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Article ; Online: Microglia C-lectin/selectin' neurons to eat.

Jiang, Yike / Shinohara, Mari L

2023 Volume 56, Issue 2, Page(s) 227–229

Abstract: β-glucosylceramide (β-GlcCer) accumulates in Gaucher disease, but how β-GlcCer, a Mincle ligand, causes characteristic neuroinflammation and neuronopathy is poorly understood. In this issue of Immunity, Shimizu et al. reveal that Mincle-dependent ... ...

Abstract	β-glucosylceramide (β-GlcCer) accumulates in Gaucher disease, but how β-GlcCer, a Mincle ligand, causes characteristic neuroinflammation and neuronopathy is poorly understood. In this issue of Immunity, Shimizu et al. reveal that Mincle-dependent activation of microglia led to phagocytosis of neurons and neurologic symptoms.
MeSH term(s)	Lectins ; Microglia ; Neurons ; Phagocytosis ; Selectins
Chemical Substances	Lectins ; Selectins
Language	English
Publishing date	2023-01-19
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
ZDB-ID	1217235-2
ISSN	1097-4180 ; 1074-7613
ISSN (online)	1097-4180
ISSN	1074-7613
DOI	10.1016/j.immuni.2023.01.020
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Zs.MG 69: Show issues

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Article ; Online: Host immune responses in the central nervous system during fungal infections.

Reyes, Estefany Y / Shinohara, Mari L

Immunological reviews

2022 Volume 311, Issue 1, Page(s) 50–74

Abstract: Fungal infections in the central nervous system (CNS) cause high morbidity and mortality. The frequency of CNS mycosis has increased over the last two decades as more individuals go through immunocompromised conditions for various reasons. Nevertheless, ... ...

Abstract	Fungal infections in the central nervous system (CNS) cause high morbidity and mortality. The frequency of CNS mycosis has increased over the last two decades as more individuals go through immunocompromised conditions for various reasons. Nevertheless, options for clinical interventions for CNS mycoses are still limited. Thus, there is an urgent need to understand the host-pathogen interaction mechanisms in CNS mycoses for developing novel treatments. Although the CNS has been regarded as an immune-privileged site, recent studies demonstrate the critical involvement of immune responses elicited by CNS-resident and CNS-infiltrated cells during fungal infections. In this review, we discuss mechanisms of fungal invasion in the CNS, fungal pathogen detection by CNS-resident cells (microglia, astrocytes, oligodendrocytes, neurons), roles of CNS-infiltrated leukocytes, and host immune responses. We consider that understanding host immune responses in the CNS is crucial for endeavors to develop treatments for CNS mycosis.
MeSH term(s)	Central Nervous System ; Host-Pathogen Interactions ; Humans ; Immunity ; Mycoses
Language	English
Publishing date	2022-06-07
Publishing country	England
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	391796-4
ISSN	1600-065X ; 0105-2896
ISSN (online)	1600-065X
ISSN	0105-2896
DOI	10.1111/imr.13101
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Article ; Online: Emerging roles of Dectin-1 in noninfectious settings and in the CNS.

Deerhake, M Elizabeth / Shinohara, Mari L

Trends in immunology

2021 Volume 42, Issue 10, Page(s) 891–903

Abstract: Dectin-1 is a C-type lectin receptor (CLR) expressed on the surface of various mammalian myeloid cells. Dectin-1 recognizes β-glucans and elicits antifungal proinflammatory immune responses. Recent studies have begun to examine the biology of Dectin-1 in ...

Abstract	Dectin-1 is a C-type lectin receptor (CLR) expressed on the surface of various mammalian myeloid cells. Dectin-1 recognizes β-glucans and elicits antifungal proinflammatory immune responses. Recent studies have begun to examine the biology of Dectin-1 in previously less explored settings, such as homeostasis, sterile inflammation, and in the central nervous system. Indeed, in certain contexts, Dectin-1 is now known to promote tolerance, and anti-inflammatory and neuroprotective responses. In this review, we provide an overview of the current understanding of the roles of Dectin-1 in immunology beyond the context of fungal infections, mainly focusing on in vivo neuroimmunology studies, which could reveal new therapeutic approaches to modify innate immune responses in neurologic disorders.
MeSH term(s)	Animals ; Central Nervous System ; Immunity, Innate ; Lectins, C-Type ; beta-Glucans
Chemical Substances	Lectins, C-Type ; beta-Glucans ; dectin 1
Language	English
Publishing date	2021-09-04
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2036831-8
ISSN	1471-4981 ; 1471-4906
ISSN (online)	1471-4981
ISSN	1471-4906
DOI	10.1016/j.it.2021.08.005
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Zs.A 1601: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MG 2: Show issues

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Article ; Online: Yes, research matters.

Shinohara, Mari L

PLoS pathogens

2017 Volume 13, Issue 8, Page(s) e1006420

Abstract: My father was diagnosed with stomach cancer recently. Luckily, it was still at an early stage, and endoscopic surgery successfully took care of it. My father was fortunate; since people with stomach cancer do not show clear symptoms in the early stages, ... ...

Abstract	My father was diagnosed with stomach cancer recently. Luckily, it was still at an early stage, and endoscopic surgery successfully took care of it. My father was fortunate; since people with stomach cancer do not show clear symptoms in the early stages, the disease is often not diagnosed until it becomes advanced. In his case, the diagnosis started from a suggestion by his doctor to check whether he had a gastric infection with Helicobacter pylori, a bacterial species found in the digestive tract. In Japan, where he lives, a majority of gastric cancer patients (more than 99%) have been infected with H. pylori [1], and the causative role of this bacterial species in promoting gastric cancer is very well established. Now, scientific understanding connecting gastric cancer to H. pylori is saving the lives of many people, including my father. Thinking about this recent personal experience, I wonder if the connection between bacteria and cancer might have been considered a crazy idea decades ago. Research makes it possible to connect seemingly unrelated matters. My laboratory works on seemingly unrelated research topics, such as fungal infections and autoimmunity. However, my question is the same whatever the topic: How do leukocytes elicit and regulate inflammation when they detect infections or endogenous signals? In fact, host receptors detecting pathogens can induce autoimmunity, and autoimmunity alters host sensitivity to pathogens due to the imbalance in the immune system. We are beginning to gain some insight into this question, as revealed by some of our recent studies. For example, the NLR family, pyrin domain containing 3 (NLRP3) inflammasome, which is known to sense a wide variety of pathogens, can also change the course of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). In particular, our study suggested that disease treatment approaches need to be changed based on the activation status of the NLRP3 inflammasome [2]. Another recent study from our laboratory demonstrated that a protein, termed osteopontin (OPN), skews the balance of population sizes between myeloid cells (i.e., innate immunity) and lymphoid cells (i.e., adaptive immunity) during infections and other biological insults [3]. An intracellular isoform of OPN (iOPN) negatively regulates emergency myelopoiesis. Thus, OPN attenuates host resistance by limiting neutrophil supply at the early stage of systemic Candida infection. In contrast, a secreted OPN (sOPN) isoform positively regulates the expansion of T lymphocytes and ends up triggering autoimmune colitis. I am an immunologist but obtained my PhD in mycology. Nevertheless, it took some time for me to appreciate that research enables us to connect the dots placed far apart. This is a truly exciting time to connect seemingly unrelated biological phenomena, because scientists are exponentially increasing our understanding of nature. This is particularly true in innate immunity, which is not only the central alarming system in host-microbe interactions but also relates to almost any human disease we can imagine. However, we are facing a dark age for science and research, in which certain interests wrongfully discredit some research fields. There are things that can be achieved only by research. I am always ready to tell anyone, "Yes, research matters!".
MeSH term(s)	Animals ; Biomedical Research ; Humans
Language	English
Publishing date	2017-08-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	2205412-1
ISSN	1553-7374 ; 1553-7366
ISSN (online)	1553-7374
ISSN	1553-7366
DOI	10.1371/journal.ppat.1006420
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Article ; Online: Dectin-1 signaling in neutrophils up-regulates PD-L1 and triggers ROS-mediated suppression of CD4

Deerhake, M Elizabeth / Cardakli, Emre D / Shinohara, Mari L

Journal of leukocyte biology

2022 Volume 112, Issue 6, Page(s) 1413–1425

Abstract: Dectin-1 is known to drive proinflammatory cytokine production by macrophages and dendritic cells which promotes Th17 ... ...

Abstract	Dectin-1 is known to drive proinflammatory cytokine production by macrophages and dendritic cells which promotes Th17 CD4
MeSH term(s)	Animals ; Neutrophils ; B7-H1 Antigen/metabolism ; Reactive Oxygen Species/metabolism ; Lectins, C-Type/metabolism ; Encephalomyelitis, Autoimmune, Experimental/metabolism ; Th17 Cells
Chemical Substances	dectin 1 ; B7-H1 Antigen ; Reactive Oxygen Species ; Lectins, C-Type
Language	English
Publishing date	2022-09-08
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1002/JLB.3A0322-152RR
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Zs.A 603: Show issues

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Article ; Online: Osteopontin (OPN)/SPP1: from its biochemistry to biological functions in the innate immune system and the central nervous system (CNS).

Lin, Elliot Yi-Hsin / Xi, Wen / Aggarwal, Nupur / Shinohara, Mari L

International immunology

2022 Volume 35, Issue 4, Page(s) 171–180

Abstract: Osteopontin (OPN) is a multifunctional protein, initially identified in osteosarcoma cells with its role of mediating osteoblast adhesion. Later studies revealed that OPN is associated with many inflammatory conditions caused by infections, allergic ... ...

Abstract	Osteopontin (OPN) is a multifunctional protein, initially identified in osteosarcoma cells with its role of mediating osteoblast adhesion. Later studies revealed that OPN is associated with many inflammatory conditions caused by infections, allergic responses, autoimmunity and tissue damage. Many cell types in the peripheral immune system express OPN with various functions, which could be beneficial or detrimental. Also, more recent studies demonstrated that OPN is highly expressed in the central nervous system (CNS), particularly in microglia during CNS diseases and development. However, understanding of mechanisms underlying OPN's functions in the CNS is still limited. In this review, we focus on peripheral myeloid cells and CNS-resident cells to discuss the expression and functions of OPN.
MeSH term(s)	Osteopontin/metabolism ; Central Nervous System ; Immune System/metabolism ; Microglia/metabolism ; Autoimmunity
Chemical Substances	Osteopontin (106441-73-0)
Language	English
Publishing date	2022-12-16
Publishing country	England
Document type	Review ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1013745-2
ISSN	1460-2377 ; 0953-8178
ISSN (online)	1460-2377
ISSN	0953-8178
DOI	10.1093/intimm/dxac060
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Zs.A 2619: 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)
Zs.MG 70: Show issues

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Article: Tissue-Resident Macrophages in Fungal Infections.

Xu, Shengjie / Shinohara, Mari L

Frontiers in immunology

2017 Volume 8, Page(s) 1798

Abstract: Invasive fungal infections result in high morbidity and mortality. Host organs targeted by fungal pathogens vary depending on the route of infection and fungal species encountered. ...

Abstract	Invasive fungal infections result in high morbidity and mortality. Host organs targeted by fungal pathogens vary depending on the route of infection and fungal species encountered.
Language	English
Publishing date	2017
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2017.01798
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Article ; Online: Integrin α3 promotes T

Park, Eunchong / Barclay, William E / Barrera, Alejandro / Liao, Tzu-Chieh / Salzler, Harmony R / Reddy, Timothy E / Shinohara, Mari L / Ciofani, Maria

Science immunology

2023 Volume 8, Issue 88, Page(s) eadg7597

Abstract: Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS) caused by CNS-infiltrating leukocytes, including ... ...

Abstract	Multiple sclerosis (MS) is an autoimmune disease of the central nervous system (CNS) caused by CNS-infiltrating leukocytes, including T
MeSH term(s)	Animals ; Humans ; Integrin alpha3 ; Neuroinflammatory Diseases ; Central Nervous System ; Encephalomyelitis, Autoimmune, Experimental ; Multiple Sclerosis
Chemical Substances	Integrin alpha3
Language	English
Publishing date	2023-10-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ISSN	2470-9468
ISSN (online)	2470-9468
DOI	10.1126/sciimmunol.adg7597
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Article ; Online: Inflammasome activation in multiple sclerosis and experimental autoimmune encephalomyelitis (EAE).

Barclay, William / Shinohara, Mari L

Brain pathology (Zurich, Switzerland)

2017 Volume 27, Issue 2, Page(s) 213–219

Abstract: The aptly named inflammasomes are powerful signaling complexes that sense inflammatory signals under a myriad of conditions, including those from infections and endogenous sources. The inflammasomes promote inflammation by maturation and release of the ... ...

Abstract	The aptly named inflammasomes are powerful signaling complexes that sense inflammatory signals under a myriad of conditions, including those from infections and endogenous sources. The inflammasomes promote inflammation by maturation and release of the pro-inflammatory cytokines, IL-1β and IL-18. Several inflammasomes have been identified so far, but this review focuses mainly on the NLRP3 inflammasome. By still ill-defined activation mechanisms, a sensor molecule, NLRP3 (NACHT, LRR and PYD domains-containing protein 3), responds to danger signals and rapidly recruits ASC (apoptosis-associated speck-like protein containing a CARD) and pro-caspase-1 to form a large oligomeric signaling platform-the inflammasome. Involvement of the NLRP3 inflammasome in infections, metabolic disorders, autoinflammation, and autoimmunity, underscores its position as a central player in sensing microbial and damage signals and coordinating pro-inflammatory immune responses. Indeed, evidence in patients with multiple sclerosis (MS) suggests inflammasome activation occurs during disease. Experiments with the mouse model of MS, experimental autoimmune encephalomyelitis (EAE), specifically describe the NLRP3 inflammasome as critical and necessary to disease development. This review discusses recent studies in EAE and MS which describe associations of inflammasome activation with promotion of T cell pathogenicity, infiltration of cells into the central nervous system (CNS) and direct neurodegeneration during EAE and MS.
MeSH term(s)	Animals ; Carrier Proteins/metabolism ; Caspase 1/metabolism ; Central Nervous System/metabolism ; Disease Models, Animal ; Encephalomyelitis, Autoimmune, Experimental/metabolism ; Encephalomyelitis, Autoimmune, Experimental/pathology ; Humans ; Inflammasomes/metabolism ; Inflammasomes/physiology ; Inflammation ; Interleukin-18/metabolism ; Interleukin-1beta/metabolism ; Interleukin-1beta/physiology ; Mice ; Multiple Sclerosis/metabolism ; Multiple Sclerosis/pathology ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/physiology ; Signal Transduction
Chemical Substances	Carrier Proteins ; IL18 protein, human ; Inflammasomes ; Interleukin-18 ; Interleukin-1beta ; NLR Family, Pyrin Domain-Containing 3 Protein ; Caspase 1 (EC 3.4.22.36)
Language	English
Publishing date	2017-02-08
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	1051484-3
ISSN	1750-3639 ; 1015-6305
ISSN (online)	1750-3639
ISSN	1015-6305
DOI	10.1111/bpa.12477
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Zs.A 3585: Show issues

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Article: Roles of Autophagy and Autophagy-Related Proteins in Antifungal Immunity.

Kanayama, Masashi / Shinohara, Mari L

Frontiers in immunology

2016 Volume 7, Page(s) 47

Abstract: Autophagy was initially characterized as a process to digest cellular components, including damaged cell organelles or unused proteins. However, later studies showed that autophagy plays an important role to protect hosts from microbial infections. ... ...

Abstract	Autophagy was initially characterized as a process to digest cellular components, including damaged cell organelles or unused proteins. However, later studies showed that autophagy plays an important role to protect hosts from microbial infections. Accumulating evidences showed the contribution of autophagy itself and autophagy-related proteins (ATGs) in the clearance of bacteria, virus, and parasites. A number of studies also revealed the molecular mechanisms by which autophagy is initiated and developed. Furthermore, it is now understood that some ATGs are shared between two distinct processes; autophagy and LC3-associated phagocytosis (LAP). Thus, our understanding on autophagy has been greatly enhanced in the last decade. By contrast, roles of autophagy and ATGs in fungal infections are still elusive relative to those in bacterial and viral infections. Based on limited numbers of reports, ATG-mediated host responses appear to significantly vary depending on invading fungal species. In this review, we discuss how autophagy and ATGs are involved in antifungal immune responses based on recent discoveries.
Language	English
Publishing date	2016
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2016.00047
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