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Article ; Online: SCARF1-Induced Efferocytosis Plays an Immunomodulatory Role in Humans, and Autoantibodies Targeting SCARF1 Are Produced in Patients with Systemic Lupus Erythematosus.

Jorge, April M / Lao, Taotao / Kim, Rachel / Licciardi, Samantha / El Khoury, Joseph / Luster, Andrew D / Means, Terry K / Ramirez-Ortiz, Zaida G

Journal of immunology (Baltimore, Md. : 1950)

2022 Volume 208, Issue 4, Page(s) 955–967

Abstract: Deficiency in the clearance of cellular debris is a major pathogenic factor in the emergence of autoimmune diseases. We previously demonstrated that mice deficient for scavenger receptor class F member 1 (SCARF1) develop a lupus-like autoimmune disease ... ...

Abstract	Deficiency in the clearance of cellular debris is a major pathogenic factor in the emergence of autoimmune diseases. We previously demonstrated that mice deficient for scavenger receptor class F member 1 (SCARF1) develop a lupus-like autoimmune disease with symptoms similar to human systemic lupus erythematosus (SLE), including a pronounced accumulation of apoptotic cells (ACs). Therefore, we hypothesized that SCARF1 will be important for clearance of ACs and maintenance of self-tolerance in humans, and that dysregulation of this process could contribute to SLE. In this article, we show that SCARF1 is highly expressed on phagocytic cells, where it functions as an efferocytosis receptor. In healthy individuals, we discovered that engagement of SCARF1 by ACs on BDCA1
MeSH term(s)	Animals ; Autoantibodies/blood ; Autoantibodies/immunology ; Biomarkers ; Disease Models, Animal ; Disease Susceptibility ; Gene Expression Profiling ; Humans ; Immunoglobulin G/blood ; Immunoglobulin G/immunology ; Immunomodulation/genetics ; Immunophenotyping ; Lupus Erythematosus, Systemic/diagnosis ; Lupus Erythematosus, Systemic/etiology ; Lupus Erythematosus, Systemic/metabolism ; Mice ; Mice, Transgenic ; Mitogen-Activated Protein Kinases/metabolism ; Phagocytes/immunology ; Phagocytes/metabolism ; Phagocytosis/immunology ; Phosphorylation ; STAT Transcription Factors/metabolism ; Scavenger Receptors, Class F/genetics ; Scavenger Receptors, Class F/immunology ; Scavenger Receptors, Class F/metabolism
Chemical Substances	Autoantibodies ; Biomarkers ; Immunoglobulin G ; SCARF1 protein, human ; STAT Transcription Factors ; Scavenger Receptors, Class F ; Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2022-01-26
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.2100532
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Article: Dysregulated Pulmonary Inflammatory Responses Exacerbate the Outcome of Secondary Aspergillosis Following Influenza.

Lee, Chrono K / Oliveira, Lorena V N / Akalin, Ali / Specht, Charles A / Lourenco, Diana / Gomez, Christina L / Ramirez-Ortiz, Zaida G / Wang, Jennifer P / Levitz, Stuart M

bioRxiv : the preprint server for biology

2023

Abstract: Inhalation of airborne conidia of the ubiquitous fungus : Importance: Severe influenza is a risk factor for fatal invasive pulmonary aspergillosis; however, the mechanistic basis for the lethality is unclear. Utilizing an influenza-associated ... ...

Abstract	Inhalation of airborne conidia of the ubiquitous fungus Importance: Severe influenza is a risk factor for fatal invasive pulmonary aspergillosis; however, the mechanistic basis for the lethality is unclear. Utilizing an influenza-associated pulmonary aspergillosis (IAPA) model, we found that mice infected with influenza A virus followed by
Language	English
Publishing date	2023-06-30
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.06.27.546808
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Article ; Online: Dysregulated pulmonary inflammatory responses exacerbate the outcome of secondary aspergillosis following influenza.

Lee, Chrono K / Oliveira, Lorena V N / Akalin, Ali / Specht, Charles A / Lourenco, Diana / Gomez, Christina L / Ramirez-Ortiz, Zaida G / Wang, Jennifer P / Levitz, Stuart M

mBio

2023 Volume 14, Issue 5, Page(s) e0163323

Abstract: Importance: Severe influenza is a risk factor for fatal invasive pulmonary aspergillosis; however, the mechanistic basis for the lethality is unclear. Utilizing an influenza-associated pulmonary aspergillosis (IAPA) model, we found that mice infected ... ...

Abstract	Importance: Severe influenza is a risk factor for fatal invasive pulmonary aspergillosis; however, the mechanistic basis for the lethality is unclear. Utilizing an influenza-associated pulmonary aspergillosis (IAPA) model, we found that mice infected with influenza A virus followed by
MeSH term(s)	Humans ; Animals ; Mice ; Influenza, Human/complications ; Aspergillosis/microbiology ; Lung/microbiology ; Invasive Pulmonary Aspergillosis/microbiology ; Pulmonary Aspergillosis ; Aspergillus fumigatus ; Inflammation/complications
Language	English
Publishing date	2023-09-08
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.01633-23
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Article ; Online: Current Insights in Cutaneous Lupus Erythematosus Immunopathogenesis.

Garelli, Colton J / Refat, Maggi Ahmed / Nanaware, Padma P / Ramirez-Ortiz, Zaida G / Rashighi, Mehdi / Richmond, Jillian M

Frontiers in immunology

2020 Volume 11, Page(s) 1353

Abstract: Cutaneous Lupus Erythematosus (CLE) is a clinically diverse group of autoimmune skin diseases with shared histological features of interface dermatitis and autoantibodies deposited at the dermal-epidermal junction. Various genetic and environmental ... ...

Abstract	Cutaneous Lupus Erythematosus (CLE) is a clinically diverse group of autoimmune skin diseases with shared histological features of interface dermatitis and autoantibodies deposited at the dermal-epidermal junction. Various genetic and environmental triggers of CLE promote infiltration of T cells, B cells, neutrophils, antigen presenting cells, and NK cells into lesional skin. In this mini-review, we will discuss the clinical features of CLE, insights into CLE immunopathogenesis, and novel treatment approaches.
MeSH term(s)	Humans ; Lupus Erythematosus, Cutaneous/drug therapy ; Lupus Erythematosus, Cutaneous/immunology ; Lupus Erythematosus, Cutaneous/pathology
Language	English
Publishing date	2020-07-02
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.01353
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Article ; Online: The role of dendritic cells in the innate recognition of pathogenic fungi (A. fumigatus, C. neoformans and C. albicans).

Ramirez-Ortiz, Zaida G / Means, Terry K

Virulence

2012 Volume 3, Issue 7, Page(s) 635–646

Abstract: Dendritic cells (DCs) are the bridge between the innate and adaptive immune system. DCs are responsible for sensing and patrolling the environment, initiating a host response and instructing the proper adaptive immune response against pathogens. Recent ... ...

Abstract	Dendritic cells (DCs) are the bridge between the innate and adaptive immune system. DCs are responsible for sensing and patrolling the environment, initiating a host response and instructing the proper adaptive immune response against pathogens. Recent advances in medical treatments have led to increased use of immunosuppressive drugs, leading to the emergence of fungal species that cause life-threatening infections in humans. Three of these opportunistic fungal pathogens: Aspergillus fumigatus, Candida albicans and Cryptococcus neoformans pose the biggest concern for the immune-compromised host. Here we will review the interactions between DCs and these fungal pathogens, the receptors expressed on DCs that mediate these responses and the signaling mechanisms that shape the adaptive host response.
MeSH term(s)	Aspergillosis/immunology ; Aspergillosis/microbiology ; Aspergillus fumigatus/immunology ; Candida albicans/immunology ; Candidiasis/immunology ; Candidiasis/microbiology ; Cryptococcosis/immunology ; Cryptococcosis/microbiology ; Cryptococcus neoformans/immunology ; Dendritic Cells/immunology ; Humans ; Immunocompromised Host
Language	English
Publishing date	2012-10-17
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2657572-3
ISSN	2150-5608 ; 2150-5594
ISSN (online)	2150-5608
ISSN	2150-5594
DOI	10.4161/viru.22295
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Article ; Online: The receptor TREML4 amplifies TLR7-mediated signaling during antiviral responses and autoimmunity.

Ramirez-Ortiz, Zaida G / Prasad, Amit / Griffith, Jason W / Pendergraft, William F / Cowley, Glenn S / Root, David E / Tai, Melissa / Luster, Andrew D / El Khoury, Joseph / Hacohen, Nir / Means, Terry K

Nature immunology

2015 Volume 16, Issue 5, Page(s) 495–504

Abstract: The molecules and pathways that fine-tune innate inflammatory responses mediated by Toll-like receptor 7 (TLR7) remain to be fully elucidated. Using an unbiased genome-scale screen with short hairpin RNA (shRNA), we identified the receptor TREML4 as an ... ...

Abstract	The molecules and pathways that fine-tune innate inflammatory responses mediated by Toll-like receptor 7 (TLR7) remain to be fully elucidated. Using an unbiased genome-scale screen with short hairpin RNA (shRNA), we identified the receptor TREML4 as an essential positive regulator of TLR7 signaling. Macrophages from Treml4(-/-) mice were hyporesponsive to TLR7 agonists and failed to produce type I interferons due to impaired phosphorylation of the transcription factor STAT1 by the mitogen-activated protein kinase p38 and decreased recruitment of the adaptor MyD88 to TLR7. TREML4 deficiency reduced the production of inflammatory cytokines and autoantibodies in MRL/lpr mice, which are prone to systemic lupus erythematosus (SLE), and inhibited the antiviral immune response to influenza virus. Our data identify TREML4 as a positive regulator of TLR7 signaling and provide insight into the molecular mechanisms that control antiviral immunity and the development of autoimmunity.
MeSH term(s)	Animals ; Autoantibodies/metabolism ; Autoimmunity/genetics ; Cells, Cultured ; Cytokines/metabolism ; Humans ; Immunity, Innate/genetics ; Inflammation Mediators/metabolism ; Interferon Type I/metabolism ; Lupus Erythematosus, Systemic/immunology ; Macrophages/physiology ; Macrophages/virology ; Membrane Glycoproteins/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Inbred MRL lpr ; Mice, Knockout ; Myeloid Differentiation Factor 88/metabolism ; Orthomyxoviridae/immunology ; Orthomyxoviridae Infections/immunology ; RNA, Small Interfering/genetics ; Receptors, Immunologic/genetics ; Receptors, Immunologic/metabolism ; STAT1 Transcription Factor/metabolism ; Signal Transduction/genetics ; Toll-Like Receptor 7/metabolism ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	Autoantibodies ; Cytokines ; Inflammation Mediators ; Interferon Type I ; Membrane Glycoproteins ; Myeloid Differentiation Factor 88 ; RNA, Small Interfering ; Receptors, Immunologic ; STAT1 Transcription Factor ; Tlr7 protein, mouse ; Toll-Like Receptor 7 ; Treml4 protein, mouse ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2015-04-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/ni.3143
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Zs.A 5294: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
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Article: A Nonredundant Role for Plasmacytoid Dendritic Cells in Host Defense against the Human Fungal Pathogen Aspergillus fumigatus

Ramirez-Ortiz, Zaida G / Lee, Chrono K / Wang, Jennifer P / Boon, Louis / Specht, Charles A / Levitz, Stuart M

Cell host & microbe. 2011 May 19, v. 9, no. 5

2011

Abstract: While plasmacytoid dendritic cells (pDCs), a natural type I interferon (IFN)-producing cell type, are regarded as critical for innate immunity to viruses, their role in defense against fungal infections remains unknown. We examined the interactions of ... ...

Abstract	While plasmacytoid dendritic cells (pDCs), a natural type I interferon (IFN)-producing cell type, are regarded as critical for innate immunity to viruses, their role in defense against fungal infections remains unknown. We examined the interactions of pDCs with hyphae of the invasive human fungal pathogen Aspergillus fumigatus. Human pDCs spread over hyphae and inhibited their growth. Antifungal activity was retained in pDC lysates, did not require direct fungal contact, and was partially reversed by zinc. Incubation with hyphae resulted in pDC cytotoxicity, partly due to fungal gliotoxin secretion. Following hyphal stimulation, pDCs released proinflammatory cytokines via a TLR9-independent mechanism. Pulmonary challenge of mice with A. fumigatus resulted in a substantial influx of pDCs into lungs, and pDC-depleted mice were hypersusceptible to invasive aspergillosis. These data demonstrate the antifungal activity of pDCs against A. fumigatus and establish their nonredundant role in host defenses against invasive aspergillosis in vivo.
Keywords	Aspergillus fumigatus ; antifungal properties ; aspergillosis ; cytokines ; cytotoxicity ; dendritic cells ; fungi ; growth retardation ; humans ; hyphae ; innate immunity ; interferons ; lungs ; mice ; pathogens ; secretion ; viruses ; zinc
Language	English
Dates of publication	2011-0519
Size	p. 415-424.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	2278004-X
ISSN	1931-3128
ISSN	1931-3128
DOI	10.1016/j.chom.2011.04.007
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: A nonredundant role for plasmacytoid dendritic cells in host defense against the human fungal pathogen Aspergillus fumigatus.

Ramirez-Ortiz, Zaida G / Lee, Chrono K / Wang, Jennifer P / Boon, Louis / Specht, Charles A / Levitz, Stuart M

Cell host & microbe

2010 Volume 9, Issue 5, Page(s) 415–424

Abstract	While plasmacytoid dendritic cells (pDCs), a natural type I interferon (IFN)-producing cell type, are regarded as critical for innate immunity to viruses, their role in defense against fungal infections remains unknown. We examined the interactions of pDCs with hyphae of the invasive human fungal pathogen Aspergillus fumigatus. Human pDCs spread over hyphae and inhibited their growth. Antifungal activity was retained in pDC lysates, did not require direct fungal contact, and was partially reversed by zinc. Incubation with hyphae resulted in pDC cytotoxicity, partly due to fungal gliotoxin secretion. Following hyphal stimulation, pDCs released proinflammatory cytokines via a TLR9-independent mechanism. Pulmonary challenge of mice with A. fumigatus resulted in a substantial influx of pDCs into lungs, and pDC-depleted mice were hypersusceptible to invasive aspergillosis. These data demonstrate the antifungal activity of pDCs against A. fumigatus and establish their nonredundant role in host defenses against invasive aspergillosis in vivo.
MeSH term(s)	Animals ; Aspergillosis/immunology ; Aspergillosis/microbiology ; Aspergillus fumigatus/immunology ; Aspergillus fumigatus/pathogenicity ; Cell Survival ; Cytokines/metabolism ; Dendritic Cells/immunology ; Dendritic Cells/microbiology ; Disease Models, Animal ; Female ; Gliotoxin/toxicity ; Humans ; Hyphae/immunology ; Hyphae/pathogenicity ; Lung/immunology ; Lung/microbiology ; Lung/pathology ; Male ; Mice ; Mice, Inbred C57BL
Chemical Substances	Cytokines ; Gliotoxin (67-99-2)
Language	English
Publishing date	2010-11-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2278004-X
ISSN	1934-6069 ; 1931-3128
ISSN (online)	1934-6069
ISSN	1931-3128
DOI	10.1016/j.chom.2011.04.007
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Article ; Online: CD82 controls CpG-dependent TLR9 signaling.

Khan, Nida S / Lukason, Daniel P / Feliu, Marianela / Ward, Rebecca A / Lord, Allison K / Reedy, Jennifer L / Ramirez-Ortiz, Zaida G / Tam, Jenny M / Kasperkovitz, Pia V / Negoro, Paige E / Vyas, Tammy D / Xu, Shuying / Brinkmann, Melanie M / Acharaya, Mridu / Artavanis-Tsakonas, Katerina / Frickel, Eva-Maria / Becker, Christine E / Dagher, Zeina / Kim, You-Me /

Latz, Eicke / Ploegh, Hidde L / Mansour, Michael K / Miranti, Cindy K / Levitz, Stuart M / Vyas, Jatin M

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2019 Volume 33, Issue 11, Page(s) 12500–12514

Abstract: The tetraspanin CD82 is a potent suppressor of tumor metastasis and regulates several processes including signal transduction, cell adhesion, motility, and aggregation. However, the mechanisms by which CD82 participates in innate immunity are unknown. We ...

Abstract	The tetraspanin CD82 is a potent suppressor of tumor metastasis and regulates several processes including signal transduction, cell adhesion, motility, and aggregation. However, the mechanisms by which CD82 participates in innate immunity are unknown. We report that CD82 is a key regulator of TLR9 trafficking and signaling. TLR9 recognizes unmethylated cytosine-phosphate-guanine (CpG) motifs present in viral, bacterial, and fungal DNA. We demonstrate that TLR9 and CD82 associate in macrophages, which occurs in the endoplasmic reticulum (ER) and post-ER. Moreover, CD82 is essential for TLR9-dependent myddosome formation in response to CpG stimulation. Finally, CD82 modulates TLR9-dependent NF-κB nuclear translocation, which is critical for inflammatory cytokine production. To our knowledge, this is the first time a tetraspanin has been implicated as a key regulator of TLR signaling. Collectively, our study demonstrates that CD82 is a specific regulator of TLR9 signaling, which may be critical in cancer immunotherapy approaches and coordinating the innate immune response to pathogens.-Khan, N. S., Lukason, D. P., Feliu, M., Ward, R. A., Lord, A. K., Reedy, J. L., Ramirez-Ortiz, Z. G., Tam, J. M., Kasperkovitz, P. V., Negoro, P. E., Vyas, T. D., Xu, S., Brinkmann, M. M., Acharaya, M., Artavanis-Tsakonas, K., Frickel, E.-M., Becker, C. E., Dagher, Z., Kim, Y.-M., Latz, E., Ploegh, H. L., Mansour, M. K., Miranti, C. K., Levitz, S. M., Vyas, J. M. CD82 controls CpG-dependent TLR9 signaling.
MeSH term(s)	Active Transport, Cell Nucleus/drug effects ; Active Transport, Cell Nucleus/genetics ; Active Transport, Cell Nucleus/immunology ; Animals ; Cell Nucleus/genetics ; Cell Nucleus/immunology ; Cytokines/genetics ; Cytokines/immunology ; Endoplasmic Reticulum/genetics ; Endoplasmic Reticulum/immunology ; Endoplasmic Reticulum/pathology ; Inflammation/genetics ; Inflammation/immunology ; Inflammation/pathology ; Kangai-1 Protein/genetics ; Kangai-1 Protein/immunology ; Macrophages/immunology ; Macrophages/pathology ; Mice ; Mice, Knockout ; NF-kappa B/genetics ; NF-kappa B/immunology ; Oligodeoxyribonucleotides/pharmacology ; RAW 264.7 Cells ; Signal Transduction/drug effects ; Signal Transduction/genetics ; Signal Transduction/immunology ; Toll-Like Receptor 9/genetics ; Toll-Like Receptor 9/immunology
Chemical Substances	CPG-oligonucleotide ; Cd82 antigen, mouse ; Cytokines ; Kangai-1 Protein ; NF-kappa B ; Oligodeoxyribonucleotides ; Tlr9 protein, mouse ; Toll-Like Receptor 9
Language	English
Publishing date	2019-08-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.201901547R
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Article ; Online: The scavenger receptor SCARF1 mediates the clearance of apoptotic cells and prevents autoimmunity.

Ramirez-Ortiz, Zaida G / Pendergraft, William F / Prasad, Amit / Byrne, Michael H / Iram, Tal / Blanchette, Christopher J / Luster, Andrew D / Hacohen, Nir / El Khoury, Joseph / Means, Terry K

Nature immunology

2013 Volume 14, Issue 9, Page(s) 917–926

Abstract: The clearance of apoptotic cells is critical for the control of tissue homeostasis; however, the full range of receptors on phagocytes responsible for the recognition of apoptotic cells remains to be identified. Here we found that dendritic cells (DCs), ... ...

Abstract	The clearance of apoptotic cells is critical for the control of tissue homeostasis; however, the full range of receptors on phagocytes responsible for the recognition of apoptotic cells remains to be identified. Here we found that dendritic cells (DCs), macrophages and endothelial cells used the scavenger receptor SCARF1 to recognize and engulf apoptotic cells via the complement component C1q. Loss of SCARF1 impaired the uptake of apoptotic cells. Consequently, in SCARF1-deficient mice, dying cells accumulated in tissues, which led to a lupus-like disease, with the spontaneous generation of autoantibodies to DNA-containing antigens, activation of cells of the immune system, dermatitis and nephritis. The discovery of such interactions of SCARF1 with C1q and apoptotic cells provides insight into the molecular mechanisms involved in the maintenance of tolerance and prevention of autoimmune disease.
MeSH term(s)	Animals ; Apoptosis/genetics ; Apoptosis/immunology ; Autoimmune Diseases/genetics ; Autoimmune Diseases/immunology ; Autoimmune Diseases/metabolism ; Autoimmunity/genetics ; Complement C1q/chemistry ; Complement C1q/immunology ; Complement C1q/metabolism ; Female ; Inflammation/genetics ; Inflammation/immunology ; Inflammation/metabolism ; Male ; Mice ; Mice, Knockout ; Nephritis/genetics ; Nephritis/immunology ; Nephritis/pathology ; Phagocytosis/genetics ; Phagocytosis/immunology ; Phosphorylation ; Protein Binding ; Scavenger Receptors, Class F/genetics ; Scavenger Receptors, Class F/immunology ; Scavenger Receptors, Class F/metabolism ; Serine/metabolism
Chemical Substances	Scavenger Receptors, Class F ; Serine (452VLY9402) ; Complement C1q (80295-33-6)
Language	English
Publishing date	2013-07-28
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2016987-5
ISSN	1529-2916 ; 1529-2908
ISSN (online)	1529-2916
ISSN	1529-2908
DOI	10.1038/ni.2670
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