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Article ; Online: Role of inhibitory signaling in peripheral B cell tolerance.

Getahun, Andrew

2022 Volume 307, Issue 1, Page(s) 27–42

Abstract: At least 20% of B cells in the periphery expresses an antigen receptor with a degree of self-reactivity. If activated, these autoreactive B cells pose a risk as they can contribute to the development of autoimmune diseases. To prevent their activation, ... ...

Abstract	At least 20% of B cells in the periphery expresses an antigen receptor with a degree of self-reactivity. If activated, these autoreactive B cells pose a risk as they can contribute to the development of autoimmune diseases. To prevent their activation, both B cell-intrinsic and extrinsic tolerance mechanisms are in place in healthy individuals. In this review article, I will focus on B cell-intrinsic mechanisms that prevent the activation of autoreactive B cells in the periphery. I will discuss how inhibitory signaling circuits are established in autoreactive B cells, focusing on the Lyn-SHIP-1-SHP-1 axis, how they contribute to peripheral immune tolerance, and how disruptions of these circuits can contribute to the development of autoimmunity.
MeSH term(s)	Autoimmune Diseases ; Autoimmunity ; B-Lymphocytes ; Humans ; Immune Tolerance ; Receptors, Antigen, B-Cell ; Signal Transduction
Chemical Substances	Receptors, Antigen, B-Cell
Language	English
Publishing date	2022-02-06
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	391796-4
ISSN	1600-065X ; 0105-2896
ISSN (online)	1600-065X
ISSN	0105-2896
DOI	10.1111/imr.13070
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Article ; Online: Failed Downregulation of PI3K Signaling Makes Autoreactive B Cells Receptive to Bystander T Cell Help.

Fiske, Brigita E / Getahun, Andrew

Journal of immunology (Baltimore, Md. : 1950)

2024 Volume 212, Issue 7, Page(s) 1150–1160

Abstract: The role of T cell help in autoantibody responses is not well understood. Because tolerance mechanisms govern both T and B cell responses, one might predict that both T cell tolerance and B cell tolerance must be defeated in autoantibody responses ... ...

Abstract	The role of T cell help in autoantibody responses is not well understood. Because tolerance mechanisms govern both T and B cell responses, one might predict that both T cell tolerance and B cell tolerance must be defeated in autoantibody responses requiring T cell help. To define whether autoreactive B cells depend on T cells to generate autoantibody responses, we studied the role of T cells in murine autoantibody responses resulting from acute B cell-specific deletion of regulatory phosphatases. Ars/A1 B cells are DNA reactive and require continuous inhibitory signaling by the tyrosine phosphatase SHP-1 and the inositol phosphatases SHIP-1 and PTEN to maintain unresponsiveness. Acute B cell-restricted deletion of any of these phosphatases results in an autoantibody response. In this study, we show that CD40-CD40L interactions are required to support autoantibody responses of B cells whose anergy has been compromised. If the B cell-intrinsic driver of loss of tolerance is failed negative regulation of PI3K signaling, bystander T cells provide sufficient CD40-mediated signal 2 to support an autoantibody response. However, although autoantibody responses driven by acute B cell-targeted deletion of SHP-1 also require T cells, bystander T cell help does not suffice. These results demonstrate that upregulation of PI3K signaling in autoreactive B cells, recapitulating the effect of multiple autoimmunity risk alleles, promotes autoantibody responses both by increasing B cells' cooperation with noncognate T cell help and by altering BCR signaling. Receptiveness to bystander T cell help enables autoreactive B cells to circumvent the fail-safe of T cell tolerance.
MeSH term(s)	Mice ; Animals ; Phosphatidylinositol 3-Kinases ; T-Lymphocytes ; Down-Regulation ; B-Lymphocytes ; Autoantibodies ; Receptors, Antigen, B-Cell
Chemical Substances	Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Autoantibodies ; Receptors, Antigen, B-Cell
Language	English
Publishing date	2024-02-14
Publishing country	United States
Document type	Journal Article
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.2300108
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Article: Failed down-regulation of PI3K signaling makes autoreactive B cells receptive to bystander T cell help.

Fiske, Brigita E / Getahun, Andrew

bioRxiv : the preprint server for biology

2023

Abstract: The role of T cell help in autoantibody responses is not well understood. Since tolerance mechanisms govern both T and B cell responses, one might predict that both T cell tolerance and B cell tolerance must be defeated in autoantibody responses ... ...

Abstract	The role of T cell help in autoantibody responses is not well understood. Since tolerance mechanisms govern both T and B cell responses, one might predict that both T cell tolerance and B cell tolerance must be defeated in autoantibody responses requiring T cell help. To define whether autoreactive B cells depend on T cells to generate autoantibody responses, we studied the role of T cells in autoantibody responses resulting from acute cell-specific deletion of regulatory phosphatases. Ars/A1 B cells are DNA-reactive and require continuous inhibitory signaling by the tyrosine phosphatase SHP-1 and the inositol phosphatases SHIP-1 and PTEN to maintain unresponsiveness. Acute B cell-restricted deletion of any of these phosphatases results in an autoantibody response. Here we show that CD40-CD40L interactions are required to support autoantibody responses of B cells whose anergy has been compromised. If the B cell-intrinsic driver of loss of tolerance is failed negative regulation of PI3K signaling, bystander T cells provide sufficient CD40-mediated signal 2 to support an autoantibody response. However, while autoantibody responses driven by acute B cell-targeted deletion of SHP-1 also require T cells, bystander T cell help does not suffice. These results demonstrate that upregulation of PI3K signaling in autoreactive B cells, recapitulating the effect of multiple autoimmunity risk alleles, promotes autoantibody responses both by increasing B cellsâ€™ cooperation with non-cognate T cell help, as well as by altering BCR signaling. Receptiveness to bystander T cell help enables autoreactive B cells to circumvent the fail-safe of T cell tolerance. Significance: Phosphatase suppression of PI3K signaling is an important mechanism by which peripheral autoreactive B cells are kept in an unresponsive/anergic state. Loss of this suppression, due to genetic alleles that confer risk of autoimmunity, often occurs in autoreactive B cells of individuals who develop autoimmune disease. Here we demonstrate that de-repression of PI3K signaling promotes autoantibody responses of a DNA-reactive B cell clone by relaxing dependence of autoantibody responses on T cell-derived helper signals. These results suggest that impaired regulation of PI3K signaling can promote autoantibody responses in two ways: by restoring antigen receptor signaling and by enabling autoreactive B cells to circumvent restrictions imposed by T cell tolerance mechanisms.
Language	English
Publishing date	2023-01-23
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.01.23.525206
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Article ; Online: Non-Antibody-Secreting Functions of B Cells and Their Contribution to Autoimmune Disease.

Getahun, Andrew / Cambier, John C

Annual review of cell and developmental biology

2019 Volume 35, Page(s) 337–356

Abstract: B cells play multiple important roles in the pathophysiology of autoimmune disease. Beyond producing pathogenic autoantibodies, B cells can act as antigen-presenting cells and producers of cytokines, including both proinflammatory and anti-inflammatory ... ...

Abstract	B cells play multiple important roles in the pathophysiology of autoimmune disease. Beyond producing pathogenic autoantibodies, B cells can act as antigen-presenting cells and producers of cytokines, including both proinflammatory and anti-inflammatory cytokines. Here we review our current understanding of the non-antibody-secreting roles that B cells may play during development of autoimmunity, as learned primarily from reductionist preclinical models. Attention is also given to concepts emerging from clinical studies using B cell depletion therapy, which shed light on the roles of these mechanisms in human autoimmune disease.
MeSH term(s)	Animals ; Autoimmune Diseases/immunology ; Autoimmune Diseases/pathology ; Autoimmunity ; B-Lymphocyte Subsets/immunology ; Cytokines/immunology ; Disease Models, Animal ; Humans ; Inflammation/immunology
Chemical Substances	Cytokines
Language	English
Publishing date	2019-03-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1293750-2
ISSN	1530-8995 ; 1081-0706
ISSN (online)	1530-8995
ISSN	1081-0706
DOI	10.1146/annurev-cellbio-100617-062518
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Article ; Online: Comparative analysis of the repertoire of insulin-reactive B cells in type 1 diabetes-prone and resistant mice.

Banach, Maureen / Harley, Isaac T W / Getahun, Andrew / Cambier, John C

Frontiers in immunology

2022 Volume 13, Page(s) 961209

Abstract: Seropositivity for autoantibodies against multiple islet antigens is associated with development of autoimmune type 1 diabetes (T1D), suggesting a role for B cells in disease. The importance of B cells in T1D is indicated by the effectiveness of B cell- ... ...

Abstract	Seropositivity for autoantibodies against multiple islet antigens is associated with development of autoimmune type 1 diabetes (T1D), suggesting a role for B cells in disease. The importance of B cells in T1D is indicated by the effectiveness of B cell-therapies in mouse models and patients. B cells contribute to T1D by presenting islet antigens, including insulin, to diabetogenic T cells that kill pancreatic beta cells. The role of B cell receptor (BCR) affinity in T1D development is unclear. Here, we employed single cell RNA sequencing to define the relationship between BCR affinity for insulin and B cell phenotype during disease development. We utilized immunoglobulin (Ig) heavy chain (VH125) mouse models in which high-affinity insulin-reactive B cells (IBCs) were previously shown to be anergic in diabetes-resistant VH125.C57BL/6-H2g7 and activated in VH125. NOD mice developing disease. Here, high-affinity IBCs were found in the spleen of prediabetic VH125. NOD mice and exhibited marginal zone or follicular phenotypes. Ig light chains expressed by these B cells are unmutated and biased toward Vκ4-74 and Vκ4-57 usage. Receptors expressed by anergic high-affinity IBCs of diabetes-resistant VH125.C57BL/6-H2g7 are also unmutated; however, in this genetic background light chains are polymorphic relative to those of NOD. Light chains derived from NOD and C57BL/6-H2g7 genetic backgrounds conferred divergent kinetics of binding to insulin when paired with the VH125 heavy chain. These findings suggest that relaxation of tolerance mechanisms in the NOD mouse leads to accumulation and partial activation of B cells expressing germline encoded high-affinity BCRs that support development of autoimmunity.
MeSH term(s)	Mice ; Animals ; Diabetes Mellitus, Type 1 ; Insulin/metabolism ; Mice, Inbred NOD ; Mice, Inbred C57BL ; Receptors, Antigen, B-Cell/metabolism ; Autoantibodies ; Immunoglobulin Heavy Chains/genetics ; Immunoglobulin Light Chains
Chemical Substances	Insulin ; Receptors, Antigen, B-Cell ; Autoantibodies ; Immunoglobulin Heavy Chains ; Immunoglobulin Light Chains
Language	English
Publishing date	2022-10-04
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.961209
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Article ; Online: Identifying opportunities for prevention of adverse outcomes following female genital fistula repair: protocol for a mixed-methods study in Uganda.

El Ayadi, Alison M / Obore, Susan / Kirya, Fred / Miller, Suellen / Korn, Abner / Nalubwama, Hadija / Neuhaus, John / Getahun, Monica / Eyul, Patrick / Twine, Robert / Andrew, Erin V W / Barageine, Justus K

Reproductive health

2024 Volume 21, Issue 1, Page(s) 2

Abstract: Background: Female genital fistula is a traumatic debilitating injury, frequently caused by prolonged obstructed labor, affecting between 500,000-2 million women in lower-resource settings. Vesicovaginal fistula causes urinary incontinence, and other ... ...

Abstract	Background: Female genital fistula is a traumatic debilitating injury, frequently caused by prolonged obstructed labor, affecting between 500,000-2 million women in lower-resource settings. Vesicovaginal fistula causes urinary incontinence, and other morbidity may occur during fistula development. Women with fistula are stigmatized, limit social and economic engagement, and experience psychiatric morbidity. Improved surgical access has reduced fistula consequences yet post-repair risks impacting quality of life and well-being include fistula repair breakdown or recurrence and ongoing or changing urine leakage or incontinence. Limited evidence on risk factors contributing to adverse outcomes hinders interventions to mitigate adverse events. This study aims to quantify these adverse risks and inform clinical and counseling interventions to optimize women's health and quality of life following fistula repair through: identifying predictors and characteristics of post-repair fistula breakdown and recurrence (Objective 1) and post-repair incontinence (Objective 2), and to identify feasible and acceptable intervention strategies (Objective 3). Methods: This mixed-methods study incorporates a prospective cohort of women with successful vesicovaginal fistula repair at approximately 12 fistula repair centers in Uganda (Objectives 1-2) followed by qualitative inquiry among key stakeholders (Objective 3). Cohort participants will have a baseline visit at the time of surgery followed by data collection at 2 weeks, 6 weeks, 3 months and quarterly thereafter for 3 years. Primary predictors to be evaluated include patient-related factors, fistula-related factors, fistula repair-related factors, and post-repair behaviors and exposures, collected via structured questionnaire at all data collection points. Clinical exams will be conducted at baseline, 2 weeks post-surgery, and for outcome confirmation at symptom development. Primary outcomes are fistula repair breakdown or fistula recurrence and post-repair incontinence. In-depth interviews will be conducted with cohort participants (n ~ 40) and other key stakeholders (~ 40 including family, peers, community members and clinical/social service providers) to inform feasibility and acceptability of recommendations. Discussion: Participant recruitment is underway. This study is expected to identify key predictors that can directly improve fistula repair and post-repair programs and women's outcomes, optimizing health and quality of life. Furthermore, our study will create a comprehensive longitudinal dataset capable of supporting broad inquiry into post-fistula repair health. Trial Registration ClinicalTrials.gov Identifier: NCT05437939.
MeSH term(s)	Female ; Humans ; Genital Diseases, Female ; Genitalia, Female ; Prospective Studies ; Quality of Life ; Uganda ; Vesicovaginal Fistula/etiology ; Vesicovaginal Fistula/prevention & control ; Vesicovaginal Fistula/surgery
Language	English
Publishing date	2024-01-04
Publishing country	England
Document type	Journal Article ; Observational Study
ZDB-ID	2149029-6
ISSN	1742-4755 ; 1742-4755
ISSN (online)	1742-4755
ISSN	1742-4755
DOI	10.1186/s12978-023-01732-7
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Article ; Online: A Precision B Cell-Targeted Therapeutic Approach to Autoimmunity Caused by Phosphatidylinositol 3-Kinase Pathway Dysregulation.

Franks, S Elizabeth / Getahun, Andrew / Cambier, John C

Journal of immunology (Baltimore, Md. : 1950)

2019 Volume 202, Issue 12, Page(s) 3381–3393

Abstract: The inositol lipid phosphatases PTEN and SHIP-1 play a crucial role in maintaining B cell anergy and are reduced in expression in B cells from systemic lupus erythematosus and type 1 diabetes patients, consequent to aberrant regulation by miRNA-7 and 155. ...

Abstract	The inositol lipid phosphatases PTEN and SHIP-1 play a crucial role in maintaining B cell anergy and are reduced in expression in B cells from systemic lupus erythematosus and type 1 diabetes patients, consequent to aberrant regulation by miRNA-7 and 155. With an eye toward eventual use in precision medicine therapeutic approaches in autoimmunity, we explored the ability of p110δ inhibition to compensate for PI3K pathway dysregulation in mouse models of autoimmunity. Low dosages of the p110δ inhibitor idelalisib, which spare the ability to mount an immune response to exogenous immunogens, are able to block the development of autoimmunity driven by compromised PI3K pathway regulation resultant from acutely induced B cell-targeted haploinsufficiency of PTEN and SHIP-1. These conditions do not block autoimmunity driven by B cell loss of the regulatory tyrosine phosphatase SHP-1. Finally, we show that B cells in NOD mice express reduced PTEN, and low-dosage p110δ inhibitor therapy blocks disease progression in this model of type 1 diabetes. These studies may aid in the development of precision treatments that act by enforcing PI3K pathway regulation in patients carrying specific risk alleles.
MeSH term(s)	Animals ; Autoimmunity ; B-Lymphocytes/immunology ; Class I Phosphatidylinositol 3-Kinases/antagonists & inhibitors ; Diabetes Mellitus, Type 1/immunology ; Diabetes Mellitus, Type 1/therapy ; Haploinsufficiency ; Humans ; Immunotherapy/methods ; Lupus Erythematosus, Systemic/immunology ; Lupus Erythematosus, Systemic/therapy ; Mice ; Mice, Inbred NOD ; MicroRNAs/genetics ; Molecular Targeted Therapy ; PTEN Phosphohydrolase/genetics ; PTEN Phosphohydrolase/metabolism ; Phosphatidylinositol 3-Kinase/metabolism ; Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases/genetics ; Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases/metabolism ; Signal Transduction
Chemical Substances	MIRN155 microRNA, human ; MIRN7 microRNA, human ; MicroRNAs ; Class I Phosphatidylinositol 3-Kinases (EC 2.7.1.137) ; PIK3CD protein, human (EC 2.7.1.137) ; Phosphatidylinositol 3-Kinase (EC 2.7.1.137) ; PTEN Phosphohydrolase (EC 3.1.3.67) ; INPP5D protein, human (EC 3.1.3.86) ; Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases (EC 3.1.3.86)
Language	English
Publishing date	2019-05-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1801394
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Article: Identifying Opportunities for Prevention of Adverse Outcomes Following Female Genital Fistula Repair: Protocol for a Mixed-Methods Study in Uganda.

Research square

2023

Abstract	Background: Female genital fistula is a traumatic debilitating injury, frequently caused by prolonged obstructed labor, affecting between 500,000-2 million women in lower-resource settings. Vesicovaginal fistula causes urinary incontinence. Other gynecologic, neurologic and orthopedic morbidity may occur during fistula development. Women with fistula are stigmatized; limit engagement in social, economic, or religious activities; and report high psychiatric morbidity. Improved global surgical access has reduced fistula consequences yet post-repair risks impacting quality of life and well-being include fistula repair breakdown or recurrence and ongoing or changing urine leakage or incontinence. Limited evidence on risk factors contributing to adverse outcomes hinders interventions to mitigate adverse events, protecting health and quality of life after surgery. This study seeks to identify predictors and characteristics of post-repair fistula breakdown and recurrence (Aim 1) and post-repair incontinence (Aim 2), and to identify feasible and acceptable intervention strategies (Aim 3). Methods: This mixed-methods study incorporates a prospective cohort study of women with successful vesicovaginal fistula repair at approximately 12 fistula repair centers and affiliated care sites in Uganda (Aims 1-2) followed by qualitative inquiry among key stakeholders (Aim 3). Cohort participants will have a baseline visit at the time of surgery followed by data collection at 2 weeks, 6 weeks, 3 months and quarterly thereafter for 3 years. Primary predictors to be evaluated include patient-related factors, fistula-related factors, fistula repair-related factors, and post-repair behaviors and exposures, collected via structured questionnaire at all data collection points. Clinical exams will be conducted at baseline, 2 weeks post-surgery, and for outcome confirmation at symptom development. Primary outcomes are fistula repair breakdown or fistula recurrence and post-repair incontinence. In-depth interviews will be conducted with cohort participants (n ~ 40) and other key stakeholders (~ 40 including family, peers, community members and clinical/social service providers) to develop feasible and acceptable intervention concepts for adjustment of identified risk factors. Discussion: Participant recruitment is underway. This study is expected to identify key predictors that can directly improve fistula repair and post-repair programs and women's outcomes, optimizing health and quality of life. Furthermore, our study will create a comprehensive longitudinal dataset capable of supporting broad inquiry into post-fistula repair health. Trial registration: ClinicalTrials.gov Identifier: NCT05437939.
Language	English
Publishing date	2023-05-05
Publishing country	United States
Document type	Preprint
DOI	10.21203/rs.3.rs-2879899/v1
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Article ; Online: Of ITIMs, ITAMs, and ITAMis: revisiting immunoglobulin Fc receptor signaling.

Getahun, Andrew / Cambier, John C

Immunological reviews

2015 Volume 268, Issue 1, Page(s) 66–73

Abstract: Receptors for immunoglobulin Fc regions play multiple critical roles in the immune system, mediating functions as diverse as phagocytosis, triggering degranulation of basophils and mast cells, promoting immunoglobulin class switching, and preventing ... ...

Abstract	Receptors for immunoglobulin Fc regions play multiple critical roles in the immune system, mediating functions as diverse as phagocytosis, triggering degranulation of basophils and mast cells, promoting immunoglobulin class switching, and preventing excessive activation. Transmembrane signaling associated with these functions is mediated primarily by two amino acid sequence motifs, ITAMs (immunoreceptor tyrosine-based activation motifs) and ITIMs (immunoreceptor tyrosine-based inhibition motifs) that act as the receptors' interface with activating and inhibitory signaling pathways, respectively. While ITAMs mobilize activating tyrosine kinases and their consorts, ITIMs mobilize opposing tyrosine and inositol-lipid phosphatases. In this review, we will discuss our current understanding of signaling by these receptors/motifs and their sometimes blurred lines of function.
MeSH term(s)	Amino Acid Motifs ; Animals ; Anti-Inflammatory Agents ; B-Lymphocytes/immunology ; B-Lymphocytes/metabolism ; Humans ; Immunoglobulins/immunology ; Immunoglobulins/metabolism ; Immunoglobulins, Intravenous/pharmacology ; Immunoglobulins, Intravenous/therapeutic use ; Immunomodulation ; Ligands ; Protein Binding/immunology ; Protein Interaction Domains and Motifs ; Protein Tyrosine Phosphatases/metabolism ; Receptors, Fc/chemistry ; Receptors, Fc/genetics ; Receptors, Fc/metabolism ; Receptors, IgG/chemistry ; Receptors, IgG/genetics ; Receptors, IgG/metabolism ; Signal Transduction
Chemical Substances	Anti-Inflammatory Agents ; Immunoglobulins ; Immunoglobulins, Intravenous ; Ligands ; Receptors, Fc ; Receptors, IgG ; Protein Tyrosine Phosphatases (EC 3.1.3.48)
Language	English
Publishing date	2015-11
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	391796-4
ISSN	1600-065X ; 0105-2896
ISSN (online)	1600-065X
ISSN	0105-2896
DOI	10.1111/imr.12336
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Article ; Online: Caring for Children in Relation to Financial Hardship, Advance Care Planning, and Genetic Testing Among Adolescent and Young Adults with Cancer.

Tan, Kelly R / Meernik, Clare / Anderson, Chelsea / Deal, Allison M / Engel, Stephanie / Getahun, Darios / Kent, Erin E / Kirchhoff, Anne C / Kwan, Marilyn L / Mitra, Sara / Park, Eliza M / Smitherman, Andrew / Chao, Chun R / Kushi, Lawrence / Nichols, Hazel B

Journal of adolescent and young adult oncology

2023 Volume 13, Issue 1, Page(s) 147–155

Abstract: Purpose: ...

Abstract	Purpose:
MeSH term(s)	Child ; Humans ; Female ; Young Adult ; Adolescent ; Financial Stress ; Neoplasms/epidemiology ; Thyroid Neoplasms ; Cancer Survivors/psychology ; Advance Care Planning ; Genetic Testing
Language	English
Publishing date	2023-06-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	2607978-1
ISSN	2156-535X ; 2156-5333
ISSN (online)	2156-535X
ISSN	2156-5333
DOI	10.1089/jayao.2023.0010
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