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Article ; Online: Persistent Unexplained Transaminitis in COPA Syndrome.

Thaivalappil, Silpa S / Garrod, Andrea S / Borowitz, Stephen M / Watkin, Levi B / Lawrence, Monica G

2020 Volume 41, Issue 1, Page(s) 205–208

MeSH term(s)	Alleles ; Biomarkers ; Child, Preschool ; Coat Protein Complex I/genetics ; DNA Mutational Analysis ; Humans ; Immune System Diseases/diagnosis ; Immune System Diseases/genetics ; Immune System Diseases/metabolism ; Immune System Diseases/therapy ; Immunohistochemistry ; Lung/metabolism ; Lung/pathology ; Male ; Mutation ; Syndrome ; Tomography, X-Ray Computed ; Transaminases/metabolism
Chemical Substances	Biomarkers ; Coat Protein Complex I ; Transaminases (EC 2.6.1.-)
Language	English
Publishing date	2020-09-24
Publishing country	Netherlands
Document type	Case Reports ; Letter ; Research Support, Non-U.S. Gov't
ZDB-ID	779361-3
ISSN	1573-2592 ; 0271-9142
ISSN (online)	1573-2592
ISSN	0271-9142
DOI	10.1007/s10875-020-00832-4
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Article ; Online: Reduced pro-inflammatory dendritic cell phenotypes are a potential indicator of successful peanut oral immunotherapy.

Anvari, Sara / Watkin, Levi B / Minard, Charles G / Schuster, Kimberly / Hassan, Oluwatomi / Anagnostou, Aikaterini / Orange, Jordan S / Corry, David B / Davis, Carla M

PloS one

2022 Volume 17, Issue 5, Page(s) e0264674

Abstract: Dendritic cells are important mediators in the early presentation of antigen and regulation of the differentiation of T cells. Peanut oral immunotherapy (POIT) results in desensitization in most peanut allergic individuals (responders), but not in others ...

Abstract	Dendritic cells are important mediators in the early presentation of antigen and regulation of the differentiation of T cells. Peanut oral immunotherapy (POIT) results in desensitization in most peanut allergic individuals (responders), but not in others due to allergic reactions (non-responders). Delineation of early immunologic changes contributing to desensitization would help clarify the POIT mechanism of action. We analyzed dendritic cells in 15 pediatric subjects (5-12 years) undergoing a phase 1 single-center POIT study. We examined dendritic cells at baseline, 6-, 12-, 18- and 24-weeks after initiation of POIT and responders of therapy were compared to non-responders and healthy controls. The distribution frequency of myeloid DCs (mDCs) and plasmacytoid DCs (pDCs) from peripheral blood samples were measured in vitro. A general linear mixed model was used, and included fixed effects for cohort (responder, non-responder, or healthy control), time (0-, 6-, 12-, 18-, and 24-weeks), and the cohort-time interaction term. P-values were adjusted for multiple hypothesis testing using Tukey's method. We observed that POIT responders had reduced TNFa producing myeloid dendritic cells (mDCs) compared to non-responders. Additionally, non-responders had increased OX40L expressing mDCs at 18-weeks compared to responders. In conclusion, our findings suggest that a reduced pro-inflammatory phenotype in DCs could potentially serve as a predictor of early outcome and success of POIT desensitization.
MeSH term(s)	Arachis ; Child ; Dendritic Cells ; Desensitization, Immunologic/methods ; Humans ; Peanut Hypersensitivity/therapy ; Phenotype
Language	English
Publishing date	2022-05-26
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0264674
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Article ; Online: Vaccination and heterologous immunity: educating the immune system.

Gil, Anna / Kenney, Laurie L / Mishra, Rabinarayan / Watkin, Levi B / Aslan, Nuray / Selin, Liisa K

Transactions of the Royal Society of Tropical Medicine and Hygiene

2015 Volume 109, Issue 1, Page(s) 62–69

Abstract: This review discusses three inter-related topics: (1) the immaturity of the neonatal and infant immune response; (2) heterologous immunity, where prior infection history with unrelated pathogens alters disease outcome resulting in either enhanced ... ...

Abstract	This review discusses three inter-related topics: (1) the immaturity of the neonatal and infant immune response; (2) heterologous immunity, where prior infection history with unrelated pathogens alters disease outcome resulting in either enhanced protective immunity or increased immunopathology to new infections, and (3) epidemiological human vaccine studies that demonstrate vaccines can have beneficial or detrimental effects on subsequent unrelated infections. The results from the epidemiological and heterologous immunity studies suggest that the immune system has tremendous plasticity and that each new infection or vaccine that an individual is exposed to during a lifetime will potentially alter the dynamics of their immune system. It also suggests that each new infection or vaccine that an infant receives is not only perturbing the immune system but is educating the immune system and laying down the foundation for all subsequent responses. This leads to the question, is there an optimum way to educate the immune system? Should this be taken into consideration in our vaccination protocols?
MeSH term(s)	Animals ; Cross Reactions ; Humans ; Immunity, Heterologous/drug effects ; Immunity, Heterologous/immunology ; Immunity, Innate/drug effects ; Immunity, Innate/immunology ; Immunologic Memory/drug effects ; Infant ; Infant, Newborn ; T-Lymphocytes ; Vaccination ; Viral Vaccines/immunology ; Virus Diseases/immunology ; Virus Diseases/prevention & control
Chemical Substances	Viral Vaccines
Language	English
Publishing date	2015-01
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	441375-1
ISSN	1878-3503 ; 0035-9203
ISSN (online)	1878-3503
ISSN	0035-9203
DOI	10.1093/trstmh/tru198
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Article ; Online: Severity of Acute Infectious Mononucleosis Correlates with Cross-Reactive Influenza CD8 T-Cell Receptor Repertoires.

Aslan, Nuray / Watkin, Levi B / Gil, Anna / Mishra, Rabinarayan / Clark, Fransenio G / Welsh, Raymond M / Ghersi, Dario / Luzuriaga, Katherine / Selin, Liisa K

mBio

2017 Volume 8, Issue 6

Abstract: Fifty years after the discovery of Epstein-Barr virus (EBV), it remains unclear how primary infection with this virus leads to massive CD8 T-cell expansion and acute infectious mononucleosis (AIM) in young adults. AIM can vary greatly in severity, from a ...

Abstract	Fifty years after the discovery of Epstein-Barr virus (EBV), it remains unclear how primary infection with this virus leads to massive CD8 T-cell expansion and acute infectious mononucleosis (AIM) in young adults. AIM can vary greatly in severity, from a mild transient influenza-like illness to a prolonged severe syndrome. We questioned whether expansion of a unique HLA-A2.01-restricted, cross-reactive CD8 T-cell response between influenza virus A-M1
MeSH term(s)	Antigens, Viral/immunology ; CD8-Positive T-Lymphocytes/immunology ; Cross Reactions/immunology ; Epitopes, T-Lymphocyte/immunology ; Epitopes, T-Lymphocyte/metabolism ; Female ; HLA-A2 Antigen/immunology ; Herpesvirus 4, Human/immunology ; Humans ; Immunity, Heterologous ; Immunologic Memory ; Infectious Mononucleosis/immunology ; Influenza A virus/immunology ; Influenza, Human/immunology ; Interferon-gamma/metabolism ; Lymphocyte Activation ; Male ; Receptors, Antigen, T-Cell/immunology ; Receptors, Antigen, T-Cell/metabolism ; Severity of Illness Index ; Viral Matrix Proteins/immunology ; Young Adult
Chemical Substances	Antigens, Viral ; Epitopes, T-Lymphocyte ; HLA-A2 Antigen ; IFNG protein, human ; M1 protein, Influenza A virus ; Receptors, Antigen, T-Cell ; Viral Matrix Proteins ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2017-12-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	2557172-2
ISSN	2150-7511 ; 2161-2129
ISSN (online)	2150-7511
ISSN	2161-2129
DOI	10.1128/mBio.01841-17
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Article ; Online: Unique influenza A cross-reactive memory CD8 T-cell receptor repertoire has a potential to protect against EBV seroconversion.

Watkin, Levi B / Mishra, Rabinarayan / Gil, Anna / Aslan, Nuray / Ghersi, Dario / Luzuriaga, Katherine / Selin, Liisa K

The Journal of allergy and clinical immunology

2017 Volume 140, Issue 4, Page(s) 1206–1210

MeSH term(s)	Adolescent ; Adult ; CD8-Positive T-Lymphocytes/immunology ; Cross Reactions ; Female ; Herpesvirus 4, Human/immunology ; Humans ; Influenza A virus/immunology ; Male ; Middle Aged ; Receptors, Antigen, T-Cell/immunology ; Seroconversion
Chemical Substances	Receptors, Antigen, T-Cell
Language	English
Publishing date	2017-06-16
Publishing country	United States
Document type	Letter ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2017.05.037
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Article ; Online: Innate PLZF+CD4+ αβ T cells develop and expand in the absence of Itk.

Prince, Amanda L / Watkin, Levi B / Yin, Catherine C / Selin, Liisa K / Kang, Joonsoo / Schwartzberg, Pamela L / Berg, Leslie J

Journal of immunology (Baltimore, Md. : 1950)

2014 Volume 193, Issue 2, Page(s) 673–687

Abstract: T cell development in the thymus produces multiple lineages of cells, including innate T cells. Studies in mice harboring alterations in TCR signaling proteins or transcriptional regulators have revealed an expanded population of CD4(+) innate T cells in ...

Abstract	T cell development in the thymus produces multiple lineages of cells, including innate T cells. Studies in mice harboring alterations in TCR signaling proteins or transcriptional regulators have revealed an expanded population of CD4(+) innate T cells in the thymus that produce IL-4 and express the transcription factor promyelocytic leukemia zinc finger (PLZF). In these mice, IL-4 produced by the CD4(+)PLZF(+) T cell population leads to the conversion of conventional CD8(+) thymocytes into innate CD8(+) T cells resembling memory T cells expressing eomesodermin. The expression of PLZF, the signature invariant NKT cell transcription factor, in these innate CD4(+) T cells suggests that they might be a subset of αβ or γδ TCR(+) NKT cells or mucosal-associated invariant T (MAIT) cells. To address these possibilities, we characterized the CD4(+)PLZF(+) innate T cells in itk(-/-) mice. We show that itk(-/-) innate PLZF(+)CD4(+) T cells are not CD1d-dependent NKT cells, MR1-dependent MAIT cells, or γδ T cells. Furthermore, although the itk(-/-) innate PLZF(+)CD4(+) T cells express αβ TCRs, neither β2-microglobulin-dependent MHC class I nor any MHC class II molecules are required for their development. In contrast to invariant NKT cells and MAIT cells, this population has a highly diverse TCRα-chain repertoire. Analysis of peripheral tissues indicates that itk(-/-) innate PLZF(+)CD4(+) T cells preferentially home to spleen and mesenteric lymph nodes owing to increased expression of gut-homing receptors, and that their expansion is regulated by commensal gut flora. These data support the conclusion that itk(-/-) innate PLZF(+)CD4(+) T cells are a novel subset of innate T cells.
MeSH term(s)	Animals ; Antigens, CD1d/immunology ; Antigens, CD1d/metabolism ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/metabolism ; Cell Differentiation/genetics ; Cell Differentiation/immunology ; Cell Proliferation ; Cells, Cultured ; Flow Cytometry ; Gene Expression/immunology ; H-2 Antigens/genetics ; H-2 Antigens/immunology ; H-2 Antigens/metabolism ; Interleukin-4/genetics ; Interleukin-4/immunology ; Interleukin-4/metabolism ; Kruppel-Like Transcription Factors/immunology ; Kruppel-Like Transcription Factors/metabolism ; Lymph Nodes/immunology ; Lymph Nodes/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Promyelocytic Leukemia Zinc Finger Protein ; Protein-Tyrosine Kinases/deficiency ; Protein-Tyrosine Kinases/genetics ; Protein-Tyrosine Kinases/immunology ; Receptors, Antigen, T-Cell, alpha-beta/genetics ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; Receptors, Antigen, T-Cell, alpha-beta/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Spleen/immunology ; Spleen/metabolism ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism ; Thymocytes/immunology ; Thymocytes/metabolism ; beta 2-Microglobulin/immunology ; beta 2-Microglobulin/metabolism
Chemical Substances	Antigens, CD1d ; H-2 Antigens ; Kruppel-Like Transcription Factors ; Promyelocytic Leukemia Zinc Finger Protein ; Receptors, Antigen, T-Cell, alpha-beta ; Zbtb16 protein, mouse ; beta 2-Microglobulin ; Interleukin-4 (207137-56-2) ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; emt protein-tyrosine kinase (EC 2.7.10.2)
Language	English
Publishing date	2014-06-13
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.1302058
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Article: First Case of

Pedroza, Luis Alberto / Guerrero, Nina / Stray-Pedersen, Asbjørg / Tafur, Cristina / Macias, Roque / Muñoz, Greta / Akdemir, Zeynep Coban / Jhangiani, Shalini N / Watkin, Levi B / Chinn, Ivan K / Lupski, James R / Orange, Jordan S

Frontiers in pediatrics

2017 Volume 5, Page(s) 17

Abstract: Severe infections ... ...

Abstract	Severe infections with
Language	English
Publishing date	2017-02-10
Publishing country	Switzerland
Document type	Case Reports
ZDB-ID	2711999-3
ISSN	2296-2360
ISSN	2296-2360
DOI	10.3389/fped.2017.00017
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Article ; Online: Copa Syndrome: a Novel Autosomal Dominant Immune Dysregulatory Disease.

Vece, Timothy J / Watkin, Levi B / Nicholas, Sarah / Canter, Debra / Braun, Michael C / Guillerman, R Paul / Eldin, Karen W / Bertolet, Grant / McKinley, Scott / de Guzman, Marietta / Forbes, Lisa / Chinn, Ivan / Orange, Jordan S

Journal of clinical immunology

2016 Volume 36, Issue 4, Page(s) 377–387

Abstract: Inherently defective immunity typically results in either ineffective host defense, immune regulation, or both. As a category of primary immunodeficiency diseases, those that impair immune regulation can lead to autoimmunity and/or autoinflammation. In ... ...

Abstract	Inherently defective immunity typically results in either ineffective host defense, immune regulation, or both. As a category of primary immunodeficiency diseases, those that impair immune regulation can lead to autoimmunity and/or autoinflammation. In this review we focus on one of the most recently discovered primary immunodeficiencies that leads to immune dysregulation: "Copa syndrome". Copa syndrome is named for the gene mutated in the disease, which encodes the alpha subunit of the coatomer complex-I that, in aggregate, is devoted to transiting molecular cargo from the Golgi complex to the endoplasmic reticulum (ER). Copa syndrome is autosomal dominant with variable expressivity and results from mutations affecting a narrow amino acid stretch in the COPA gene-encoding COPα protein. Patients with these mutations typically develop arthritis and interstitial lung disease with pulmonary hemorrhage representing a striking feature. Immunologically Copa syndrome is associated with autoantibody development, increased Th17 cells and pro-inflammatory cytokine expression including IL-1β and IL-6. Insights have also been gained into the underlying mechanism of Copa syndrome, which include excessive ER stress owing to the impaired return of proteins from the Golgi, and presumably resulting aberrant cellular autophagy. As such it represents a novel cellular disorder of intracellular trafficking associated with a specific clinical presentation and phenotype.
MeSH term(s)	Arthritis/genetics ; Arthritis/immunology ; Arthritis/pathology ; Coatomer Protein/genetics ; Humans ; Immunologic Deficiency Syndromes/genetics ; Immunologic Deficiency Syndromes/immunology ; Immunologic Deficiency Syndromes/pathology ; Kidney Diseases/genetics ; Kidney Diseases/immunology ; Kidney Diseases/pathology ; Lung Diseases/genetics ; Lung Diseases/immunology ; Lung Diseases/pathology
Chemical Substances	Coatomer Protein
Language	English
Publishing date	2016-04-05
Publishing country	Netherlands
Document type	Editorial ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	779361-3
ISSN	1573-2592 ; 0271-9142
ISSN (online)	1573-2592
ISSN	0271-9142
DOI	10.1007/s10875-016-0271-8
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Article: Analysis of the role of bleomycin hydrolase in antigen presentation and the generation of CD8 T cell responses.

Towne, Charles F / York, Ian A / Watkin, Levi B / Lazo, John S / Rock, Kenneth L

Journal of immunology (Baltimore, Md. : 1950)

2007 Volume 178, Issue 11, Page(s) 6923–6930

Abstract: Long oligopeptides (>10 residues) are generated during the catabolism of cellular proteins in the cytosol. To be presented to T cells, such peptides must be trimmed by aminopeptidases to the proper size (typically 8-10 residues) to stably bind to MHC ... ...

Abstract	Long oligopeptides (>10 residues) are generated during the catabolism of cellular proteins in the cytosol. To be presented to T cells, such peptides must be trimmed by aminopeptidases to the proper size (typically 8-10 residues) to stably bind to MHC class I molecules. Aminopeptidases also destroy epitopes by trimming them to even shorter lengths. Bleomycin hydrolase (BH) is a cytosolic aminopeptidase that has been suggested to play a key role in generating MHC class I-presented peptides. We show that BH-deficient cells from mice are unimpaired in their ability to present epitopes from N-extended precursors or whole Ags and express normal levels of MHC class I molecules. Similarly, BH-deficient mice develop normal CD8(+) T cell responses to eight epitopes from three different viruses in vivo. Therefore, BH by itself is not essential for the generation or destruction of MHC class I peptides. In contrast, when BH(-/-) mice are crossed to mice lacking another cytosolic aminopeptidase, leucine aminopeptidase, the resulting BH(-/-)leucine aminopeptidase(-/-) progeny show a selective increase in CD8(+) T cell responses to the gp276 epitope from lymphocytic choriomeningitis virus, whereas the ability to present and respond to several other epitopes is unchanged. Therefore, BH does influence presentation of some Ags, although its role is largely redundant with other aminopeptidases.
MeSH term(s)	Aminopeptidases/immunology ; Aminopeptidases/metabolism ; Animals ; Antigen Presentation/genetics ; Antigen Presentation/immunology ; CD8-Positive T-Lymphocytes/enzymology ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/virology ; Cells, Cultured ; Cysteine Endopeptidases/biosynthesis ; Cysteine Endopeptidases/deficiency ; Cysteine Endopeptidases/genetics ; Cysteine Endopeptidases/physiology ; Cytotoxicity, Immunologic/genetics ; Egg Proteins/immunology ; Egg Proteins/metabolism ; Embryonic Stem Cells/immunology ; Embryonic Stem Cells/metabolism ; Epitopes, T-Lymphocyte/immunology ; Epitopes, T-Lymphocyte/metabolism ; Fibroblasts/immunology ; Fibroblasts/metabolism ; Histocompatibility Antigens Class I/immunology ; Histocompatibility Antigens Class I/metabolism ; Immunodominant Epitopes/immunology ; Immunodominant Epitopes/metabolism ; Leucyl Aminopeptidase/deficiency ; Leucyl Aminopeptidase/genetics ; Membrane Glycoproteins/immunology ; Membrane Glycoproteins/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Minor Histocompatibility Antigens ; Ovalbumin/immunology ; Ovalbumin/metabolism ; Peptide Fragments/immunology ; Peptide Fragments/metabolism ; Viral Envelope Proteins/immunology ; Viral Envelope Proteins/metabolism
Chemical Substances	Egg Proteins ; Epitopes, T-Lymphocyte ; G protein, vesicular stomatitis virus ; Histocompatibility Antigens Class I ; Immunodominant Epitopes ; Membrane Glycoproteins ; Minor Histocompatibility Antigens ; OVA-8 ; Peptide Fragments ; Viral Envelope Proteins ; Ovalbumin (9006-59-1) ; Aminopeptidases (EC 3.4.11.-) ; ERAP1 protein, mouse (EC 3.4.11.-) ; Leucyl Aminopeptidase (EC 3.4.11.1) ; Cysteine Endopeptidases (EC 3.4.22.-) ; bleomycin hydrolase (EC 3.4.22.40)
Language	English
Publishing date	2007-04-27
Publishing country	United States
Document type	Comparative Study ; 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.178.11.6923
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Article ; Online: Cell biological steps and checkpoints in accessing NK cell cytotoxicity.

Mace, Emily M / Dongre, Prachi / Hsu, Hsiang-Ting / Sinha, Papiya / James, Ashley M / Mann, Shaina S / Forbes, Lisa R / Watkin, Levi B / Orange, Jordan S

Immunology and cell biology

2014 Volume 92, Issue 3, Page(s) 245–255

Abstract: Natural killer (NK) cell-mediated cytotoxicity is governed by the formation of a lytic immune synapse in discrete regulated steps, which give rise to an extensive array of cellular checkpoints in accessing NK cell-mediated cytolytic defense. Appropriate ... ...

Abstract	Natural killer (NK) cell-mediated cytotoxicity is governed by the formation of a lytic immune synapse in discrete regulated steps, which give rise to an extensive array of cellular checkpoints in accessing NK cell-mediated cytolytic defense. Appropriate progression through these cell biological steps is critical for the directed secretion of specialized secretory lysosomes and subsequent target cell death. Here we highlight recent discoveries in the formation of the NK cell cytolytic synapse as well as the molecular steps and cell biological checkpoints required for this essential host defense process.
MeSH term(s)	Animals ; Cell Cycle Checkpoints ; Cytotoxicity, Immunologic ; Humans ; Immunological Synapses/immunology ; Killer Cells, Natural/cytology ; Killer Cells, Natural/immunology
Language	English
Publishing date	2014-01-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	284057-1
ISSN	1440-1711 ; 0818-9641
ISSN (online)	1440-1711
ISSN	0818-9641
DOI	10.1038/icb.2013.96
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