Michal Schwartz

Last updated
Michal Schwartz
Prof. Michal Schwarz.jpg
Born (1950-01-01) 1 January 1950 (age 74)
Tel Aviv, Israel
Nationality Israeli
Scientific career
Fields Neuroimmunology [1]
Institutions Weizmann Institute of Science
Doctoral students
Website www.weizmann.ac.il/neurobiology/labs/schwartz OOjs UI icon edit-ltr-progressive.svg

Michal Schwartz (born 1 January 1950) is a professor of neuroimmunology at the Weizmann Institute of Science. She is active in the field of neurodegenerative diseases, particularly utilizing the immune system to help the brain fight terminal neurodegenerative brain diseases, such as Alzheimer's disease and dementia. [3] [1]

Contents

Schwartz's studies have shown that the immune system supports a healthy brain's function and is vital for healing and protecting the brain in case of injury or disease. [4]

Schwartz coined the term protective autoimmunity [5] and discovered roles for immune cells in repair and neurogenesis. She has been the elected chair of the International Society of Neuroimmunology (ISNI) since 2016. [6]

In 2023 Schwartz received the honorary Israel Prize for Life Sciences.

Education

Schwartz gained her Bachelor of Science in chemistry at the Hebrew University of Jerusalem in 1972. She received her Ph.D in Immunology in 1977 at the Weizmann Institute of Science, where she would later spend the majority of her career. She also spent time at the University of Michigan, Ann Arbor, researching nerve regeneration.[ when? ]

Career and research

At the Weizmann Institute, she progressed from senior scientist in the Department of Neurobiology to full professor in 1998, and was then awarded the Maurice and Ilse Katz Professorial Chair in Neuroimmunology in 2016. [7] Schwartz's work in neuroimmunology has encompassed a wide range of pathologies in the central nervous system (CNS), including injury, neurodegeneration, mental dysfunction, and aging. She coined the term protective autoimmunity and demonstrated the role of immune cells such as macrophages and T cells in spinal cord repair. She also identified specific brain areas for 'cross talk' between the CNS and the immune system. This cross-talk is important for recruiting immune cells and maintaining a healthy brain, and the disruption of this cross-talk can play a role in brain aging and neurodegenerative disease. She also showed this role in pregnancy and fetal brain development, where immune disruption in the mother can be linked to neurodevelopmental disorders in their children. Another focus of her work has been on repurposing cancer immunotherapies such as PD-1 blockers to treat neurodegenerative disorders, such as Alzheimer's disease.

Macrophages

The Schwartz team discovered that bone marrow-derived macrophages are needed for central nervous system (CNS) repair. The brain-resident myeloid cells (the microglia), and infiltrating monocyte-derived macrophages are not redundant populations, despite their myeloid phenotype, and display distinct functions in resolution of brain inflammation. [8] [9] [10]

Autoimmunity

In her research, Schwartz discovered that the ability to cope with sterile CNS injuries requires support in the form of an adaptive immune response mediated by CD4+ T cells that recognize CNS antigens. She coined the concept of protective autoimmunity, to distinguish this response from autoimmune disease, in which the anti-self response escapes control. Over the years, it became clear that adaptive immunity is needed to facilitate the recruitment of immunoregulatory cells, including bone marrow-derived macrophages and FoxP3 regulatory T cells, though the balance between regulatory T cells and effector memory cells is different in the periphery versus the brain. [11] [12] [13]

Brain Homeostasis

Schwartz’s team discovered the role of adaptive systemic immune cells, and specifically T cells recognizing brain antigens (Protective autoimmune T cells), in supporting the cognitive capacity of the healthy brain, for lifelong neurogenesis, and functional brain plasticity. These observations paved the way for numerous additional discoveries in which the brain-immune axis was described. [14] [15] [16]

The Choroid Plexus

Schwartz’s team identified the brain’s choroid plexus (CP) within the blood-cerebrospinal fluid barrier as an immunological interface between the brain and the immune system. It serves as a niche that hosts immune cells, and as a physiological entry gate for leukocytes. Focusing on this unique niche within the brain led the Schwartz group to propose that IFN-γ holds the key to regulating CP gateway activity. Her team further showed that in brain aging and neurodegenerative diseases (studied using both mouse models and human samples), dysfunction of this interface is determined both by signals originating in the brain, and signals from the aged immune system, which led to the identification of Type-I Interferon (IFN-I) at the CP as a negative player, affecting the fate of the aging brain in general, and of microglia, in particular. A similar IFN-I signature at the CP was subsequently discovered by others in Alzheimer’s disease and in the postmortem brains of infected patients who died from COVID-19. [17] [14] [10]

Immunotherapy

The discovery that adaptive immunity plays a key role in brain function and repair, the need for bone marrow-derived macrophages to resolve local brain inflammation, the fact that Alzheimer's disease (AD) and all forms of dementia are mainly age-related diseases, and the fact that the immune system is particularly affected by aging all led Schwartz to propose a new treatment for combating dementias. Schwartz suggested empowering systemic immunity, using a form of immunotherapy by modestly blocking the inhibitory immune checkpoint PD1/PD-L1 pathway.[ citation needed ] This treatment drives an immune-dependent cascade of events, that allows the harnessing of bone marrow-derived macrophages and regulatory T cells to help clear toxic factors from the diseased brain, and to arrest the local inflammation, thereby providing a comprehensive multi-factorial therapy through modification of multiple elements that go awry in AD. Schwartz’s patents for developing such immunotherapy for AD are licensed to a small Biopharma company, Immunobrain Checkpoint. The company is awaiting a clinical trial in AD patients, supported in part by the National Institute of Aging, the US National Institutes of Health, and The Alzheimer's Association. [18] [19] [20] [21] [22] [23]

Students

Schwartz has mentored approximately 40 Ph.D. students [ citation needed ], [24] [9] and approximately 39 MSc students.[ citation needed ] [25] [26] Her former Ph.D students include Jonathan Kipnis, [16] Noga Ron Harel, Jasmin Fisher, [2] Asya Rolls.[ citation needed ] [25] [26] [9]

Related Research Articles

<span class="mw-page-title-main">Stromal cell-derived factor 1</span> Mammalian protein found in Homo sapiens

The stromal cell-derived factor 1 (SDF-1), also known as C-X-C motif chemokine 12 (CXCL12), is a chemokine protein that in humans is encoded by the CXCL12 gene on chromosome 10. It is ubiquitously expressed in many tissues and cell types. Stromal cell-derived factors 1-alpha and 1-beta are small cytokines that belong to the chemokine family, members of which activate leukocytes and are often induced by proinflammatory stimuli such as lipopolysaccharide, TNF, or IL1. The chemokines are characterized by the presence of 4 conserved cysteines that form 2 disulfide bonds. They can be classified into 2 subfamilies. In the CC subfamily, the cysteine residues are adjacent to each other. In the CXC subfamily, they are separated by an intervening amino acid. The SDF1 proteins belong to the latter group. CXCL12 signaling has been observed in several cancers. The CXCL12 gene also contains one of 27 SNPs associated with increased risk of coronary artery disease.

<span class="mw-page-title-main">Microglia</span> Glial cell located throughout the brain and spinal cord

Microglia are a type of neuroglia located throughout the brain and spinal cord. Microglia account for about 10-15% of cells found within the brain. As the resident macrophage cells, they act as the first and main form of active immune defense in the central nervous system (CNS). Microglia originate in the yolk sac under a tightly regulated molecular process. These cells are distributed in large non-overlapping regions throughout the CNS. Microglia are key cells in overall brain maintenance—they are constantly scavenging the CNS for plaques, damaged or unnecessary neurons and synapses, and infectious agents. Since these processes must be efficient to prevent potentially fatal damage, microglia are extremely sensitive to even small pathological changes in the CNS. This sensitivity is achieved in part by the presence of unique potassium channels that respond to even small changes in extracellular potassium. Recent evidence shows that microglia are also key players in the sustainment of normal brain functions under healthy conditions. Microglia also constantly monitor neuronal functions through direct somatic contacts and exert neuroprotective effects when needed.

Neuroimmunology is a field combining neuroscience, the study of the nervous system, and immunology, the study of the immune system. Neuroimmunologists seek to better understand the interactions of these two complex systems during development, homeostasis, and response to injuries. A long-term goal of this rapidly developing research area is to further develop our understanding of the pathology of certain neurological diseases, some of which have no clear etiology. In doing so, neuroimmunology contributes to development of new pharmacological treatments for several neurological conditions. Many types of interactions involve both the nervous and immune systems including the physiological functioning of the two systems in health and disease, malfunction of either and or both systems that leads to disorders, and the physical, chemical, and environmental stressors that affect the two systems on a daily basis.

<span class="mw-page-title-main">Neuroimmune system</span>

The neuroimmune system is a system of structures and processes involving the biochemical and electrophysiological interactions between the nervous system and immune system which protect neurons from pathogens. It serves to protect neurons against disease by maintaining selectively permeable barriers, mediating neuroinflammation and wound healing in damaged neurons, and mobilizing host defenses against pathogens.

<span class="mw-page-title-main">Neurodegenerative disease</span> Central nervous system disease

A neurodegenerative disease is caused by the progressive loss of structure or function of neurons, in the process known as neurodegeneration. Such neuronal damage may ultimately involve cell death. Neurodegenerative diseases include amyotrophic lateral sclerosis, multiple sclerosis, Parkinson's disease, Alzheimer's disease, Huntington's disease, multiple system atrophy, tauopathies, and prion diseases. Neurodegeneration can be found in the brain at many different levels of neuronal circuitry, ranging from molecular to systemic. Because there is no known way to reverse the progressive degeneration of neurons, these diseases are considered to be incurable; however research has shown that the two major contributing factors to neurodegeneration are oxidative stress and inflammation. Biomedical research has revealed many similarities between these diseases at the subcellular level, including atypical protein assemblies and induced cell death. These similarities suggest that therapeutic advances against one neurodegenerative disease might ameliorate other diseases as well.

<span class="mw-page-title-main">Monoclonal antibody therapy</span> Form of immunotherapy

Monoclonal antibodies (mAbs) have varied therapeutic uses. It is possible to create a mAb that binds specifically to almost any extracellular target, such as cell surface proteins and cytokines. They can be used to render their target ineffective, to induce a specific cell signal, to cause the immune system to attack specific cells, or to bring a drug to a specific cell type.

<span class="mw-page-title-main">Toll-like receptor 4</span> Cell surface receptor found in humans

Toll-like receptor 4 (TLR4), also designated as CD284, is a key activator of the innate immune response and plays a central role in the fight against bacterial infections. TLR4 is a transmembrane protein of approximately 95 kDa that is encoded by the TLR4 gene.

Certain sites of the mammalian body have immune privilege, meaning they are able to tolerate the introduction of antigens without eliciting an inflammatory immune response. Tissue grafts are normally recognised as foreign antigens by the body and attacked by the immune system. However, in immune privileged sites, tissue grafts can survive for extended periods of time without rejection occurring. Immunologically privileged sites include:

<span class="mw-page-title-main">PD-L1</span> Mammalian protein found in humans

Programmed death-ligand 1 (PD-L1) also known as cluster of differentiation 274 (CD274) or B7 homolog 1 (B7-H1) is a protein that in humans is encoded by the CD274 gene.

<span class="mw-page-title-main">Colony stimulating factor 1 receptor</span> Protein found in humans

Colony stimulating factor 1 receptor (CSF1R), also known as macrophage colony-stimulating factor receptor (M-CSFR), and CD115, is a cell-surface protein encoded by the human CSF1R gene. CSF1R is a receptor that can be activated by two ligands: colony stimulating factor 1 (CSF-1) and interleukin-34 (IL-34). CSF1R is highly expressed in myeloid cells, and CSF1R signaling is necessary for the survival, proliferation, and differentiation of many myeloid cell types in vivo and in vitro. CSF1R signaling is involved in many diseases and is targeted in therapies for cancer, neurodegeneration, and inflammatory bone diseases.

<span class="mw-page-title-main">Programmed cell death protein 1</span> Mammalian protein found in humans

Programmed cell death protein 1(PD-1),. PD-1 is a protein encoded in humans by the PDCD1 gene. PD-1 is a cell surface receptor on T cells and B cells that has a role in regulating the immune system's response to the cells of the human body by down-regulating the immune system and promoting self-tolerance by suppressing T cell inflammatory activity. This prevents autoimmune diseases, but it can also prevent the immune system from killing cancer cells.

<span class="mw-page-title-main">TREM2</span> Protein-coding gene in the species Homo sapiens

Triggering receptor expressed on myeloid cells 2(TREM2) is a protein that in humans is encoded by the TREM2 gene. TREM2 is expressed on macrophages, immature monocyte-derived dendritic cells, osteoclasts, and microglia, which are immune cells in the central nervous system. In the liver, TREM2 is expressed by several cell types, including macrophages, that respond to injury. In the intestine, TREM2 is expressed by myeloid-derived dendritic cells and macrophage. TREM2 is overexpressed in many tumor types and has anti-inflammatory activities. It might therefore be a good therapeutic target.

Protective autoimmunity is a condition in which cells of the adaptive immune system contribute to maintenance of the functional integrity of a tissue, or facilitate its repair following an insult. The term ‘protective autoimmunity’ was coined by Prof. Michal Schwartz of the Weizmann Institute of Science (Israel), whose pioneering studies were the first to demonstrate that autoimmune T lymphocytes can have a beneficial role in repair, following an injury to the central nervous system (CNS). Most of the studies on the phenomenon of protective autoimmunity were conducted in experimental settings of various CNS pathologies and thus reside within the scientific discipline of neuroimmunology.

Neuroinflammation is inflammation of the nervous tissue. It may be initiated in response to a variety of cues, including infection, traumatic brain injury, toxic metabolites, or autoimmunity. In the central nervous system (CNS), including the brain and spinal cord, microglia are the resident innate immune cells that are activated in response to these cues. The CNS is typically an immunologically privileged site because peripheral immune cells are generally blocked by the blood–brain barrier (BBB), a specialized structure composed of astrocytes and endothelial cells. However, circulating peripheral immune cells may surpass a compromised BBB and encounter neurons and glial cells expressing major histocompatibility complex molecules, perpetuating the immune response. Although the response is initiated to protect the central nervous system from the infectious agent, the effect may be toxic and widespread inflammation as well as further migration of leukocytes through the blood–brain barrier may occur.

<span class="mw-page-title-main">Meningeal lymphatic vessels</span>

The meningeal lymphatic vessels are a network of conventional lymphatic vessels located parallel to the dural venous sinuses and middle meningeal arteries of the mammalian central nervous system (CNS). As a part of the lymphatic system, the meningeal lymphatics are responsible for draining immune cells, small molecules, and excess fluid from the CNS into the deep cervical lymph nodes. Cerebrospinal fluid, and interstitial fluid are exchanged, and drained by the meningeal lymphatic vessels.

<span class="mw-page-title-main">Pathophysiology of Parkinson's disease</span> Medical condition

The pathophysiology of Parkinson's disease is death of dopaminergic neurons as a result of changes in biological activity in the brain with respect to Parkinson's disease (PD). There are several proposed mechanisms for neuronal death in PD; however, not all of them are well understood. Five proposed major mechanisms for neuronal death in Parkinson's Disease include protein aggregation in Lewy bodies, disruption of autophagy, changes in cell metabolism or mitochondrial function, neuroinflammation, and blood–brain barrier (BBB) breakdown resulting in vascular leakiness.

<span class="mw-page-title-main">Jonathan Kipnis</span> Neuroscientist

Jonathan Kipnis is a neuroscientist, immunologist, and professor of pathology and immunology at the Washington University School of Medicine. His lab studies interactions between the immune system and nervous system. He is best known for his lab's discovery of meningeal lymphatic vessels in humans and mice, which has impacted research on neurodegenerative diseases such as Alzheimer's disease and multiple sclerosis, neuropsychiatric disorders, such as anxiety, and neurodevelopmental disorders such as autism and Rett syndrome.

Microglia are the primary immune cells of the central nervous system, similar to peripheral macrophages. They respond to pathogens and injury by changing morphology and migrating to the site of infection/injury, where they destroy pathogens and remove damaged cells.

Melanie Greter is a Swiss neuroimmunologist and a Swiss National Science Foundation Professor in the Institute of Experimental Immunology at the University of Zurich. Greter explores the ontogeny and function of microglia and border-associated macrophages of the central nervous system to understand how they maintain homeostasis and contribute to brain-related diseases.

Malú G. Tansey is an American Physiologist and Neuroscientist as well as the Director of the Center for Translational Research in Neurodegenerative Disease at the University of Florida. Tansey holds the titles of Evelyn F. and William L. McKnight Brain Investigator and Norman Fixel Institute for Neurological Diseases Investigator. As the principal investigator of the Tansey Lab, Tansey guides a research program centered around investigating the role of neuroimmune interactions in the development and progression of neurodegenerative and neuropsychiatric disease. Tansey's work is primarily focused on exploring the cellular and molecular basis of peripheral and central inflammation in the pathology of age-related neurodegenerative diseases like Alzheimer's disease and amyotrophic lateral sclerosis.

References

  1. 1 2 Michal Schwartz publications indexed by Google Scholar OOjs UI icon edit-ltr-progressive.svg
  2. 1 2 "Making Sense of a Complex Situation - Weizmann Wonder Wander - News, Features and Discoveries". weizmann.ac.il. Weizmann Wonder Wander - News, Features and Discoveries from the Weizmann Institute of Science. 2013-02-24. Retrieved 2022-08-05.
  3. ↑ Michal Schwartz publications from Europe PubMed Central
  4. ↑ Schwartz, Michal; Kipnis, Jonathan; Rivest, Serge; Prat, Alexandre (2013-11-06). "How Do Immune Cells Support and Shape the Brain in Health, Disease, and Aging?". The Journal of Neuroscience. 33 (45): 17587–17596. doi:10.1523/JNEUROSCI.3241-13.2013. ISSN   0270-6474. PMC   3818540 . PMID   24198349.
  5. ↑ Schwartz, Michal (January 2000). "Protective autoimmunity: potential treatment for traumatized optic nerves". Neuro-Ophthalmology. 24 (3): 395–399. doi:10.1076/noph.24.3.395.7142.[ non-primary source needed ]
  6. ↑ "Schwartz, Michal" . Retrieved 2023-11-10.
  7. ↑ "Michal Schwartz | Britannica, Biography & Facts". 9 May 2024.
  8. ↑ Shechter, Ravid; London, Anat; Varol, Chen; Raposo, Catarina; Cusimano, Melania; Yovel, Gili; Rolls, Asya; Mack, Matthias; Pluchino, Stefano; Martino, Gianvito; Jung, Steffen; Schwartz, Michal (2009). "Infiltrating Blood-Derived Macrophages Are Vital Cells Playing an Anti-inflammatory Role in Recovery from Spinal Cord Injury in Mice". PLOS Medicine. 6 (7): e1000113. doi: 10.1371/journal.pmed.1000113 . PMC   2707628 . PMID   19636355.
  9. 1 2 3 Rapalino, O.; Lazarov-Spiegler, O.; Agranov, E.; Velan, G.J.; Yoles, E.; Fraidakis, M.; Soloman, A.; Gepstein, R.; Katz, A.; Belkin, M.; Hadani, M.; Schwartz, M. (July 1998). "Implantation of stimulated homologous macrophages results in partial recovery of paraplegic rats". Nature Medicine. 4 (7): 814–821. doi:10.1038/nm0798-814. PMID   9662373.[ non-primary source needed ]
  10. 1 2 Shechter, Ravid; Miller, Omer; Yovel, Gili; Rosenzweig, Neta; London, Anat; Ruckh, Julia; Kim, Ki-Wook; Klein, Eugenia; Kalchenko, Vyacheslav; Bendel, Peter; Lira, Sergio A.; Jung, Steffen; Schwartz, Michal (2013). "Recruitment of Beneficial M2 Macrophages to Injured Spinal Cord is Orchestrated by Remote Brain Choroid Plexus". Immunity. 38 (3): 555–569. doi:10.1016/j.immuni.2013.02.012. PMC   4115271 . PMID   23477737.
  11. ↑ Hauben, Ehud; Agranov, Eugenia; Gothilf, Amalia; Nevo, Uri; Cohen, Avi; Smirnov, Igor; Steinman, Lawrence; Schwartz, Michal (2001). "Posttraumatic therapeutic vaccination with modified myelin self-antigen prevents complete paralysis while avoiding autoimmune disease". Journal of Clinical Investigation. 108 (4): 591–599. doi:10.1172/JCI12837. PMC   209402 . PMID   11518733.
  12. ↑ Yoles, Eti; Hauben, Ehud; Palgi, Orna; Agranov, Evgenia; Gothilf, Amalia; Cohen, Avi; Kuchroo, Vijay; Cohen, Irun R.; Weiner, Howard; Schwartz, Michal (2001). "Protective Autoimmunity is a Physiological Response to CNS Trauma". The Journal of Neuroscience. 21 (11): 3740–3748. doi:10.1523/JNEUROSCI.21-11-03740.2001. PMC   6762728 . PMID   11356861.
  13. ↑ Moalem, Gila; Leibowitz–Amit, Raya; Yoles, Eti; Mor, Felix; Cohen, Irun R.; Schwartz, Michal (1999). "Autoimmune T cells protect neurons from secondary degeneration after central nervous system axotomy". Nature Medicine. 5 (1): 49–55. doi:10.1038/4734. PMID   9883839. S2CID   8877114.
  14. 1 2 Baruch, Kuti; Deczkowska, Aleksandra; David, Eyal; Castellano, Joseph M.; Miller, Omer; Kertser, Alexander; Berkutzki, Tamara; Barnett-Itzhaki, Zohar; Bezalel, Dana; Wyss-Coray, Tony; Amit, Ido; Schwartz, Michal (2014). "Aging-induced type I interferon response at the choroid plexus negatively affects brain function". Science. 346 (6205): 89–93. Bibcode:2014Sci...346...89B. doi:10.1126/science.1252945. PMC   4869326 . PMID   25147279.
  15. ↑ Ziv, Yaniv; Ron, Noga; Butovsky, Oleg; Landa, Gennady; Sudai, Einav; Greenberg, Nadav; Cohen, Hagit; Kipnis, Jonathan; Schwartz, Michal (2006). "Immune cells contribute to the maintenance of neurogenesis and spatial learning abilities in adulthood". Nature Neuroscience. 9 (2): 268–275. doi:10.1038/nn1629. PMID   16415867. S2CID   205430936.
  16. 1 2 Kipnis, Jonathan; Cohen, Hagit; Cardon, Michal; Ziv, Yaniv; Schwartz, Michal (25 May 2004). "T cell deficiency leads to cognitive dysfunction: Implications for therapeutic vaccination for schizophrenia and other psychiatric conditions". Proceedings of the National Academy of Sciences. 101 (21): 8180–8185. Bibcode:2004PNAS..101.8180K. doi: 10.1073/pnas.0402268101 . PMC   419577 . PMID   15141078.[ non-primary source needed ]
  17. ↑ Deczkowska, Aleksandra; Matcovitch-Natan, Orit; Tsitsou-Kampeli, Afroditi; Ben-Hamo, Sefi; Dvir-Szternfeld, Raz; Spinrad, Amit; Singer, Oded; David, Eyal; Winter, Deborah R.; Smith, Lucas K.; Kertser, Alexander; Baruch, Kuti; Rosenzweig, Neta; Terem, Anna; Prinz, Marco; Villeda, Saul; Citri, Ami; Amit, Ido; Schwartz, Michal (2017). "Mef2C restrains microglial inflammatory response and is lost in brain ageing in an IFN-I-dependent manner". Nature Communications. 8 (1): 717. Bibcode:2017NatCo...8..717D. doi:10.1038/s41467-017-00769-0. PMC   5620041 . PMID   28959042.
  18. ↑ Baruch, Kuti; Deczkowska, Aleksandra; Rosenzweig, Neta; Tsitsou-Kampeli, Afroditi; Sharif, Alaa Mohammad; Matcovitch-Natan, Orit; Kertser, Alexander; David, Eyal; Amit, Ido; Schwartz, Michal (2016). "PD-1 immune checkpoint blockade reduces pathology and improves memory in mouse models of Alzheimer's disease". Nature Medicine. 22 (2): 135–137. doi:10.1038/nm.4022. PMID   26779813. S2CID   20699898.
  19. ↑ Ben-Yehuda, Hila; Arad, Michal; Peralta Ramos, Javier María; Sharon, Efrat; Castellani, Giulia; Ferrera, Shir; Cahalon, Liora; Colaiuta, Sarah Phoebeluc; Salame, Tomer-Meir; Schwartz, Michal (2021). "Key role of the CCR2-CCL2 axis in disease modification in a mouse model of tauopathy". Molecular Neurodegeneration. 16 (1): 39. doi: 10.1186/s13024-021-00458-z . PMC   8234631 . PMID   34172073.
  20. ↑ Dvir-Szternfeld, Raz; Castellani, Giulia; Arad, Michal; Cahalon, Liora; Colaiuta, Sarah Phoebeluc; Keren-Shaul, Hadas; Croese, Tommaso; Burgaletto, Chiara; Baruch, Kuti; Ulland, Tyler; Colonna, Marco; Weiner, Assaf; Amit, Ido; Schwartz, Michal (2021). "Alzheimer's disease modification mediated by bone marrow-derived macrophages via a TREM2-independent pathway in mouse model of amyloidosis". Nature Aging. 2 (1): 60–73. doi:10.1038/s43587-021-00149-w. PMID   37118355. S2CID   245371515.
  21. ↑ Rosenzweig, Neta; Dvir-Szternfeld, Raz; Tsitsou-Kampeli, Afroditi; Keren-Shaul, Hadas; Ben-Yehuda, Hila; Weill-Raynal, Pierre; Cahalon, Liora; Kertser, Alex; Baruch, Kuti; Amit, Ido; Weiner, Assaf; Schwartz, Michal (2019). "PD-1/PD-L1 checkpoint blockade harnesses monocyte-derived macrophages to combat cognitive impairment in a tauopathy mouse model". Nature Communications. 10 (1): 465. Bibcode:2019NatCo..10..465R. doi:10.1038/s41467-019-08352-5. PMC   6349941 . PMID   30692527.[ non-primary source needed ]
  22. ↑ Schwartz, Michal (2017). "Can immunotherapy treat neurodegeneration?". Science. 357 (6348): 254–255. Bibcode:2017Sci...357..254S. doi:10.1126/science.aai8231. PMID   28729500. S2CID   20559985.
  23. ↑ "ImmunoBrain Checkpoint Awarded $5 Million US NIA Grant for Phase 1b Alzheimer's Disease Proof-of-Mechanism Study of Anti-PD-L1 IBC-Ab002". GlobeNewswire News Room (Press release). 2021-08-27. Retrieved 2023-01-13.
  24. ↑ Ziv, Yaniv; Ron, Noga; Butovsky, Oleg; Landa, Gennady; Sudai, Einav; Greenberg, Nadav; Cohen, Hagit; Kipnis, Jonathan; Schwartz, Michal (February 2006). "Immune cells contribute to the maintenance of neurogenesis and spatial learning abilities in adulthood". Nature Neuroscience. 9 (2): 268–275. doi:10.1038/nn1629. PMID   16415867.[ non-primary source needed ]
  25. 1 2 Nevo, Uri; Kipnis, Jonathan; Golding, Ido; Shaked, Iftach; Neumann, Avidan; Akselrod, Solange; Schwartz, Michal (March 2003). "Autoimmunity as a special case of immunity: removing threats from within". Trends in Molecular Medicine. 9 (3): 88–93. doi:10.1016/S1471-4914(03)00024-8. PMID   12657429.[ non-primary source needed ]
  26. 1 2 Butovsky, O.; Landa, G; Kunis, G; Ziv, Y; Avidan, H; Greenberg, N; Schwartz, A; Smirnov, I; Pollack, A; Jung, S; Schwartz, M (23 March 2006). "Induction and blockage of oligodendrogenesis by differently activated microglia in an animal model of multiple sclerosis". Journal of Clinical Investigation. 116 (4): 905–915. doi:10.1172/JCI26836. PMC   1409740 . PMID   16557302.[ non-primary source needed ]
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