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Article ; Online: Immunotherapy for neuroblastoma by hematopoietic cell transplantation and post-transplant immunomodulation.

Ash, Shifra / Askenasy, Nadir

2023 Volume 185, Page(s) 103956

Abstract: Neuroblastoma represents a relatively common childhood tumor that imposes therapeutic difficulties. High risk neuroblastoma patients have poor prognosis, display limited response to radiochemotherapy and may be treated by hematopoietic cell ... ...

Abstract	Neuroblastoma represents a relatively common childhood tumor that imposes therapeutic difficulties. High risk neuroblastoma patients have poor prognosis, display limited response to radiochemotherapy and may be treated by hematopoietic cell transplantation. Allogeneic and haploidentical transplants have the distinct advantage of reinstitution of immune surveillance, reinforced by antigenic barriers. The key factors favorable to ignition of potent anti-tumor reactions are transition to adaptive immunity, recovery from lymphopenia and removal of inhibitory signals that inactivate immune cells at the local and systemic levels. Post-transplant immunomodulation may further foster anti-tumor reactivity, with positive but transient impact of infusions of lymphocytes and natural killer cells both from the donor, the recipient or third party. The most promising approaches include introduction of antigen-presenting cells in early post-transplant stages and neutralization of inhibitory signals. Further studies will likely shed light on the nature and actions of suppressor factors within tumor stroma and at the systemic level.
MeSH term(s)	Humans ; Child ; Graft vs Host Disease ; Transplantation, Homologous ; Hematopoietic Stem Cell Transplantation/adverse effects ; Immunotherapy ; Neuroblastoma/therapy ; Neuroblastoma/pathology
Language	English
Publishing date	2023-03-07
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	605680-5
ISSN	1879-0461 ; 0737-9587 ; 1040-8428
ISSN (online)	1879-0461
ISSN	0737-9587 ; 1040-8428
DOI	10.1016/j.critrevonc.2023.103956
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Article ; Online: Mechanisms of autoimmunity in the non-obese diabetic mouse: effector/regulatory cell equilibrium during peak inflammation.

Askenasy, Nadir

Immunology

2016 Volume 147, Issue 4, Page(s) 377–388

Abstract: Immune imbalance in autoimmune disorders such as type 1 diabetes may originate from aberrant activities of effector cells or dysfunction of suppressor cells. All possible defective mechanisms have been proposed for diabetes-prone species: (i) ... ...

Abstract	Immune imbalance in autoimmune disorders such as type 1 diabetes may originate from aberrant activities of effector cells or dysfunction of suppressor cells. All possible defective mechanisms have been proposed for diabetes-prone species: (i) quantitative dominance of diabetogenic cells and decreased numbers of regulatory T cells, (ii) excessive aggression of effectors and defective function of suppressors, (iii) perturbed interaction between effector and suppressor cells, and (iv) variations in sensitivity to negative regulation. The experimental evidence available to date presents conflicting information on these mechanisms, with identification of perturbed equilibrium on the one hand and negation of critical role of each mechanism in propagation of diabetic autoimmunity on the other hand. In our analysis, there is no evidence that inherent abnormalities in numbers and function of effector and suppressor T cells are responsible for the immune imbalance responsible for propagation of type 1 diabetes as a chronic inflammatory process. Possibly, the experimental tools for investigation of these features of immune activity are still underdeveloped and lack sufficient resolution, in the presence of the extensive biological viability and functional versatility of effector and suppressor elements.
MeSH term(s)	Animals ; Apoptosis/immunology ; Autoimmunity ; Cell Communication/immunology ; Diabetes Mellitus, Experimental ; Diabetes Mellitus, Type 1/immunology ; Diabetes Mellitus, Type 1/metabolism ; Disease Progression ; Inflammation/immunology ; Inflammation/metabolism ; Lymphocyte Activation/immunology ; Mice ; Mice, Inbred NOD ; T-Lymphocyte Subsets/immunology ; T-Lymphocyte Subsets/metabolism
Language	English
Publishing date	2016-04
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	80124-0
ISSN	1365-2567 ; 0019-2805 ; 0953-4954
ISSN (online)	1365-2567
ISSN	0019-2805 ; 0953-4954
DOI	10.1111/imm.12581
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Article ; Online: Mechanisms of diabetic autoimmunity: I--the inductive interface between islets and the immune system at onset of inflammation.

Askenasy, Nadir

Immunologic research

2016 Volume 64, Issue 2, Page(s) 360–368

Abstract: The mechanisms of autoimmune reactivity onset in type 1 diabetes (T1D) remain elusive despite extensive experimentation and discussion. We reconsider several key aspects of the early stages of autoimmunity at four levels: islets, pancreatic lymph nodes, ... ...

Abstract	The mechanisms of autoimmune reactivity onset in type 1 diabetes (T1D) remain elusive despite extensive experimentation and discussion. We reconsider several key aspects of the early stages of autoimmunity at four levels: islets, pancreatic lymph nodes, thymic function and peripheral immune homeostasis. Antigen presentation is the islets and has the capacity to provoke immune sensitization, either in the process of physiological neonatal β cell apoptosis or as a consequence of cytolytic activity of self-reactive thymocytes that escaped negative regulation. Diabetogenic effectors are efficiently expanded in both the islets and the lymph nodes under conditions of empty lymphoid niches during a period of time coinciding with a synchronized wave of β cell apoptosis surrounding weaning. A major drive of effector cell activation and expansion is inherent peripheral lymphopenia characteristic of neonates, though it remains unclear when is autoimmunity triggered in subjects displaying hyperglycemia in late adolescence. Our analysis suggests that T1D evolves through coordinated activity of multiple physiological mechanisms of stimulation within specific characteristics of the neonate immune system.
MeSH term(s)	Animals ; Apoptosis ; Autoantigens/immunology ; Autoimmunity ; Diabetes Mellitus, Type 1/immunology ; Disease Susceptibility ; Homeostasis ; Humans ; Immune System/cytology ; Immune System/immunology ; Immune System/metabolism ; Immunologic Surveillance ; Inflammation/immunology ; Islets of Langerhans/cytology ; Islets of Langerhans/immunology ; Islets of Langerhans/metabolism ; Lymphocyte Activation ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism
Chemical Substances	Autoantigens
Language	English
Publishing date	2016-04
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	632857-x
ISSN	1559-0755 ; 0257-277X
ISSN (online)	1559-0755
ISSN	0257-277X
DOI	10.1007/s12026-015-8753-y
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Zs.A 1755: Show issues

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Article ; Online: Mechanisms of diabetic autoimmunity: II--Is diabetes a central or peripheral disorder of effector and regulatory cells?

Askenasy, Nadir

Immunologic research

2016 Volume 64, Issue 1, Page(s) 36–43

Abstract: Two competing hypotheses aiming to explain the onset of autoimmune reactions are discussed in the context of genetic and environmental predisposition to type 1 diabetes (T1D). The first hypothesis has evolved along characterization of the mechanisms of ... ...

Abstract	Two competing hypotheses aiming to explain the onset of autoimmune reactions are discussed in the context of genetic and environmental predisposition to type 1 diabetes (T1D). The first hypothesis has evolved along characterization of the mechanisms of self-discrimination and attributes diabetic autoimmunity to escape of reactive T cells from central regulation in the thymus. The second considers frequent occurrence of autoimmune reactions within the immune homunculus, which are adequately suppressed by regulatory T cells originating from the thymus, and occasionally, insufficient suppression results in autoimmunity. Besides thymic dysfunction, deregulation of both effector and suppressor cells can in fact result from homeostatic aberrations at the peripheral level during initial stages of evolution of adaptive immunity. Pathogenic cells sensitized in the islets are efficiently expanded in the target tissue and pancreatic lymph nodes of lymphopenic neonates. In parallel, the same mechanisms of peripheral sensitization contribute to tolerization through education of naïve/effector T cells and expansion of regulatory T cells. Experimental evidence presented for each individual mechanism implies that T1D may result from a primary effector or suppressor immune abnormality. Disturbed self-tolerance leading to T1D may well result from peripheral deregulation of innate and adaptive immunity, with variable contribution of central thymic dysfunction.
MeSH term(s)	Animals ; Autoantigens/immunology ; Autoimmunity ; Central Tolerance ; Diabetes Mellitus, Type 1/immunology ; Gene-Environment Interaction ; Humans ; Peripheral Tolerance ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes, Regulatory/immunology
Chemical Substances	Autoantigens
Language	English
Publishing date	2016-02
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	632857-x
ISSN	1559-0755 ; 0257-277X
ISSN (online)	1559-0755
ISSN	0257-277X
DOI	10.1007/s12026-015-8725-2
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Zs.A 1755: Show issues

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Article ; Online: Interferon and tumor necrosis factor as humoral mechanisms coupling hematopoietic activity to inflammation and injury.

Askenasy, Nadir

Blood reviews

2015 Volume 29, Issue 1, Page(s) 11–15

Abstract: Enhanced hematopoiesis accompanies systemic responses to injury and infection. Tumor necrosis factor (TNF) produced by injured cells and interferons (IFNs) secreted by inflammatory cells is a co-product of the process of clearance of debris and removal ... ...

Abstract	Enhanced hematopoiesis accompanies systemic responses to injury and infection. Tumor necrosis factor (TNF) produced by injured cells and interferons (IFNs) secreted by inflammatory cells is a co-product of the process of clearance of debris and removal of still viable but dysfunctional cells. Concomitantly, these cytokines induce hematopoietic stem and progenitor cell (HSPC) activity as an intrinsic component of the systemic response. The proposed scenario includes induction of HSPC activity by type I (IFNα/β) and II (IFNγ) receptors within the quiescent bone marrow niches rendering progenitors responsive to additional signals. TNFα converges as a non-selective stimulant of HSPC activity and both cytokines synergize with other growth factors in promoting differentiation. These physiological signaling pathways of stress hematopoiesis occur quite frequent and do not cause HSPC extinction. The proposed role of IFNs and TNFs in stress hematopoiesis commends revision of their alleged involvement in bone marrow failure syndromes.
MeSH term(s)	Hematologic Diseases/metabolism ; Hematopoiesis ; Hematopoietic Stem Cells/metabolism ; Humans ; Inflammation/metabolism ; Interferons/metabolism ; Signal Transduction ; Stress, Physiological ; Tumor Necrosis Factors/metabolism
Chemical Substances	Tumor Necrosis Factors ; Interferons (9008-11-1)
Language	English
Publishing date	2015-01
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	639015-8
ISSN	1532-1681 ; 0268-960X
ISSN (online)	1532-1681
ISSN	0268-960X
DOI	10.1016/j.blre.2014.09.002
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Zs.A 2207: Show issues

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Article ; Online: Less is more: the detrimental consequences of immunosuppressive therapy in the treatment of type-1 diabetes.

Askenasy, Nadir

International reviews of immunology

2015 Volume 34, Issue 6, Page(s) 523–537

Abstract: The prevalent current approach to type 1 diabetes (T1D) is the abrogation of pathogenic potential by immunosuppressive therapy, an intuitive approach aiming to slow down disease progression by the reduction of pathogenic burden. In spite of promising ... ...

Abstract	The prevalent current approach to type 1 diabetes (T1D) is the abrogation of pathogenic potential by immunosuppressive therapy, an intuitive approach aiming to slow down disease progression by the reduction of pathogenic burden. In spite of promising initial results in rodent models, there has been little efficacy of most lymphoreductive strategies in human subjects. Our analysis suggests that lymphopenia is the common denominator of ineffective immunosuppressive therapies: Immune rebound from lymphopenia is associated per se with increased susceptibility to immune reactivity, including relapse of autoimmunity. In addition, immune homeostasis and self-tolerance are not restored. These considerations raise the following question: What is the allowed degree of immunosuppressive therapy that does not elicit recurrent autoimmunity. More effective therapeutic strategies include targeted deletion of pathogenic cells, preferably in the pancreatic islets and regional lymphatics using selective T cell activation markers, re-education and remodeling of effector responses.
MeSH term(s)	Animals ; Antibodies, Blocking/pharmacology ; Antibodies, Blocking/therapeutic use ; Antibodies, Monoclonal/pharmacology ; Antibodies, Monoclonal/therapeutic use ; Cell Transplantation ; Chemoradiotherapy/methods ; Clinical Studies as Topic ; Combined Modality Therapy ; Diabetes Mellitus, Type 1/immunology ; Diabetes Mellitus, Type 1/therapy ; Disease Models, Animal ; Humans ; Immunomodulation/drug effects ; Immunosuppression/methods ; Immunosuppressive Agents/pharmacology ; Immunosuppressive Agents/therapeutic use ; Lymphocyte Depletion ; Mice ; Prognosis ; Recurrence ; Treatment Outcome
Chemical Substances	Antibodies, Blocking ; Antibodies, Monoclonal ; Immunosuppressive Agents
Language	English
Publishing date	2015
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	632825-8
ISSN	1563-5244 ; 1545-5858 ; 0883-0185
ISSN (online)	1563-5244 ; 1545-5858
ISSN	0883-0185
DOI	10.3109/08830185.2015.1010723
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Zs.A 2156: Show issues

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Article ; Online: Enhanced killing activity of regulatory T cells ameliorates inflammation and autoimmunity.

Askenasy, Nadir

Autoimmunity reviews

2013 Volume 12, Issue 10, Page(s) 972–975

Abstract: Regulatory T cells (Treg) are pivotal suppressor elements in immune homeostasis with potential therapeutic applications in inflammatory and autoimmune disorders. Using Treg as vehicles for targeted immunomodulation, a short-lived Fas-ligand (FasL) ... ...

Abstract	Regulatory T cells (Treg) are pivotal suppressor elements in immune homeostasis with potential therapeutic applications in inflammatory and autoimmune disorders. Using Treg as vehicles for targeted immunomodulation, a short-lived Fas-ligand (FasL) chimeric protein (killer Treg) was found efficient in preventing the progression of autoimmune insulitis in NOD mice, and amelioration of chronic colitis and graft versus host disease. The main mechanisms of disease suppression by killer Treg are: a) in the acute phase induction of apoptosis in effector cells at the site of inflammation decreases the pathogenic burden, and b) persistent increase in FoxP3⁺ Treg with variable CD25 co-expression induced by FasL sustains disease suppression over extended periods of time. Reduced sensitivity of Treg to receptor-mediated apoptosis under inflammatory conditions makes them optimal vehicles for targeted immunotherapy using apoptotic agents.
MeSH term(s)	Animals ; Autoimmune Diseases/immunology ; Autoimmune Diseases/therapy ; Humans ; Immunomodulation ; Inflammation/immunology ; Inflammation/pathology ; Inflammation/therapy ; T-Lymphocytes, Regulatory/immunology
Language	English
Publishing date	2013-08
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2144145-5
ISSN	1873-0183 ; 1568-9972
ISSN (online)	1873-0183
ISSN	1568-9972
DOI	10.1016/j.autrev.2013.04.005
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Zs.A 5913: Show issues

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Article ; Online: Hematopoietic transplants for disease suppression and cure in type 1 diabetes.

Askenasy, Nadir

Current stem cell research & therapy

2013 Volume 8, Issue 4, Page(s) 333–339

Abstract: Recent clinical studies have demonstrated the capacity of immunosuppressive therapy to delay progression of inflammatory insulitis in type 1 diabetes (T1D). The procedure includes depletion of pathogenic cells by immunosuppressive therapy and support of ... ...

Abstract	Recent clinical studies have demonstrated the capacity of immunosuppressive therapy to delay progression of inflammatory insulitis in type 1 diabetes (T1D). The procedure includes depletion of pathogenic cells by immunosuppressive therapy and support of recovery by reinfusion of autologous hematopoietic progenitors. The short-term outcome of these clinical transplants is similar to the predictions drawn from NOD mice: debulking of diabetogenic cells is ineffectively achieved by immunosuppressive therapy, and resetting of immune homeostasis does not restrain autoimmunity. Murine models indicate that allogeneic transplants are potentially curative, through restored mechanisms of negative regulation that are effective in continuous and indefinite suppression of autoimmunity.
MeSH term(s)	Animals ; Clinical Trials as Topic ; Diabetes Mellitus, Type 1/immunology ; Diabetes Mellitus, Type 1/therapy ; Hematopoietic Stem Cell Transplantation ; Humans ; Immunosuppression ; Treatment Outcome
Language	English
Publishing date	2013-05-27
Publishing country	United Arab Emirates
Document type	Journal Article
ZDB-ID	2251937-3
ISSN	2212-3946 ; 1574-888X
ISSN (online)	2212-3946
ISSN	1574-888X
DOI	10.2174/1574888x113089990001
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Zs.A 6399: Show issues

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Article ; Online: Restless Leg Syndrome in Neurologic and Medical Disorders.

Askenasy, Nadir / Askenasy, Jean-Jacques

Sleep medicine clinics

2015 Volume 10, Issue 3, Page(s) 343–50, xv

Abstract: Adopting prior models of sleep-wake transitions, a flip-flop switch in synchronized neurotransmitter activity is proposed to underlie restless leg syndrome onset. In this model, leg quiescence homeostasis sustained through concerted activities of several ...

Abstract	Adopting prior models of sleep-wake transitions, a flip-flop switch in synchronized neurotransmitter activity is proposed to underlie restless leg syndrome onset. In this model, leg quiescence homeostasis sustained through concerted activities of several neurotransmitters in basal ganglia is perturbed and produces striatal motor activity along sensory activity associated with thalamocortical circuits (conscious urge and discomfort). This model explains the association of restless leg syndrome with a wide variety of associated pathologies emphasizing that perturbed function and imbalance may occur under different steady states of neurotransmitter levels. Likewise, this concept links various central and peripheral etiologies and integrates the augmenting and transient effects of therapeutic neuromodulators.
MeSH term(s)	Humans ; Neurotransmitter Agents/metabolism ; Restless Legs Syndrome/complications ; Restless Legs Syndrome/physiopathology ; Sleep/physiology ; Wakefulness/physiology
Chemical Substances	Neurotransmitter Agents
Language	English
Publishing date	2015-09
Publishing country	United States
Document type	Journal Article ; Review
ISSN	1556-4088
ISSN (online)	1556-4088
DOI	10.1016/j.jsmc.2015.05.008
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Article ; Online: Engineering donor lymphocytes with Fas ligand protein effectively prevents acute graft-versus-host disease.

Shrestha, Pradeep / Turan, Ali / Batra, Lalit / Gulen, Ayse Ece / Sun, Zhengda / Tan, Helen / Askenasy, Nadir / Shirwan, Haval / Yolcu, Esma S

Blood advances

2023 Volume 7, Issue 10, Page(s) 2181–2195

Abstract: Alloreactive T-effector cells (Teffs) are the major culprit of acute graft-versus-host disease (aGVHD) associated with hematopoietic stem cell transplantation. Ex vivo nonspecific depletion of T cells from the donor graft impedes stem cell engraftment ... ...

Abstract	Alloreactive T-effector cells (Teffs) are the major culprit of acute graft-versus-host disease (aGVHD) associated with hematopoietic stem cell transplantation. Ex vivo nonspecific depletion of T cells from the donor graft impedes stem cell engraftment and posttransplant immune reconstitution. Teffs upregulate Fas after activation and undergo Fas ligand (FasL)-mediated restimulation-induced cell death (RICD), an important mechanism of immune homeostasis. We targeted RICD as a means to eliminate host-reactive Teffs in vivo for the prevention of aGVHD. A novel form of FasL protein chimeric with streptavidin (SA-FasL) was transiently displayed on the surface of biotinylated lymphocytes, taking advantage of the high-affinity interaction between biotin and streptavidin. SA-FasL-engineered mouse and human T cells underwent apoptosis after activation in response to alloantigens in vitro and in vivo. SA-FasL on splenocytes was effective in preventing aGVHD in >70% of lethally irradiated haploidentical mouse recipients after cotransplantation with bone marrow cells, whereas all controls that underwent transplantation with nonengineered splenocytes developed aGVHD. Prevention of aGVHD was associated with an increased ratio of CD4+CD25+FoxP3+ T regulatory (Tregs) to Teffs and significantly reduced transcripts for proinflammatory cytokines in the lymphoid organs and target tissues. Depletion of Tregs from the donor graft abrogated the protection conferred by SA-FasL. This approach was also effective in a xenogeneic aGVHD setting where SA-FasL-engineered human PBMCs were transplanted into NSG mice. Direct display of SA-FasL protein on donor cells as an effective means of eliminating alloreactive Teffs in the host represents a practical approach with significant translation potential for the prevention of aGVHD.
MeSH term(s)	Mice ; Humans ; Animals ; Fas Ligand Protein ; Streptavidin ; Graft vs Host Disease/prevention & control ; T-Lymphocytes ; Lymphocytes
Chemical Substances	Fas Ligand Protein ; Streptavidin (9013-20-1)
Language	English
Publishing date	2023-02-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	2915908-8
ISSN	2473-9537 ; 2473-9529
ISSN (online)	2473-9537
ISSN	2473-9529
DOI	10.1182/bloodadvances.2022008495
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