, and 7 shared interactors. (geetha2024dynamiccontrolof pages 1-2, geetha2024dynamiccontrolof pages 8-10)
A 2024 clinical-genetics review reports that STAT1 GOF is the most common STAT1 defect, with >100 different variants described in >400 patients, and chronic mucocutaneous candidiasis (CMC) occurring in >60% of individuals with STAT1 GOF. Mechanistically, GOF variants often cause increased or prolonged STAT1 phosphorylation after cytokine stimulation (including variant-class-dependent effects on dephosphorylation). (meesilpavikkai2024unravelingtheimmunogenetics pages 4-7)
A 2024 infections-focused review summarizes a cohort description of 274 STAT1 GOF patients, reporting recurrent bacterial infections in ~75% and pneumonias in ~50%, with viral susceptibility in ~one-third (noting recurrent HSV/VZV and rare severe complications such as JCV-associated PML). (wang2024infectionsininborn pages 3-4)
A 2024 review summarizes autosomal recessive complete STAT1 deficiency as abolishing type I/II/III IFN and IL-27 signaling and reports 24 patients described “so far” in that review; it notes severe early-life infections and high mortality (“majority … died within the first year of life”) and severe vaccine reactions (e.g., 5 of 24 with severe reactions after live vaccination, as summarized). (meesilpavikkai2024unravelingtheimmunogenetics pages 4-7)
A 2023 clinical review similarly emphasizes that STAT1 LOF impairs IFN responses leading to severe infections and reports HSCT as a key intervention for severe deficiency; in one summary of 24 published patients, 10 received HSCT and 7 survived. (ott2023jaksandstats pages 13-14)
A 2023 case series reports three adults with STAT1 GOF and CMC treated with JAK inhibitors. In one detailed case, baricitinib 2 mg/day (initiated with prophylactic fluconazole and valacyclovir) led to marked improvement in mucocutaneous inflammation within a month and healing of aphthous ulcers by six months; infections/side effects were observed in some cases (e.g., herpes virus infection, sinusitis, bronchitis) and one patient did not tolerate ruxolitinib and required HSCT. (borgstrom2023threeadultcases pages 5-7, borgstrom2023threeadultcases pages 12-13)
A 2023 review argues that interferon-driven JAK–STAT signaling contributes to pancreatic islet HLA-I hyperexpression in T1D and frames JAK inhibition as a practical near-term approach to modulate this axis. It reports:
* In NOD mice, JAK inhibitors reduced insulitis, reduced islet HLA-I, and lowered diabetes incidence, with some evidence for reversal of new-onset disease. (russell2023theroleof pages 7-9)
* In human beta-cell/islet models, baricitinib prevented IFNα-induced HLA-I upregulation in EndoC-βH1 cells, and TYK2 inhibition (e.g., BMS-986165) or TYK2 knockdown prevented IFN-driven HLA-I upregulation in human islets. (russell2023theroleof pages 7-9)
* A translational clinical anecdote: a 15-year-old STAT1 GOF patient treated with ruxolitinib became euglycemic and discontinued insulin for 12 months. (russell2023theroleof pages 7-9, russell2023theroleof pages 9-10)
Figure evidence of proposed intervention points (receptors/JAKs/STATs/negative regulators) is available from this review. (russell2023theroleof media e63e0201)
A 2024 Signal Transduction and Targeted Therapy review compiles a broad translational landscape of JAK/TYK inhibitors in clinical use and development, including long-term clinical data for widely used agents (e.g., ruxolitinib, tofacitinib) and multiple phase I/II studies for more selective inhibitors. This provides context for why repurposing JAK inhibitors is often proposed for IFN/STAT1-driven pathology: the pharmacologic class is mature and clinically accessible, though selectivity and infection risk remain central safety concerns. (lv2024thejakstatpathway pages 31-31)
The following table consolidates the most directly citable functional-annotation evidence gathered here (mechanism, localization, transcriptional programs, disease statistics, and applications) with URLs.
| Aspect | Key points | Recent sources (2023-2024 with first author/year) | URLs |
|---|---|---|---|
| Identity / domains | • Verified target is human STAT1 matching UniProt P42224, a STAT-family transcription factor in IFN signaling. • Conserved STAT architecture: N-terminal, coiled-coil, DNA-binding, linker, SH2, C-terminal transactivation domain. • Canonical gene products include STAT1 homodimeric and STAT1-containing heterodimeric transcription factor functions, consistent with UniProt description of ISGF3 component p91/p84. (babadei2024transcriptionalcontrolof pages 2-3, meesilpavikkai2024unravelingtheimmunogenetics pages 1-3) |
Babadei 2024; Meesilpavikkai 2024 | https://doi.org/10.1016/j.jbc.2024.107771 https://doi.org/10.12932/ap-270124-1776 |
| Activation / PTMs | • Receptor-associated JAKs phosphorylate STAT1 on Tyr701, enabling dimerization and transcriptional activation. • Ser727 phosphorylation in the C-terminal region modulates transcriptional output; recent review also highlights context-dependent Thr748 phosphorylation biology. • GOF alleles often show prolonged or increased pSTAT1 after cytokine stimulation due to altered phosphorylation/dephosphorylation dynamics. (babadei2024transcriptionalcontrolof pages 2-3, meesilpavikkai2024unravelingtheimmunogenetics pages 4-7) |
Babadei 2024; Meesilpavikkai 2024 | https://doi.org/10.1016/j.jbc.2024.107771 https://doi.org/10.12932/ap-270124-1776 |
| Complexes & DNA elements | • STAT1 homodimers (GAF) bind GAS elements, especially downstream of IFN-γ. • STAT1-STAT2-IRF9 (ISGF3) binds ISRE elements, especially downstream of type I/III IFNs. • Composite ISRE+GAS promoters function as regulatory switches integrating pSTAT1, pSTAT2, IRF9, and IRF1. (babadei2024transcriptionalcontrolof pages 2-3, efstathiou2024respiratorysyncytialvirus pages 1-2, sekrecka2023timedependentrecruitmentof pages 1-2) |
Babadei 2024; Efstathiou 2024; Sekrecka 2023 | https://doi.org/10.1016/j.jbc.2024.107771 https://doi.org/10.3389/fimmu.2024.1395809 https://doi.org/10.1007/s00018-023-04830-8 |
| Localization | • In resting cells, STAT1 is largely cytoplasmic or shuttling in unphosphorylated/preassociated forms; after tyrosine phosphorylation it forms dimers that translocate to the nucleus. • Nuclear import depends on interaction with importin α/KPNA1; RSV NS1 can block STAT1 nuclear translocation despite preserved phosphorylation. • STAT1 executes its transcriptional role in the nucleus at IFN-responsive promoters/enhancers. (babadei2024transcriptionalcontrolof pages 1-2, efstathiou2024respiratorysyncytialvirus pages 1-2) |
Babadei 2024; Efstathiou 2024 | https://doi.org/10.1016/j.jbc.2024.107771 https://doi.org/10.3389/fimmu.2024.1395809 |
| Transcriptional programs / kinetics | • A cross-cell-type study summarized in review identified 975 ISGs, with 166 core ISGs robustly induced by IFN-I. • Time-resolved multi-omics identified 319 IFNα-responsive integrated genes and 286 IFNγ-inducible integrated genes bound by STAT/IRF complexes; 108 were IFNα-specific and 75 IFNγ-specific. • GAS genes tend to be early, ISRE genes more intermediate/late, while composite promoters show heterogeneous sustained responses driven by GAF, ISGF3, and IRF1. (sekrecka2023timedependentrecruitmentof pages 8-9, sekrecka2023timedependentrecruitmentof pages 1-2, babadei2024transcriptionalcontrolof pages 1-2) |
Sekrecka 2023; Babadei 2024 | https://doi.org/10.1007/s00018-023-04830-8 https://doi.org/10.1016/j.jbc.2024.107771 |
| Human genetic disorders & stats | • STAT1 GOF is the most common STAT1 defect: >100 variants reported in >400 patients; CMC >60%, and one review notes 98% CMC in a series and ~half of all CMC attributable to STAT1 GOF. • A cohort of 274 patients with STAT1 GOF showed broad infectious phenotypes: recurrent bacterial infections in ~75%, pneumonias in ~50%, viral infections in ~one-third; another review notes bacterial infections in more than half and viral infections in about half. • AR complete STAT1 deficiency is rare but severe: 24 patients summarized in one review; a larger review cites 32 patients with severe viral/mycobacterial disease, including universal BCGosis in one series; among 24 HSCT cases, 10 transplanted and 7 survived. (meesilpavikkai2024unravelingtheimmunogenetics pages 4-7, wang2024infectionsininborn pages 3-4, ott2023jaksandstats pages 13-14) |
Meesilpavikkai 2024; Wang 2024; Ott 2023 | https://doi.org/10.12932/ap-270124-1776 https://doi.org/10.3390/pathogens13110955 https://doi.org/10.1007/s10875-023-01483-x |
| Therapeutic applications | • JAK inhibitors are the main targeted strategy in STAT1 GOF and related IFN-driven pathology; real-world adult case series showed baricitinib improved mucocutaneous disease, though infections/side effects occurred and one patient later required HSCT. • In T1D models, JAK inhibition reduced IFN-driven HLA-I hyperexpression: baricitinib protected human beta-cell models; TYK2 inhibition also blocked IFN-induced HLA-I upregulation. • Translational activity includes a reported 15-year-old STAT1 GOF patient who became euglycemic off insulin for 12 months on ruxolitinib, and the BANDIT placebo-controlled trial testing baricitinib in new-onset T1D. (borgstrom2023threeadultcases pages 12-13, russell2023theroleof pages 7-9, russell2023theroleof pages 9-10, russell2023theroleof media e63e0201) |
Borgström 2023; Russell 2023 | https://doi.org/10.1007/s10875-022-01351-0 https://doi.org/10.3389/fendo.2023.1270325 |
Table: This table summarizes verified functional annotation evidence for human STAT1 (UniProt P42224), spanning molecular mechanism, localization, transcriptional programs, disease genetics, and current therapeutic applications. It emphasizes recent 2023-2024 sources and key quantitative findings useful for evidence-based gene annotation.
References
(babadei2024transcriptionalcontrolof pages 2-3): Olga Babadei, Birgit Strobl, Mathias Müller, and Thomas Decker. Transcriptional control of interferon-stimulated genes. Journal of Biological Chemistry, 300:107771, Oct 2024. URL: https://doi.org/10.1016/j.jbc.2024.107771, doi:10.1016/j.jbc.2024.107771. This article has 22 citations and is from a domain leading peer-reviewed journal.
(meesilpavikkai2024unravelingtheimmunogenetics pages 1-3): Kornvalee Meesilpavikkai, N. Hirankarn, Virgil A.S.H. Dalm, P. M. Hagen, Willem A. Dik, and Hanna IJspeert. Unraveling the immunogenetics of stat proteins: clinical perspectives on gain-of-function and loss-of-function variants. Asian Pacific journal of allergy and immunology, May 2024. URL: https://doi.org/10.12932/ap-270124-1776, doi:10.12932/ap-270124-1776. This article has 7 citations and is from a peer-reviewed journal.
(ott2023jaksandstats pages 1-2): Nils Ott, Laura Faletti, Maximilian Heeg, Virginia Andreani, and Bodo Grimbacher. Jaks and stats from a clinical perspective: loss-of-function mutations, gain-of-function mutations, and their multidimensional consequences. Journal of Clinical Immunology, 43:1326-1359, May 2023. URL: https://doi.org/10.1007/s10875-023-01483-x, doi:10.1007/s10875-023-01483-x. This article has 97 citations and is from a domain leading peer-reviewed journal.
(efstathiou2024respiratorysyncytialvirus pages 1-2): Claudia Efstathiou, Yamei Zhang, Shubhangi Kandwal, Darren Fayne, Eleanor J. Molloy, and Nigel J. Stevenson. Respiratory syncytial virus ns1 inhibits anti-viral interferon-α-induced jak/stat signaling, by limiting the nuclear translocation of stat1. Frontiers in Immunology, Jun 2024. URL: https://doi.org/10.3389/fimmu.2024.1395809, doi:10.3389/fimmu.2024.1395809. This article has 16 citations and is from a peer-reviewed journal.
(babadei2024transcriptionalcontrolof pages 1-2): Olga Babadei, Birgit Strobl, Mathias Müller, and Thomas Decker. Transcriptional control of interferon-stimulated genes. Journal of Biological Chemistry, 300:107771, Oct 2024. URL: https://doi.org/10.1016/j.jbc.2024.107771, doi:10.1016/j.jbc.2024.107771. This article has 22 citations and is from a domain leading peer-reviewed journal.
(sekrecka2023timedependentrecruitmentof pages 8-9): Agata Sekrecka, Katarzyna Kluzek, Michal Sekrecki, Mahdi Eskandarian Boroujeni, Sanaz Hassani, Shota Yamauchi, Kiyonao Sada, Joanna Wesoly, and Hans A. R. Bluyssen. Time-dependent recruitment of gaf, isgf3 and irf1 complexes shapes ifnα and ifnγ-activated transcriptional responses and explains mechanistic and functional overlap. Cellular and Molecular Life Sciences: CMLS, Jun 2023. URL: https://doi.org/10.1007/s00018-023-04830-8, doi:10.1007/s00018-023-04830-8. This article has 37 citations.
(sekrecka2023timedependentrecruitmentof pages 1-2): Agata Sekrecka, Katarzyna Kluzek, Michal Sekrecki, Mahdi Eskandarian Boroujeni, Sanaz Hassani, Shota Yamauchi, Kiyonao Sada, Joanna Wesoly, and Hans A. R. Bluyssen. Time-dependent recruitment of gaf, isgf3 and irf1 complexes shapes ifnα and ifnγ-activated transcriptional responses and explains mechanistic and functional overlap. Cellular and Molecular Life Sciences: CMLS, Jun 2023. URL: https://doi.org/10.1007/s00018-023-04830-8, doi:10.1007/s00018-023-04830-8. This article has 37 citations.
(geetha2024dynamiccontrolof pages 1-2): Aarathy Ravi Sundar Jose Geetha, Katrin Fischer, Olga Babadei, Georg Smesnik, Alex Vogt, Ekaterini Platanitis, Mathias Müller, Matthias Farlik, and Thomas Decker. Dynamic control of gene expression by isgf3 and irf1 during ifnβ and ifnγ signaling. The EMBO Journal, 43:2233-2263, Apr 2024. URL: https://doi.org/10.1038/s44318-024-00092-7, doi:10.1038/s44318-024-00092-7. This article has 15 citations.
(geetha2024dynamiccontrolof pages 8-10): Aarathy Ravi Sundar Jose Geetha, Katrin Fischer, Olga Babadei, Georg Smesnik, Alex Vogt, Ekaterini Platanitis, Mathias Müller, Matthias Farlik, and Thomas Decker. Dynamic control of gene expression by isgf3 and irf1 during ifnβ and ifnγ signaling. The EMBO Journal, 43:2233-2263, Apr 2024. URL: https://doi.org/10.1038/s44318-024-00092-7, doi:10.1038/s44318-024-00092-7. This article has 15 citations.
(meesilpavikkai2024unravelingtheimmunogenetics pages 4-7): Kornvalee Meesilpavikkai, N. Hirankarn, Virgil A.S.H. Dalm, P. M. Hagen, Willem A. Dik, and Hanna IJspeert. Unraveling the immunogenetics of stat proteins: clinical perspectives on gain-of-function and loss-of-function variants. Asian Pacific journal of allergy and immunology, May 2024. URL: https://doi.org/10.12932/ap-270124-1776, doi:10.12932/ap-270124-1776. This article has 7 citations and is from a peer-reviewed journal.
(wang2024infectionsininborn pages 3-4): Chen Wang and Alexandra F. Freeman. Infections in inborn errors of stats. Pathogens, 13:955, Nov 2024. URL: https://doi.org/10.3390/pathogens13110955, doi:10.3390/pathogens13110955. This article has 0 citations.
(ott2023jaksandstats pages 13-14): Nils Ott, Laura Faletti, Maximilian Heeg, Virginia Andreani, and Bodo Grimbacher. Jaks and stats from a clinical perspective: loss-of-function mutations, gain-of-function mutations, and their multidimensional consequences. Journal of Clinical Immunology, 43:1326-1359, May 2023. URL: https://doi.org/10.1007/s10875-023-01483-x, doi:10.1007/s10875-023-01483-x. This article has 97 citations and is from a domain leading peer-reviewed journal.
(borgstrom2023threeadultcases pages 5-7): Emilie W. Borgström, Marie Edvinsson, Lucía P. Pérez, Anna C. Norlin, Sara L. Enoksson, Susanne Hansen, Anders Fasth, Vanda Friman, Olle Kämpe, Robert Månsson, Hernando Y. Estupiñán, Qing Wang, Tan Ziyang, Tadepally Lakshmikanth, Carl Inge E. Smith, Petter Brodin, and Peter Bergman. Three adult cases of stat1 gain-of-function with chronic mucocutaneous candidiasis treated with jak inhibitors. Journal of Clinical Immunology, 43:136-150, Sep 2023. URL: https://doi.org/10.1007/s10875-022-01351-0, doi:10.1007/s10875-022-01351-0. This article has 30 citations and is from a domain leading peer-reviewed journal.
(borgstrom2023threeadultcases pages 12-13): Emilie W. Borgström, Marie Edvinsson, Lucía P. Pérez, Anna C. Norlin, Sara L. Enoksson, Susanne Hansen, Anders Fasth, Vanda Friman, Olle Kämpe, Robert Månsson, Hernando Y. Estupiñán, Qing Wang, Tan Ziyang, Tadepally Lakshmikanth, Carl Inge E. Smith, Petter Brodin, and Peter Bergman. Three adult cases of stat1 gain-of-function with chronic mucocutaneous candidiasis treated with jak inhibitors. Journal of Clinical Immunology, 43:136-150, Sep 2023. URL: https://doi.org/10.1007/s10875-022-01351-0, doi:10.1007/s10875-022-01351-0. This article has 30 citations and is from a domain leading peer-reviewed journal.
(russell2023theroleof pages 7-9): Mark A. Russell, Sarah J. Richardson, and Noel G. Morgan. The role of the interferon/jak-stat axis in driving islet hla-i hyperexpression in type 1 diabetes. Frontiers in Endocrinology, Oct 2023. URL: https://doi.org/10.3389/fendo.2023.1270325, doi:10.3389/fendo.2023.1270325. This article has 30 citations.
(russell2023theroleof pages 9-10): Mark A. Russell, Sarah J. Richardson, and Noel G. Morgan. The role of the interferon/jak-stat axis in driving islet hla-i hyperexpression in type 1 diabetes. Frontiers in Endocrinology, Oct 2023. URL: https://doi.org/10.3389/fendo.2023.1270325, doi:10.3389/fendo.2023.1270325. This article has 30 citations.
(russell2023theroleof media e63e0201): Mark A. Russell, Sarah J. Richardson, and Noel G. Morgan. The role of the interferon/jak-stat axis in driving islet hla-i hyperexpression in type 1 diabetes. Frontiers in Endocrinology, Oct 2023. URL: https://doi.org/10.3389/fendo.2023.1270325, doi:10.3389/fendo.2023.1270325. This article has 30 citations.
(lv2024thejakstatpathway pages 31-31): You Lv, Jianxun Qi, Jeff J. Babon, Longxing Cao, Guohuang Fan, Jiajia Lang, Jin Zhang, Pengbing Mi, B. Kobe, and Faming Wang. The jak-stat pathway: from structural biology to cytokine engineering. Signal Transduction and Targeted Therapy, Aug 2024. URL: https://doi.org/10.1038/s41392-024-01934-w, doi:10.1038/s41392-024-01934-w. This article has 122 citations and is from a peer-reviewed journal.
(meesilpavikkai2024unravelingtheimmunogenetics pages 12-14): Kornvalee Meesilpavikkai, N. Hirankarn, Virgil A.S.H. Dalm, P. M. Hagen, Willem A. Dik, and Hanna IJspeert. Unraveling the immunogenetics of stat proteins: clinical perspectives on gain-of-function and loss-of-function variants. Asian Pacific journal of allergy and immunology, May 2024. URL: https://doi.org/10.12932/ap-270124-1776, doi:10.12932/ap-270124-1776. This article has 7 citations and is from a peer-reviewed journal.