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Article ; Online: Risk of noise-induced hearing loss in the spine surgeon.

Meade, Matthew H / Kwan, Stephanie A / Michael, Mark E / Minissale, Nicholas J / Buchan, Levi / Gleimer, Jeffrey R / Woods, Barrett I / Kepler, Christopher

North American Spine Society journal

2023 Volume 17, Page(s) 100297

Abstract: Background: Occupation-related noise-induced hearing loss (NIHL) has both negative economic and quality of life implications. The risk spine surgeons undertake in regards to NIHL during operative intervention is unknown. Governing bodies, including the ... ...

Abstract	Background: Occupation-related noise-induced hearing loss (NIHL) has both negative economic and quality of life implications. The risk spine surgeons undertake in regards to NIHL during operative intervention is unknown. Governing bodies, including the National Institute for Occupational Safety and Health, have recommended exposure limits not to exceed 85 decibels (dB) over 8 hours. The purpose of this study is to characterize noise exposure to spine surgeons in the operating room (OR). Methods: Prospective collection of intraoperative recordings of spinal surgeries (cervical and thoracic/lumbar) was undertaken. Data gathered included procedure, operative duration, presence of background music, and noise information. Noise information included maximum decibel level (MDL), Peak level (LCPeak), Equivalent continuous sound pressure level, time weighted average (TWA), dose, and projected dose. Noise measurements were compared with baseline controls with and without music (empty ORs). Results: Two hundred seven noise recordings were analyzed. One hundred eighteen of those being spinal surgeries, 49 baseline recordings without music, and 40 with music. Maximum decibel level reached a maximum value of 111.5 dBA, with an average amongst surgical recordings of 103 dBA. Maximum decibel level exceeded 85 dBA in 100% of cases and was greater than 100 dBA in 78%. The maximum LCPeak recorded was 132.9 dBC with an average of 120 dBC. Furthermore, the average dose was 7.8% with an average projected dose of 26.5%. The highest dose occurred during a laminectomy at 72.9% of daily allowable noise. Maximum projected dose yielded 156% during a 3-level anterior cervical discectomy and fusion. Conclusions: Spine surgeons are routinely exposed to damaging noise levels (>85 dBA) during operative intervention. With spine surgeons often performing multiple surgeries a day, the cumulative risk of noise exposure cannot be ignored. The synergistic effects of continuous and impact noise places spine surgeons at risk for the development of occupation-related NIHL.
Language	English
Publishing date	2023-11-24
Publishing country	United States
Document type	Journal Article
ISSN	2666-5484
ISSN (online)	2666-5484
DOI	10.1016/j.xnsj.2023.100297
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Article ; Online: Thymocyte selection: chemokine signaling is not only about the destination.

Gleimer, Michael / von Boehmer, Harald

Current biology : CB

2010 Volume 20, Issue 7, Page(s) R316–8

Abstract: The development and function of lymphocytes depend upon their precise migration in response to chemoattractant cytokines, or chemokines. Two recent reports suggest that, during thymic beta-selection, the binding of the chemokine CXCL12 to the receptor ... ...

Abstract	The development and function of lymphocytes depend upon their precise migration in response to chemoattractant cytokines, or chemokines. Two recent reports suggest that, during thymic beta-selection, the binding of the chemokine CXCL12 to the receptor CXCR4 on thymocytes provides not only directional but also developmental cues.
MeSH term(s)	Animals ; Apoptosis ; Cell Differentiation ; Cell Proliferation ; Chemokine CXCL12/metabolism ; Chemokines/metabolism ; Chemotaxis, Leukocyte ; Humans ; Lymphocyte Activation ; Models, Immunological ; Receptors, CXCR4/metabolism ; Signal Transduction/immunology ; T-Lymphocytes/cytology ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism
Chemical Substances	Chemokine CXCL12 ; Chemokines ; Receptors, CXCR4
Language	English
Publishing date	2010-04-13
Publishing country	England
Document type	Journal Article
ZDB-ID	1071731-6
ISSN	1879-0445 ; 0960-9822
ISSN (online)	1879-0445
ISSN	0960-9822
DOI	10.1016/j.cub.2010.02.018
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Article ; Online: PLZF Controls the Expression of a Limited Number of Genes Essential for NKT Cell Function.

Gleimer, Michael / von Boehmer, Harald / Kreslavsky, Taras

Frontiers in immunology

2012 Volume 3, Page(s) 374

Abstract: Natural killer (NKT) T cells exhibit tissue distribution, surface phenotype, and functional responses that are strikingly different from those of conventional T cells. The transcription factor PLZF is responsible for most of these properties, as its ... ...

Abstract	Natural killer (NKT) T cells exhibit tissue distribution, surface phenotype, and functional responses that are strikingly different from those of conventional T cells. The transcription factor PLZF is responsible for most of these properties, as its ectopic expression in conventional T cells is sufficient to confer to them an NKT-like phenotype. The molecular program downstream of PLZF, however, is largely unexplored. Here we report that PLZF regulates the expression of a surprisingly small set of genes, many with known immune functions. This includes several established components of the NKT cell developmental program. Expression of the transcriptional regulators Id2, previously shown to be required for iNKT cell survival in the liver and c-Maf, which shapes the NKT cytokine profile, was compromised in PLZF-deficient cells. Ectopic expression of c-Maf complemented the cells' defect in producing IL-4 and IL-10. PLZF also induced a program of cell surface receptors which shape the NKT cell's response to external stimuli, including the costimulatory receptor ICOS and the cytokine receptors IL12rb1 and IL18r1. As an ensemble, the known functions of the molecules whose expression is affected by PLZF explain many defects observed in PLZF(-/-) NKT cells.
Language	English
Publishing date	2012-12-21
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2012.00374
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Article ; Online: Alphabeta versus gammadelta lineage choice at the first TCR-controlled checkpoint.

Kreslavsky, Taras / Gleimer, Michael / von Boehmer, Harald

Current opinion in immunology

2010 Volume 22, Issue 2, Page(s) 185–192

Abstract: Alphabeta and gammadelta T cells develop in the thymus from a common precursor. Although lineages initially were defined by the type of TCR they express, it soon became clear that the TCR type per se does not play a deterministic role in the lineage ... ...

Abstract	Alphabeta and gammadelta T cells develop in the thymus from a common precursor. Although lineages initially were defined by the type of TCR they express, it soon became clear that the TCR type per se does not play a deterministic role in the lineage decision, since in various transgenic and knockout models, as well as in a small fraction of cells in wt mice, the TCRgammadelta can drive the differentiation of alphabeta lineage cells and the TCRalphabeta can drive differentiation of gammadelta lineage cells. Thus until recently it was unclear what determines lineage choice and at which stage the two lineages diverge. Recent observations suggest that TCR signal strength determines lineage fate and that lineage choice is made at or shortly after the first TCR-controlled checkpoint. While it is clear that the decision between alphabeta and gammadelta lineages is made at the first TCR-controlled checkpoint and the alphabeta sublineages split off later, it is less clear whether gammadelta sublineages divert already at the first TCR-controlled checkpoint or later. Recent experiments support the former view.
MeSH term(s)	Animals ; Cell Lineage ; Humans ; Lymphopoiesis ; Precursor Cells, T-Lymphoid/immunology ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; Receptors, Antigen, T-Cell, gamma-delta/immunology ; Receptors, Notch/immunology ; Signal Transduction/immunology ; T-Lymphocytes/immunology
Chemical Substances	Receptors, Antigen, T-Cell, alpha-beta ; Receptors, Antigen, T-Cell, gamma-delta ; Receptors, Notch
Language	English
Publishing date	2010-01-13
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	1035767-1
ISSN	1879-0372 ; 0952-7915
ISSN (online)	1879-0372
ISSN	0952-7915
DOI	10.1016/j.coi.2009.12.006
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Article: Stress management: MHC class I and class I-like molecules as reporters of cellular stress.

Gleimer, Michael / Parham, Peter

Immunity

2003 Volume 19, Issue 4, Page(s) 469–477

Abstract: The evolutionarily ancient intracellular stress response protects cells from the effects of external and internal forces which perturb cellular metabolism. Members of the major histocompatibility complex (MHC) class I-like superfamily act as cell surface ...

Abstract	The evolutionarily ancient intracellular stress response protects cells from the effects of external and internal forces which perturb cellular metabolism. Members of the major histocompatibility complex (MHC) class I-like superfamily act as cell surface indicators of the intracellular stress response. Cellular immunity employs these indicators as a cue for elimination of damaged, infected, and malignant cells, promoting the health of the individual and the evolutionary success of the species.
MeSH term(s)	Animals ; Biomarkers ; Chaperonin 60/metabolism ; Evolution, Molecular ; Histocompatibility Antigens Class I/genetics ; Histocompatibility Antigens Class I/physiology ; Humans ; Mice ; Multigene Family ; Receptors, Immunologic/metabolism ; Receptors, Natural Killer Cell ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism
Chemical Substances	Biomarkers ; Chaperonin 60 ; Histocompatibility Antigens Class I ; Receptors, Immunologic ; Receptors, Natural Killer Cell
Language	English
Publishing date	2003-08-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/s1074-7613(03)00272-3
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Article ; Online: αβ versus γδ fate choice: counting the T-cell lineages at the branch point.

Kreslavsky, Taras / Gleimer, Michael / Garbe, Annette I / von Boehmer, Harald

Immunological reviews

2010 Volume 238, Issue 1, Page(s) 169–181

Abstract: Both αβ and γδ T cells develop in the thymus from a common progenitor. Historically distinguished by their T-cell receptor (TCR), these lineages are now defined on the basis of distinct molecular programs. Intriguingly, in many transgenic and knockout ... ...

Abstract	Both αβ and γδ T cells develop in the thymus from a common progenitor. Historically distinguished by their T-cell receptor (TCR), these lineages are now defined on the basis of distinct molecular programs. Intriguingly, in many transgenic and knockout systems these programs are mismatched with the TCR type, leading to the development of γδ lineage cells driven by αβTCR and vice versa. These puzzling observations were recently explained by the demonstration that TCR signal strength, rather than TCR type per se, instructs lineage fate, with stronger TCR signal favoring γδ and weaker signal favoring αβ lineage fates. These studies also highlighted the ERK (extracellular signal regulated kinase)-Egr (early growth response)-Id3 (inhibitor of differentiation 3) axis as a potential molecular switch downstream of TCR that determines lineage choice. Indeed, removal of Id3 was sufficient to redirect TCRγδ transgenic cells to the αβ lineage, even in the presence of strong TCR signal. However, in TCR non-transgenic Id3 knockout mice the overall number of γδ lineage cells was increased due to an outgrowth of a Vγ1Vδ6.3 subset, suggesting that not all γδ T cells depend on this molecular switch for lineage commitment. Thus, the γδ lineage may in fact be a collection of two or more lineages not sharing a common molecular program and thus equipollent to the αβ lineage. TCR signaling is not the only factor that is required for development of αβ and γδ lineage cells; other pathways, such as signaling from Notch and CXCR4 receptors, cooperate with the TCR in this process.
MeSH term(s)	Animals ; Cell Differentiation/genetics ; Cell Lineage/genetics ; Humans ; Inhibitor of Differentiation Proteins/genetics ; Inhibitor of Differentiation Proteins/immunology ; Mice ; Mice, Knockout ; Mice, Transgenic ; Protein Binding/immunology ; Receptor Cross-Talk/immunology ; Receptors, Antigen, T-Cell, alpha-beta/immunology ; Receptors, Antigen, T-Cell, gamma-delta/immunology ; Signal Transduction/immunology ; T-Lymphocytes/immunology
Chemical Substances	Inhibitor of Differentiation Proteins ; Receptors, Antigen, T-Cell, alpha-beta ; Receptors, Antigen, T-Cell, gamma-delta ; Idb3 protein, mouse (135845-89-5)
Language	English
Publishing date	2010-10-22
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	391796-4
ISSN	1600-065X ; 0105-2896
ISSN (online)	1600-065X
ISSN	0105-2896
DOI	10.1111/j.1600-065X.2010.00947.x
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Article ; Online: A Distinctive Cytoplasmic Tail Contributes to Low Surface Expression and Intracellular Retention of the Patr-AL MHC Class I Molecule.

Goyos, Ana / Guethlein, Lisbeth A / Horowitz, Amir / Hilton, Hugo G / Gleimer, Michael / Brodsky, Frances M / Parham, Peter

Journal of immunology (Baltimore, Md. : 1950)

2015 Volume 195, Issue 8, Page(s) 3725–3736

Abstract: Chimpanzees have orthologs of the six fixed, functional human MHC class I genes. But, in addition, the chimpanzee has a seventh functional gene, Patr-AL, which is not polymorphic but contributes substantially to population diversity by its presence on ... ...

Abstract	Chimpanzees have orthologs of the six fixed, functional human MHC class I genes. But, in addition, the chimpanzee has a seventh functional gene, Patr-AL, which is not polymorphic but contributes substantially to population diversity by its presence on only 50% of MHC haplotypes. The ancestral AL gene emerged long before the separation of human and chimpanzee ancestors and then subsequently and specifically lost function during human evolution, but was maintained in chimpanzees. Patr-AL is an alloantigen that participates in negative and positive selection of the T cell repertoire. The three-dimensional structure and the peptide-binding repertoire of Patr-AL and HLA-A02 are surprisingly similar. In contrast, the expression of these two molecules is very different, as shown using specific mAbs and polyclonal Abs made against Patr-AL. Peripheral blood cells and B cell lines express low levels of Patr-AL at the cell surface. Higher levels are seen for 221-cell transfectants expressing Patr-AL, but in these cells a large majority of Patr-AL molecules are retained in the early compartments of the secretory pathway: mainly the endoplasmic reticulum, but also cis-Golgi. Replacing the cytoplasmic tail of Patr-AL with that of HLA-A02 increased the cell-surface expression of Patr-AL substantially. Four substitutions distinguish the Patr-AL and HLA-A*02 cytoplasmic tails. Systematic mutagenesis showed that each substitution contributes changes in cell-surface expression. The combination of residues present in Patr-AL appears unique, but each individual residue is present in other primate MHC class I molecules, notably MHC-E, the most ancient of the functional human MHC class I molecules.
MeSH term(s)	Animals ; B-Lymphocytes/cytology ; B-Lymphocytes/immunology ; Cell Line, Transformed ; Cell Membrane/genetics ; Cell Membrane/immunology ; Endoplasmic Reticulum/genetics ; Endoplasmic Reticulum/immunology ; Gene Expression Regulation/genetics ; Gene Expression Regulation/immunology ; Golgi Apparatus/genetics ; Golgi Apparatus/immunology ; HLA-A2 Antigen/genetics ; HLA-A2 Antigen/immunology ; Humans ; Pan troglodytes ; Protein Structure, Tertiary
Chemical Substances	HLA-A*02 antigen ; HLA-A2 Antigen
Language	English
Publishing date	2015-10-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
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.1500397
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Article ; Online: β-Selection-induced proliferation is required for αβ T cell differentiation.

Kreslavsky, Taras / Gleimer, Michael / Miyazaki, Masaki / Choi, Yoon / Gagnon, Etienne / Murre, Cornelis / Sicinski, Piotr / von Boehmer, Harald

Immunity

2012 Volume 37, Issue 5, Page(s) 840–853

Abstract: Proliferation and differentiation are tightly coordinated to produce an appropriate number of differentiated cells and often exhibit an antagonistic relationship. Developing T cells, which arise in the thymus from a minute number of bone-marrow-derived ... ...

Abstract	Proliferation and differentiation are tightly coordinated to produce an appropriate number of differentiated cells and often exhibit an antagonistic relationship. Developing T cells, which arise in the thymus from a minute number of bone-marrow-derived progenitors, undergo a major expansion upon pre-T cell receptor (TCR) expression. The burst of proliferation coincides with differentiation toward the αβ T cell lineage-but the two processes were previously thought to be independent from one another, although both were driven by signaling from pre-TCR and Notch receptors. Here we report that proliferation at this step was not only absolutely required for differentiation but also that its ectopic activation was sufficient to substantially rescue differentiation in the absence of Notch signaling. Consistently, pharmacological inhibition of the cell cycle machinery also blocked differentiation in vivo. Thus the proliferation step is strictly required prior to differentiation of immature thymocytes.
MeSH term(s)	Animals ; Cell Differentiation/immunology ; Cell Division/immunology ; Cell Division/physiology ; Cell Growth Processes/physiology ; Cell Lineage ; Cells, Cultured ; Lymphocyte Activation ; Mice ; Receptors, Antigen, T-Cell/immunology ; Receptors, Antigen, T-Cell/metabolism ; Receptors, Notch/immunology ; Receptors, Notch/metabolism ; Signal Transduction/immunology ; Signal Transduction/physiology ; T-Lymphocytes/cytology ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism ; Thymocytes/immunology ; Thymocytes/metabolism ; Thymocytes/physiology ; Transcription Factors/immunology ; Transcription Factors/metabolism
Chemical Substances	Receptors, Antigen, T-Cell ; Receptors, Notch ; Transcription Factors
Language	English
Publishing date	2012-11-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2012.08.020
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Article: Synergistic polymorphism at two positions distal to the ligand-binding site makes KIR2DL2 a stronger receptor for HLA-C than KIR2DL3.

Moesta, Achim K / Norman, Paul J / Yawata, Makoto / Yawata, Nobuyo / Gleimer, Michael / Parham, Peter

Journal of immunology (Baltimore, Md. : 1950)

2008 Volume 180, Issue 6, Page(s) 3969–3979

Abstract: Interactions between HLA-C ligands and inhibitory killer cell Ig-like receptors (KIR) control the development and response of human NK cells. This regulatory mechanism is usually described by mutually exclusive interactions of KIR2DL1 with C2 having ... ...

Abstract	Interactions between HLA-C ligands and inhibitory killer cell Ig-like receptors (KIR) control the development and response of human NK cells. This regulatory mechanism is usually described by mutually exclusive interactions of KIR2DL1 with C2 having lysine 80, and KIR2DL2/3 with C1 having asparagine 80. Consistent with this simple rule, we found from functional analysis and binding assays to 93 HLA-A, HLA-B, and HLA-C isoforms that KIR2DL1003 bound all C2, and only C2, allotypes. The allotypically related KIR2DL2001 and KIR2DL3001 interacted with all C1, but they violated the simple rule through interactions with several C2 allotypes, notably Cw0501 and Cw0202, and two HLA-B allotypes (B4601 and B7301) that share polymorphisms with HLA-C. Although the specificities of the "cross-reactions" were similar for KIR2DL2001 and KIR2DL3001, they were stronger for KIR2DL2001, as were the reactions with C1. Mutagenesis explored the avidity difference between KIR2DL2001 and KIR2DL3001. Recombinant mutants mapped the difference to the Ig-like domains, where site-directed mutagenesis showed that the combination, but not the individual substitutions, of arginine for proline 16 in D1 and cysteine for arginine 148 in D2 made KIR2DL2001 a stronger receptor than KIR2DL3001. Neither residue 16 or 148 is part of, or near to, the ligand-binding site. Instead, their juxtaposition near the flexible hinge between D1 and D2 suggests that their polymorphisms affect the ligand-binding site by changing the hinge angle and the relative orientation of the two domains. This study demonstrates how allelic polymorphism at sites distal to the ligand-binding site of KIR2DL2/3 has diversified this receptor's interactions with HLA-C.
MeSH term(s)	Alleles ; Amino Acid Substitution/genetics ; Amino Acid Substitution/immunology ; Binding Sites/genetics ; Binding Sites/immunology ; Cell Line, Tumor ; Cytotoxicity, Immunologic/genetics ; HLA-C Antigens/genetics ; HLA-C Antigens/metabolism ; Humans ; Killer Cells, Natural/immunology ; Killer Cells, Natural/metabolism ; Ligands ; Mutagenesis, Site-Directed ; Polymorphism, Genetic ; Protein Binding/genetics ; Protein Binding/immunology ; Receptors, KIR2DL1/genetics ; Receptors, KIR2DL1/immunology ; Receptors, KIR2DL1/metabolism ; Receptors, KIR2DL2/biosynthesis ; Receptors, KIR2DL2/genetics ; Receptors, KIR2DL2/metabolism ; Receptors, KIR2DL3/biosynthesis ; Receptors, KIR2DL3/genetics ; Receptors, KIR2DL3/metabolism
Chemical Substances	HLA-C Antigens ; KIR2DL1 protein, human ; KIR2DL2 protein, human ; KIR2DL3 protein, human ; Ligands ; Receptors, KIR2DL1 ; Receptors, KIR2DL2 ; Receptors, KIR2DL3
Language	English
Publishing date	2008-03-05
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
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.180.6.3969
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Article: Continuous T cell receptor signaling required for synapse maintenance and full effector potential.

Huppa, Johannes B / Gleimer, Michael / Sumen, Cenk / Davis, Mark M

Nature immunology

2003 Volume 4, Issue 8, Page(s) 749–755

Abstract: Although signals through the T cell receptor (TCR) are essential for the initiation of T helper cell activation, it is unclear what function such signals have during the prolonged T cell-antigen-presenting cell contact. Here we simultaneously tracked TCR- ...

Abstract	Although signals through the T cell receptor (TCR) are essential for the initiation of T helper cell activation, it is unclear what function such signals have during the prolonged T cell-antigen-presenting cell contact. Here we simultaneously tracked TCR-CD3 complex and phosphoinositide 3-kinase activity in single T cells using three-dimensional video microscopy. Despite rapid internalization of most of the TCR-CD3, TCR-dependent signaling was still evident up to 10 h after conjugate formation. Blocking this interaction caused dissolution of the synapse and proportional reductions in interleukin 2 production and cellular proliferation. Thus TCR signaling persists for hours, has a cumulative effect and is necessary for the maintenance of the immunological synapse.
MeSH term(s)	Animals ; Antigen Presentation ; CD3 Complex/immunology ; CD3 Complex/metabolism ; Calcium/immunology ; Calcium/metabolism ; Cell Communication/immunology ; Lymphocyte Activation/immunology ; Mice ; Receptors, Antigen, T-Cell/immunology ; Receptors, Antigen, T-Cell/metabolism ; Signal Transduction/immunology ; T-Lymphocytes, Helper-Inducer/immunology
Chemical Substances	CD3 Complex ; CD3 antigen, zeta chain ; Receptors, Antigen, T-Cell ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2003-08
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/ni951
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