Is Alzheimer disease a failure of mobilizing immune defense? Lessons from cognitively fit oldest-old

2019 ◽  
Vol 21 (1) ◽  
pp. 7-19 ◽  
Keyword(s):  
Alzheimer Disease ◽  
Cognitive Aging ◽  
Oldest Old ◽  
Adaptive Immune Response ◽  
Effector T Cells ◽  
Immune Defense ◽  
Supporting Evidence ◽  
Therapeutic Approaches ◽  
Related Data ◽  
Adaptive Immune

Multifaceted evidence supports the hypothesis that inflammatory-immune mechanisms contribute to Alzheimer disease (AD) neuropathology and genetic association of several immune specific genes (TREM2, CR1, and CD33) suggests that maladaptive immune responses may be pivotal drivers of AD pathogenesis. We reviewed microglia-related data from postmortem AD studies and examined supporting evidence from AD animal models to answer the following questions: i) What is the temporal sequence of immune activation in AD progression and what is its impact on cognition? ii) Are there discordant, "primed", microglia responses in AD vs successful cognitive aging? iii) Does central nervous system (CNS) repair in aging depend on recruitment of the elements of cellular adaptive immune response such as effector T cells, and can the recruitment of systemic immune cells ameliorate AD neuropathology? iv) How effective are the immune-system-based therapeutic approaches currently employed for the treatment of AD?

scholarly journals Is Alzheimer disease a failure of mobilizing immune defense? Lessons from cognitively fit oldest-old

2019 ◽  
Vol 21 (1) ◽  
pp. 7-19 ◽  
Keyword(s):  
Alzheimer Disease ◽  
Cognitive Aging ◽  
Oldest Old ◽  
Adaptive Immune Response ◽  
Effector T Cells ◽  
Immune Defense ◽  
Supporting Evidence ◽  
Therapeutic Approaches ◽  
Related Data ◽  
Adaptive Immune

Multifaceted evidence supports the hypothesis that inflammatory-immune mechanisms contribute to Alzheimer disease (AD) neuropathology and genetic association of several immune specific genes (TREM2, CR1, and CD33) suggests that maladaptive immune responses may be pivotal drivers of AD pathogenesis. We reviewed microglia-related data from postmortem AD studies and examined supporting evidence from AD animal models to answer the following questions: i) What is the temporal sequence of immune activation in AD progression and what is its impact on cognition? ii) Are there discordant, “primed”, microglia responses in AD vs successful cognitive aging? iii) Does central nervous system (CNS) repair in aging depend on recruitment of the elements of cellular adaptive immune response such as effector T cells, and can the recruitment of systemic immune cells ameliorate AD neuropathology? iv) How effective are the immune-system-based therapeutic approaches currently employed for the treatment of AD?

Is Alzheimer disease a failure of mobilizing immune defense? Lessons from cognitively fit oldest-old

2019 ◽  
Vol 21 (1) ◽  
pp. 7-19
Keyword(s):  
Alzheimer Disease ◽  
Immune Responses ◽  
Cognitive Aging ◽  
Oldest Old ◽  
Adaptive Immune Response ◽  
Effector T Cells ◽  
Immune Defense ◽  
Supporting Evidence ◽  
Therapeutic Approaches ◽  
Adaptive Immune

Multifaceted evidence supports the hypothesis that inflammatory-immune mechanisms contribute to Alzheimer disease (AD) neuropathology and genetic association of several immune specific genes (TREM2, CR1, and CD33) suggests that maladaptive immune responses may be pivotal drivers of AD pathogenesis. We reviewed microgliarelated data from postmortem AD studies and examined supporting evidence from AD animal models to answer the following questions: i) What is the temporal sequence of immune activation in AD progression and what is its impact on cognition? ii) Are there discordant, “primed,” microglia responses in AD vs successful cognitive aging? iii) Does central nervous system (CNS) repair in aging depend on recruitment of the elements of cellular adaptive immune response such as effector T cells, and can the recruitment of systemic immune cells ameliorate AD neuropathology? iv) How effective are the immune-system-based therapeutic approaches currently employed for the treatment of AD?

Immunization with neural-derived peptides as a neuroprotective therapy for spinal cord injury

2021 ◽  
Vol 1 (2) ◽  
Author(s):  
Andrea Paola Ibarra-García ◽  
Antonio Ibarra
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Adaptive Immune Response ◽  
Therapeutic Approaches ◽  
Secondary Degeneration ◽  
Adaptive Immune ◽  
Cord Injury ◽  
Neuroprotective Therapy ◽  
Immunomodulatory Peptides ◽  
Significant Motor

Spinal cord injury (SCI) induces several destructive events that develop immediately after the primary insult. These phenomena increase tissue damage; that is why, numerous therapeutic approaches are studied in order to neutralize these destructive mechanisms. In line with this, several studies indicate that after injury, neural tissue could be protected by an adaptive immune response directed against self-antigens. Immunization with neural-derived peptides (INDP) reduces secondary degeneration of neurons after spinal cord insult and promotes a significant motor recovery. The combination of antioxidants or other immunomodulatory peptides after SCI can improve the protective effect induced by INDP. INDP in acute SCI is a promising strategy, so further studies should be addressed to be able to formulate the best strategy.

scholarly journals Netrin-1: A Modulator of Acute and Chronic Inflammation

2021 ◽  
Vol 23 (1) ◽  
pp. 275
Author(s):  
Laura Ziegon ◽  
Martin Schlegel
Keyword(s):  
Chronic Inflammation ◽  
Neuronal Development ◽  
Adaptive Immune Response ◽  
Immune Defense ◽  
Acute Injury ◽  
Biological Processes ◽  
First Line ◽  
Adaptive Immune ◽  
The Family ◽  
Acute And Chronic Inflammation

Netrins belong to the family of laminin-like secreted proteins, which guide axonal migration and neuronal growth in the developing central nervous system. Over the last 20 years, it has been established that netrin-1 acts as a chemoattractive or chemorepulsive cue in diverse biological processes far beyond neuronal development. Netrin-1 has been shown to play a central role in cell adhesion, cell migration, proliferation, and cell survival in neuronal and non-neuronal tissue. In this context, netrin-1 was found to orchestrate organogenesis, angiogenesis, tumorigenesis, and inflammation. In inflammation, as in neuronal development, netrin-1 plays a dichotomous role directing the migration of leukocytes, especially monocytes in the inflamed tissue. Monocyte-derived macrophages have long been known for a similar dual role in inflammation. In response to pathogen-induced acute injury, monocytes are rapidly recruited to damaged tissue as the first line of immune defense to phagocyte pathogens, present antigens to initiate the adaptive immune response, and promote wound healing in the resolution phase. On the other hand, dysregulated macrophages with impaired phagocytosis and egress capacity accumulate in chronic inflammation sites and foster the maintenance—and even the progression—of chronic inflammation. In this review article, we will highlight the dichotomous roles of netrin-1 and its impact on acute and chronic inflammation.

scholarly journals IL-12 Family Cytokines in Cancer and Immunotherapy

Cancers ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 167
Author(s):  
Bhalchandra Mirlekar ◽  
Yuliya Pylayeva-Gupta
Keyword(s):  
Immune Responses ◽  
Tumor Growth ◽  
Tumor Immunity ◽  
Effector T Cells ◽  
Immune Functions ◽  
Therapeutic Approaches ◽  
Dual Roles ◽  
Adaptive Immune ◽  
Promote Tumor Growth ◽  
Tumor Clearance

The IL-12 family cytokines are a group of unique heterodimeric cytokines that include IL-12, IL-23, IL-27, IL-35 and, most recently, IL-39. Recent studies have solidified the importance of IL-12 cytokines in shaping innate and adaptive immune responses in cancer and identified multipronged roles for distinct IL-12 family members, ranging from effector to regulatory immune functions. These cytokines could serve as promising candidates for the development of immunomodulatory therapeutic approaches. Overall, IL-12 can be considered an effector cytokine and has been found to engage anti-tumor immunity by activating the effector Th1 response, which is required for the activation of cytotoxic T and NK cells and tumor clearance. IL-23 and IL-27 play dual roles in tumor immunity, as they can both activate effector immune responses and promote tumor growth by favoring immune suppression. IL-35 is a potent regulatory cytokine and plays a largely pro-tumorigenic role by inhibiting effector T cells. In this review, we summarize the recent findings on IL-12 family cytokines in the control of tumor growth with an emphasis primarily on immune regulation. We underscore the clinical implications for the use of these cytokines either in the setting of monotherapy or in combination with other conventional therapies for the more effective treatment of malignancies.

Dendritic Cells as Arbiters of Peritoneal Immune Responses

2006 ◽  
Vol 26 (1) ◽  
pp. 8-25 ◽  
Author(s):  
Michelle L. McCully ◽  
Joaquín Madrenas
Keyword(s):  
Immune Response ◽  
Dendritic Cells ◽  
Immune Responses ◽  
Adaptive Immune Response ◽  
Immune Defense ◽  
Dendritic Cell Differentiation ◽  
Adaptive Immune ◽  
The Past ◽  
Key Players ◽  
And Function

During the past few years, there has been a substantial increase in the understanding of innate immunity. Dendritic cells are emerging as key players in the orchestration of this early phase of immune responses, with a role that will translate into the subsequent type of adaptive immune response against infection. Here we provide an overview of dendritic cell differentiation and function, with particular emphasis on those features unique to the immune defense of the peritoneal cavity and in the context of peritoneal dialysis-associated immune responses. The reader is referred to the primary references included in the accompanying list for specific details in this fascinating field.

Acute psychological stress alerts the adaptive immune response: Stress-induced mobilization of effector T cells

2006 ◽  
Vol 176 (1-2) ◽  
pp. 141-152 ◽  
Author(s):  
Djordje Atanackovic ◽  
Benjamin Schnee ◽  
Gunter Schuch ◽  
Christiane Faltz ◽  
Julia Schulze ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Psychological Stress ◽  
Adaptive Immune Response ◽  
Effector T Cells ◽  
Adaptive Immune ◽  
Acute Psychological Stress
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