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Article ; Online: Neutrophils in lupus nephritis.

Nishi, Hiroshi / Mayadas, Tanya N

2018 Volume 31, Issue 2, Page(s) 193–200

Abstract: Purpose of review: Systemic lupus erythematosus (SLE) is a multiorgan autoimmune disease characterized by IgG-autoantibodies to nuclear antigens that can deposit in the kidney and trigger lupus nephritis. Neutrophils accumulate in the kidneys of ... ...

Abstract	Purpose of review: Systemic lupus erythematosus (SLE) is a multiorgan autoimmune disease characterized by IgG-autoantibodies to nuclear antigens that can deposit in the kidney and trigger lupus nephritis. Neutrophils accumulate in the kidneys of patients with proliferative LUPUS NEPHRITIS and neutrophil products and a subset of granulocytes, called low-density granulocytes (LDG) may contribute to lupus nephritis pathogenesis. Here, we will discuss recent studies implicating neutrophils in the pathogenesis of human SLE nephritis and then examine studies that provide mechanistic insights into how these cells are recruited to the glomerulus following immune complex deposition and how their products may promote lupus nephritis. Recent findings: SLE patients display unique blood transcriptional signatures linked to Type I interferon and myeloblast differentiation, which could help stratify lupus nephritis progression. Multiphoton intravital microscopy of kidney glomerular capillaries revealed a role for neutrophil FcγRs in the rapid capture of neutrophils following immune complex deposition. The view that reduced degradation of neutrophil extracellular traps (NETS) contributes to lupus nephritis progression, is now challenged by experimental data in lupus-prone mice that genetically fail to produce NETS but still are afflicted. Summary: A greater understanding of the neutrophil dependent mechanisms that promote lupus nephritis may potentially inform on newer therapeutic options that target neutrophil accumulation and reactivity in the nephritic kidney.
MeSH term(s)	Animals ; Autoantibodies/immunology ; Autoimmunity ; Extracellular Traps/immunology ; Humans ; Lupus Nephritis/immunology ; Neutrophils/immunology
Chemical Substances	Autoantibodies
Language	English
Publishing date	2018-12-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1045317-9
ISSN	1531-6963 ; 1040-8711
ISSN (online)	1531-6963
ISSN	1040-8711
DOI	10.1097/BOR.0000000000000577
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Article ; Online: The many faces of Mac-1 in autoimmune disease.

Rosetti, Florencia / Mayadas, Tanya N

Immunological reviews

2016 Volume 269, Issue 1, Page(s) 175–193

Abstract: Mac-1 (CD11b/CD18) is a β2 integrin classically regarded as a pro-inflammatory molecule because of its ability to promote phagocyte cytotoxic functions and enhance the function of several effector molecules such as FcγR, uPAR, and CD14. Nevertheless, ... ...

Abstract	Mac-1 (CD11b/CD18) is a β2 integrin classically regarded as a pro-inflammatory molecule because of its ability to promote phagocyte cytotoxic functions and enhance the function of several effector molecules such as FcγR, uPAR, and CD14. Nevertheless, recent reports have revealed that Mac-1 also plays significant immunoregulatory roles, and genetic variants in ITGAM, the gene that encodes CD11b, confer risk for the autoimmune disease systemic lupus erythematosus (SLE). This has renewed interest in the physiological roles of this integrin and raised new questions on how its seemingly opposing biological functions may be regulated. Here, we provide an overview of the CD18 integrins and how their activation may be regulated as this may shed light on how the opposing roles of Mac-1 may be elicited. We then discuss studies that exemplify Mac-1's pro-inflammatory versus regulatory roles particularly in the context of IgG immune complex-mediated inflammation. This includes a detailed examination of molecular mechanisms that could explain the risk-conferring effect of rs1143679, a single nucleotide non-synonymous Mac-1 polymorphism associated with SLE.
MeSH term(s)	Animals ; CD11b Antigen/genetics ; CD11b Antigen/metabolism ; Genetic Predisposition to Disease ; Humans ; Immune Complex Diseases/immunology ; Immunomodulation ; Lupus Erythematosus, Systemic/immunology ; Phagocytosis ; Polymorphism, Genetic ; Risk
Chemical Substances	CD11b Antigen ; ITGAM protein, human
Language	English
Publishing date	2016-01
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.12373
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Article ; Online: Midkine, a middle manager of β2 integrins.

Herter, Jan M / Mayadas, Tanya N

Blood

2014 Volume 123, Issue 12, Page(s) 1777–1779

MeSH term(s)	Animals ; CD18 Antigens/physiology ; Humans ; Inflammation/physiopathology ; Intercellular Signaling Peptides and Proteins/physiology ; Midkine ; Neutrophils/physiology
Chemical Substances	CD18 Antigens ; Intercellular Signaling Peptides and Proteins ; Mdk protein, mouse ; Midkine (137497-38-2)
Language	English
Publishing date	2014-03-20
Publishing country	United States
Document type	Journal Article ; Comment
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood-2014-02-553073
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Article ; Online: Monocytes transition to macrophages within the inflamed vasculature via monocyte CCR2 and endothelial TNFR2.

Mysore, Vijayashree / Tahir, Suhail / Furuhashi, Kazuhiro / Arora, Jatin / Rosetti, Florencia / Cullere, Xavier / Yazbeck, Pascal / Sekulic, Miroslav / Lemieux, Madeleine E / Raychaudhuri, Soumya / Horwitz, Bruce H / Mayadas, Tanya N

The Journal of experimental medicine

2022 Volume 219, Issue 5

Abstract: Monocytes undergo phenotypic and functional changes in response to inflammatory cues, but the molecular signals that drive different monocyte states remain largely undefined. We show that monocytes acquire macrophage markers upon glomerulonephritis and ... ...

Abstract	Monocytes undergo phenotypic and functional changes in response to inflammatory cues, but the molecular signals that drive different monocyte states remain largely undefined. We show that monocytes acquire macrophage markers upon glomerulonephritis and may be derived from CCR2+CX3CR1+ double-positive monocytes, which are preferentially recruited, dwell within glomerular capillaries, and acquire proinflammatory characteristics in the nephritic kidney. Mechanistically, the transition to immature macrophages begins within the vasculature and relies on CCR2 in circulating cells and TNFR2 in parenchymal cells, findings that are recapitulated in vitro with monocytes cocultured with TNF-TNFR2-activated endothelial cells generating CCR2 ligands. Single-cell RNA sequencing of cocultures defines a CCR2-dependent monocyte differentiation path associated with the acquisition of immune effector functions and generation of CCR2 ligands. Immature macrophages are detected in the urine of lupus nephritis patients, and their frequency correlates with clinical disease. In conclusion, CCR2-dependent functional specialization of monocytes into macrophages begins within the TNF-TNFR2-activated vasculature and may establish a CCR2-based autocrine, feed-forward loop that amplifies renal inflammation.
MeSH term(s)	Endothelial Cells ; Humans ; Ligands ; Macrophages ; Monocytes ; Receptors, CCR2/genetics ; Receptors, Tumor Necrosis Factor, Type II/genetics
Chemical Substances	CCR2 protein, human ; Ligands ; Receptors, CCR2 ; Receptors, Tumor Necrosis Factor, Type II ; TNFRSF1B protein, human
Language	English
Publishing date	2022-04-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	218343-2
ISSN	1540-9538 ; 0022-1007
ISSN (online)	1540-9538
ISSN	0022-1007
DOI	10.1084/jem.20210562
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Article ; Online: DOCK4 Regulation of Rho GTPases Mediates Pulmonary Vascular Barrier Function.

Yazbeck, Pascal / Cullere, Xavier / Bennett, Paul / Yajnik, Vijay / Wang, Huan / Kawada, Kenji / Davis, Vanessa M / Parikh, Asit / Kuo, Andrew / Mysore, Vijayashree / Hla, Timothy / Milstone, David S / Mayadas, Tanya N

Arteriosclerosis, thrombosis, and vascular biology

2022 Volume 42, Issue 7, Page(s) 886–902

Abstract: Background: The vascular endothelium maintains tissue-fluid homeostasis by controlling the passage of large molecules and fluid between the blood and interstitial space. The interaction of catenins and the actin cytoskeleton with VE-cadherin (vascular ... ...

Abstract	Background: The vascular endothelium maintains tissue-fluid homeostasis by controlling the passage of large molecules and fluid between the blood and interstitial space. The interaction of catenins and the actin cytoskeleton with VE-cadherin (vascular endothelial cadherin) is the primary mechanism for stabilizing AJs (adherens junctions), thereby preventing lung vascular barrier disruption. Members of the Rho (Ras homology) family of GTPases and conventional GEFs (guanine exchange factors) of these GTPases have been demonstrated to play important roles in regulating endothelial permeability. Here, we evaluated the role of DOCK4 (dedicator of cytokinesis 4)-an unconventional Rho family GTPase GEF in vascular function. Methods: We generated mice deficient in DOCK4' used DOCK4 silencing and reconstitution approaches in human pulmonary artery endothelial cells' used assays to evaluate protein localization, endothelial cell permeability, and small GTPase activation. Results: Our data show that DOCK4-deficient mice are viable. However, these mice have hemorrhage selectively in the lung, incomplete smooth muscle cell coverage in pulmonary vessels, increased basal microvascular permeability, and impaired response to S1P (sphingosine-1-phosphate)-induced reversal of thrombin-induced permeability. Consistent with this, DOCK4 rapidly translocates to the cell periphery and associates with the detergent-insoluble fraction following S1P treatment, and its absence prevents S1P-induced Rac-1 activation and enhancement of barrier function. Moreover, DOCK4-silenced pulmonary artery endothelial cells exhibit enhanced basal permeability in vitro that is associated with enhanced Rho GTPase activation. Conclusions: Our findings indicate that DOCK4 maintains AJs necessary for lung vascular barrier function by establishing the normal balance between RhoA (Ras homolog family member A) and Rac-1-mediated actin cytoskeleton remodeling, a previously unappreciated function for the atypical GEF family of molecules. Our studies also identify S1P as a potential upstream regulator of DOCK4 activity.
MeSH term(s)	Adherens Junctions/metabolism ; Animals ; Capillary Permeability/physiology ; Cells, Cultured ; Endothelial Cells/metabolism ; Endothelium, Vascular/metabolism ; GTPase-Activating Proteins/genetics ; GTPase-Activating Proteins/metabolism ; Guanine Nucleotide Exchange Factors/genetics ; Guanine Nucleotide Exchange Factors/metabolism ; Lung/metabolism ; Mice ; rho GTP-Binding Proteins/metabolism
Chemical Substances	Dock4 protein, mouse ; GTPase-Activating Proteins ; Guanine Nucleotide Exchange Factors ; rho GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2022-04-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1221433-4
ISSN	1524-4636 ; 1079-5642
ISSN (online)	1524-4636
ISSN	1079-5642
DOI	10.1161/ATVBAHA.122.317565
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Zs.A 1705: Show issues

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Article ; Online: TNF receptors: signaling pathways and contribution to renal dysfunction.

Al-Lamki, Rafia S / Mayadas, Tanya N

Kidney international

2015 Volume 87, Issue 2, Page(s) 281–296

Abstract: Tumor necrosis factor (TNF), initially reported to induce tumor cell apoptosis and cachexia, is now considered a central mediator of a broad range of biological activities from cell proliferation, cell death and differentiation to induction of ... ...

Abstract	Tumor necrosis factor (TNF), initially reported to induce tumor cell apoptosis and cachexia, is now considered a central mediator of a broad range of biological activities from cell proliferation, cell death and differentiation to induction of inflammation and immune modulation. TNF exerts its biological responses via interaction with two cell surface receptors: TNFR1 and TNFR2. (TNFRs). These receptors trigger shared and distinct signaling pathways upon TNF binding, which in turn result in cellular outputs that may promote tissue injury on one hand but may also induce protective, beneficial responses. Yet the role of TNF and its receptors specifically in renal disease is still not well understood. This review describes the expression of the TNFRs, the signaling pathways induced by them and the biological responses of TNF and its receptors in various animal models of renal diseases, and discusses the current outcomes from use of TNF biologics and TNF biomarkers in renal disorders.
MeSH term(s)	Acute Kidney Injury/etiology ; Acute Kidney Injury/metabolism ; Animals ; Carcinoma, Renal Cell/etiology ; Carcinoma, Renal Cell/metabolism ; Diabetic Nephropathies/etiology ; Diabetic Nephropathies/metabolism ; Graft Rejection/etiology ; Graft Rejection/metabolism ; Humans ; Kidney Diseases/etiology ; Kidney Diseases/metabolism ; Kidney Diseases/therapy ; Kidney Neoplasms/etiology ; Kidney Neoplasms/metabolism ; Kidney Transplantation/adverse effects ; Models, Biological ; Nephritis/etiology ; Nephritis/metabolism ; Receptors, Tumor Necrosis Factor/antagonists & inhibitors ; Receptors, Tumor Necrosis Factor/metabolism ; Signal Transduction ; Tumor Necrosis Factor-alpha/antagonists & inhibitors ; Tumor Necrosis Factor-alpha/metabolism ; Ureteral Obstruction/complications ; Ureteral Obstruction/metabolism
Chemical Substances	Receptors, Tumor Necrosis Factor ; Tumor Necrosis Factor-alpha
Language	English
Publishing date	2015-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	120573-0
ISSN	1523-1755 ; 0085-2538
ISSN (online)	1523-1755
ISSN	0085-2538
DOI	10.1038/ki.2014.285
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Zs.A 797: Show issues

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Article ; Online: Overview: studying integrins in vivo.

Lowell, Clifford A / Mayadas, Tanya N

Methods in molecular biology (Clifton, N.J.)

2011 Volume 757, Page(s) 369–397

Abstract: Integrins are adhesive proteins that have evolved to mediate cell-cell and cell-matrix communication that is indispensable for development and postnatal physiology. Despite their widespread expression, the genetic deletion of specific integrin family ... ...

Abstract	Integrins are adhesive proteins that have evolved to mediate cell-cell and cell-matrix communication that is indispensable for development and postnatal physiology. Despite their widespread expression, the genetic deletion of specific integrin family members in lower organisms as well as mammals leads to relatively distinct abnormalities. Many of the processes in which integrins participate have a requirement for strong adhesion coincident with times of mechanical stress. In Drosophila, the absence of specific integrins leads to detachment of muscle from the gut and body wall and separation of the two epithelial layers in the wing. In mice and humans, a deletion of either subunit of the laminin-binding integrin, α6β4 leads to severe skin blistering and defects in other epithelial layers. In addition, integrins have also evolved to serve more subspecialized roles ranging from the establishment of a stem cell niche in Drosophila and mammals, to the regulation of pathogenic tumor vascularization, platelet adhesion, and leukocyte transmigration in mammalian systems. However, some cells seem to function normally in the absence of all integrins, as revealed by the very surprising finding that deletion of all the major integrin types on dendritic cells of mice has no effect on the ability of these cells to migrate within the interstitium of the skin and enter into lymphatics. In addition to serving as transmembrane mechanical links, integrins in vertebrates synergize with a number of receptors including growth factor receptors, to enhance responses. This leads to the activation of a large signaling network that affects cell proliferation and differentiation, as well as cell shape and migration. In vivo studies, in lower organisms, knockout mouse models as well as in inherited human diseases together have provided important insights into how this major, primordial family of adhesion receptors have remained true to their name "integrins" as their diverse functions have in common the ability to integrate extracellular stimuli into intracellular signals that affect cell behavior.
MeSH term(s)	Animals ; Humans ; Integrins/deficiency ; Integrins/genetics ; Integrins/metabolism ; Leukocyte-Adhesion Deficiency Syndrome/genetics ; Leukocyte-Adhesion Deficiency Syndrome/metabolism ; Signal Transduction ; Thrombasthenia/genetics ; Thrombasthenia/metabolism
Chemical Substances	Integrins
Language	English
Publishing date	2011-09-10
Publishing country	United States
Document type	Journal Article ; Review
ISSN	1940-6029
ISSN (online)	1940-6029
DOI	10.1007/978-1-61779-166-6_22
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Article ; Online: Inhibitory affinity modulation of FcγRIIA ligand binding by glycosphingolipids by inside-out signaling.

Okubo, Koshu / Brenner, Michael D / Cullere, Xavier / Saggu, Gurpanna / Patchen, Myra L / Bose, Nandita / Mihori, Saki / Yuan, Zhou / Lowell, Clifford A / Zhu, Cheng / Mayadas, Tanya N

Cell reports

2021 Volume 35, Issue 7, Page(s) 109142

Abstract: The interaction of the human FcγRIIA with immune complexes (ICs) promotes neutrophil activation and thus must be tightly controlled to avoid damage to healthy tissue. Here, we demonstrate that a fungal-derived soluble β-1,3/1,6-glucan binds to the ... ...

Abstract	The interaction of the human FcγRIIA with immune complexes (ICs) promotes neutrophil activation and thus must be tightly controlled to avoid damage to healthy tissue. Here, we demonstrate that a fungal-derived soluble β-1,3/1,6-glucan binds to the glycosphingolipid long-chain lactosylceramide (LacCer) to reduce FcγRIIA-mediated recruitment to immobilized ICs under flow, a process requiring high-affinity FcγRIIA-immunoglobulin G (IgG) interactions. The inhibition requires Lyn phosphorylation of SHP-1 phosphatase and the FcγRIIA immunotyrosine-activating motif. β-glucan reduces the effective 2D affinity of FcγRIIA for IgG via Lyn and SHP-1 and, in vivo, inhibits FcγRIIA-mediated neutrophil recruitment to intravascular IgG deposited in the kidney glomeruli in a glycosphingolipid- and Lyn-dependent manner. In contrast, β-glucan did not affect FcγR functions that bypass FcγR affinity for IgG. In summary, we have identified a pathway for modulating the 2D affinity of FcγRIIA for ligand that relies on LacCer-Lyn-SHP-1-mediated inhibitory signaling triggered by β-glucan, a previously described activator of innate immunity.
MeSH term(s)	Glycosphingolipids/metabolism ; Humans ; Ligands ; Receptors, IgG/metabolism ; Signal Transduction
Chemical Substances	Fc gamma receptor IIA ; Glycosphingolipids ; Ligands ; Receptors, IgG
Language	English
Publishing date	2021-05-19
Publishing country	United States
Document type	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	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2021.109142
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Article ; Online: Protective heterologous T cell immunity in COVID-19 induced by the trivalent MMR and Tdap vaccine antigens.

Mysore, Vijayashree / Cullere, Xavier / Settles, Matthew L / Ji, Xinge / Kattan, Michael W / Desjardins, Michaël / Durbin-Johnson, Blythe / Gilboa, Tal / Baden, Lindsey R / Walt, David R / Lichtman, Andrew H / Jehi, Lara / Mayadas, Tanya N

Med (New York, N.Y.)

2021 Volume 2, Issue 9, Page(s) 1050–1071.e7

Abstract: Background: T cells control viral infection, promote vaccine durability, and in coronavirus disease 2019 (COVID-19) associate with mild disease. We investigated whether prior measles-mumps-rubella (MMR) or tetanus-diphtheria-pertussis (Tdap) vaccination ...

Abstract	Background: T cells control viral infection, promote vaccine durability, and in coronavirus disease 2019 (COVID-19) associate with mild disease. We investigated whether prior measles-mumps-rubella (MMR) or tetanus-diphtheria-pertussis (Tdap) vaccination elicits cross-reactive T cells that mitigate COVID-19. Methods: Antigen-presenting cells (APC) loaded Findings: High correlation was observed between T cell responses to SARS-CoV-2 (spike-S1 and nucleocapsid) and MMR and Tdap proteins in COVID-19-convalescent and -vaccinated individuals. The overlapping T cell population contained an effector memory T cell subset (effector memory re-expressing CD45RA on T cells [T Conclusions: Tdap and MMR memory T cells reactivated by SARS-CoV-2 may provide protection against severe COVID-19. Funding: This study was supported by a National Institutes of Health (R01HL065095, R01AI152522, R01NS097719) donation from Barbara and Amos Hostetter and the Chleck Foundation.
MeSH term(s)	COVID-19/prevention & control ; Humans ; Measles ; Mumps Vaccine ; Receptors, Antigen, T-Cell ; Rubella Vaccine ; SARS-CoV-2 ; Spike Glycoprotein, Coronavirus ; T-Lymphocytes ; Whooping Cough
Chemical Substances	Mumps Vaccine ; Receptors, Antigen, T-Cell ; Rubella Vaccine ; Spike Glycoprotein, Coronavirus ; spike protein, SARS-CoV-2
Language	English
Publishing date	2021-08-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	2666-6340
ISSN (online)	2666-6340
DOI	10.1016/j.medj.2021.08.004
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Article: Protective heterologous T cell immunity in COVID-19 induced by MMR and Tdap vaccine antigens.

bioRxiv : the preprint server for biology

2021

Abstract: T cells are critical for control of viral infection and effective vaccination. We investigated whether prior Measles-Mumps-Rubella (MMR) or Tetanus-Diphtheria-pertussis (Tdap) vaccination elicit cross-reactive T cells that mitigate COVID-19. Using co- ... ...

Abstract	T cells are critical for control of viral infection and effective vaccination. We investigated whether prior Measles-Mumps-Rubella (MMR) or Tetanus-Diphtheria-pertussis (Tdap) vaccination elicit cross-reactive T cells that mitigate COVID-19. Using co-cultures of antigen presenting cells (APC) loaded with antigens and autologous T cells, we found a high correlation between responses to SARS-CoV-2 (Spike-S1 and Nucleocapsid) and MMR and Tdap vaccine proteins in both SARS-CoV-2 infected individuals and individuals immunized with mRNA-based SARS-CoV-2 vaccines. The overlapping T cell population contained effector memory T cells (TEMRA) previously implicated in anti-viral immunity and their activation required APC-derived IL-15. TCR- and scRNA-sequencing detected cross-reactive clones with TEMRA features among the cells recognizing SARS-CoV-2, MMR and Tdap epitopes. A propensity-weighted analysis of 73,582 COVID-19 patients revealed that severe disease outcomes (hospitalization and transfer to intensive care unit or death) were reduced in MMR or Tdap vaccinated individuals by 38-32% and 23-20% respectively. In summary, SARS-CoV-2 re-activates memory T cells generated by Tdap and MMR vaccines, which may reduce disease severity.
Language	English
Publishing date	2021-05-04
Publishing country	United States
Document type	Preprint
DOI	10.1101/2021.05.03.441323
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