An Overview of the Immune Response or an Immunologist’S View of the Nervous System Control of the Immune System

The Cannabis plant contains numerous components, including cannabinoids and other active molecules. The phyto-cannabinoid activity is mediated by the endocannabinoid system. Cannabinoids affect the nervous system and play significant roles in the regulation of the immune system. While Cannabis is not yet registered as a drug, the potential of cannabinoid-based medicines for the treatment of various conditions has led many countries to authorize their clinical use. However, the data from basic and medical research dedicated to medical Cannabis is currently limited. A variety of pathological conditions involve dysregulation of the immune system. For example, in cancer, immune surveillance and cancer immuno-editing result in immune tolerance. On the other hand, in autoimmune diseases increased immune activity causes tissue damage. Immuno-modulating therapies can regulate the immune system and therefore the immune-regulatory properties of cannabinoids, suggest their use in the therapy of immune related disorders. In this contemporary review, we discuss the roles of the endocannabinoid system in immunity and explore the emerging data about the effects of cannabinoids on the immune response in different pathologies. In addition, we discuss the complexities of using cannabinoid-based treatments in each of these conditions.

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Role of 5-HT7 receptors in the immune system in health and disease

Molecular Medicine ◽

10.1186/s10020-019-0126-x ◽

2019 ◽

Vol 26 (1) ◽

Cited By ~ 6

Author(s):

Alejandro Quintero-Villegas ◽

Sergio Iván Valdés-Ferrer

Keyword(s):

Central Nervous System ◽

Immune Response ◽

Nervous System ◽

Immune System ◽

Blood Platelets ◽

Pain Tolerance ◽

Immune Mediated ◽

The Central Nervous System ◽

Health And Disease

AbstractIn mammalians, serotonin (5-HT) has critical roles in the central nervous system (CNS), including mood stability, pain tolerance, or sleep patterns. However, the vast majority of serotonin is produced by intestinal enterochromaffin cells of the gastrointestinal tract and circulating blood platelets, also acting outside of the CNS. Serotonin effects are mediated through its interaction with 5-HT receptors (5-HTRs), a superfamily with a repertoire of at least fourteen well-characterized members. 5-HT7 receptors are the last 5-HTR member to be identified, with well-defined functions in the nervous, gastrointestinal, and vascular systems. The effects of serotonin on the immune response are less well understood. Mast cells are known to produce serotonin, while T cells, dendritic cells, monocytes, macrophages and microglia express 5-HT7 receptor. Here, we review the known roles of 5-HT7 receptors in the immune system, as well as their potential therapeutic implication in inflammatory and immune-mediated disorders.

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Can depression be associated with the immune response

10.5327/1516-3180.443 ◽

2021 ◽

Author(s):

Maurício Machado Lenhardt ◽

Dauana Schwartz ◽

Bruna K. de F. Silva

Keyword(s):

Central Nervous System ◽

Immune Response ◽

Nervous System ◽

Depressive Symptoms ◽

Immune System ◽

Literature Review ◽

The Central Nervous System ◽

Biochemical Components ◽

Therapeutic Protocols ◽

Pro Inflammatory Cytokines

Introduction: Depression is a disease of uncertain installation and etiology, the imbalance of neurotransmitters is involved in this process, and stress can be an activator of pro-inflammatory cytokines and trigger depressive symptoms. The organism undergoes modulations due to biochemical changes and these are linked to molecular and biochemical components and by the survival instinct, the human body is stimulated to release substances as a form of protection. The objective of this study is to describe the possible association between a loss of homeostasis of the central nervous system (CNS), changes in the modulation of the immune system, and the development of depressive symptoms. Methods: This is an integrative literature review, available in the virtual health databases: PubMed, MEDLINE, SciELO, and Google Scholar published between the years 2010 to 2020. Results: Studies indicate that cytokines can interfere with the homeostasis of the CNS and that the imbalance of catecholamines and indoleamine is involved in the process of depression. In this sense, studies have focused on neuromodulation by blocking neurotransmitters and neuroreceptors to regulate the immune system. Conclusion: It’s already established that the imbalance in the release and reuptake of neurotransmitters is associated with the onset of the depression, however, current studies show that there may also be an association with the homeostasis of the immune system. Therapeutic protocols aren’t based on the correlation between the immune system and the onset of the disease, so further studies are needed to strengthen this relationship.

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MEKANISME IMUNODEPRESI PASCASTROKE

Majalah Kedokteran Neurosains Perhimpunan Dokter Spesialis Saraf Indonesia ◽

10.52386/neurona.v36i3.78 ◽

2019 ◽

Vol 36 (3) ◽

Author(s):

Al Rasyid

Keyword(s):

Immune Response ◽

Nervous System ◽

Ischemic Stroke ◽

Immune System ◽

Immune Responses ◽

Functional Outcome ◽

Hpa Axis ◽

Post Stroke ◽

Cholinergic Pathway

POST-STROKE IMMUNODEPRESSION MECHANISMSABSTRACTImmunodepression refers to a condition when immune system has reduced capacity to fulfill its functions therefore leading to infection. Infections develop frequently after stroke, and have been associated with poor clinical and functional outcome. Several studies show ischemic stroke, leads to impairment of immune responses, which increases susceptibility of an infection. This review analyzes the mechanisms of post-stroke immunodepression involving nervous system, such as adrenergic pathway, cholinergic pathway, or HPA axis, comprehensively based on recent clinical and experimental evidences. A better understanding of immune system modification after stroke could encourage further studies regarding immunomodulation therapy use in fighting infection.Keywords: Immune response, infection, post-stroke immunodepressionABSTRAKImunodepresi merupakan suatu kondisi saat sistem imun tidak dapat menjalankan perannya dengan baik sehingga dapat menimbulkan suatu infeksi. Infeksi sendiri merupakan komplikasi yang umum terjadi pascastroke, dihubungkan dengan luaran klinis dan fungsional yang buruk pada pasien stroke. Berbagai studi klinis menyimpulkan kondisi iskemik pada stroke menyebabkan gangguan pada respons imun sehingga menimbulkan kerentanan terhadap infeksi. Tulisan ini membahas mekanisme imunodepresi pascastroke terkait sistem saraf, baik jalur adrenergik, kolinergik, dan aksis HPA, secara komprehensif berbasis bukti klinis maupun eksperimental. Pemahaman konsep modifikasi sistem imun pascastroke dapat mendorong studi-studi lanjutan terkait penggunaan terapi imunomodulasi untuk melawan komplikasi infeksi.Kata kunci: Imunodepresi pascastroke, infeksi, respons imun

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Psychological Stress and the Cutaneous Immune Response: Roles of the HPA Axis and the Sympathetic Nervous System in Atopic Dermatitis and Psoriasis

Dermatology Research and Practice ◽

10.1155/2012/403908 ◽

2012 ◽

Vol 2012 ◽

pp. 1-11 ◽

Cited By ~ 51

Author(s):

Jessica M. F. Hall ◽

desAnges Cruser ◽

Alan Podawiltz ◽

Diana I. Mummert ◽

Harlan Jones ◽

...

Keyword(s):

Immune Response ◽

Nervous System ◽

Atopic Dermatitis ◽

Immune System ◽

Sympathetic Nervous System ◽

Psychological Stress ◽

Hpa Axis ◽

Skin Diseases ◽

Treatment Strategies ◽

Sympathetic Nervous

Psychological stress, an evolutionary adaptation to the fight-or-flight response, triggers a number of physiological responses that can be deleterious under some circumstances. Stress signals activate the hypothalamus-pituitary-adrenal (HPA) axis and the sympathetic nervous system. Elements derived from those systems (e.g., cortisol, catecholamines and neuropeptides) can impact the immune system and possible disease states. Skin provides a first line of defense against many environmental insults. A number of investigations have indicated that the skin is especially sensitive to psychological stress, and experimental evidence shows that the cutaneous innate and adaptive immune systems are affected by stressors. For example, psychological stress has been shown to reduce recovery time of the stratum corneum barrier after its removal (innate immunity) and alters antigen presentation by epidermal Langerhans cells (adaptive immunity). Moreover, psychological stress may trigger or exacerbate immune mediated dermatological disorders. Understanding how the activity of the psyche-nervous -immune system axis impinges on skin diseases may facilitate coordinated treatment strategies between dermatologists and psychiatrists. Herein, we will review the roles of the HPA axis and the sympathetic nervous system on the cutaneous immune response. We will selectively highlight how the interplay between psychological stress and the immune system affects atopic dermatitis and psoriasis.

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Learned Placebo Effects in the Immune System

Zeitschrift für Psychologie ◽

10.1027/2151-2604/a000184 ◽

2014 ◽

Vol 222 (3) ◽

pp. 148-153 ◽

Cited By ~ 2

Author(s):

Sabine Vits ◽

Manfred Schedlowski

Keyword(s):

Nervous System ◽

Immune System ◽

Associative Learning ◽

Placebo Response ◽

Immunosuppressive Drug ◽

Immune Functions ◽

Placebo Effects ◽

New Therapeutic Approaches ◽

Biological Variables ◽

Experimental Approaches

Associative learning processes are one of the major neuropsychological mechanisms steering the placebo response in different physiological systems and end organ functions. Learned placebo effects on immune functions are based on the bidirectional communication between the central nervous system (CNS) and the peripheral immune system. Based on this “hardware,” experimental evidence in animals and humans showed that humoral and cellular immune functions can be affected by behavioral conditioning processes. We will first highlight and summarize data documenting the variety of experimental approaches conditioning protocols employed, affecting different immunological functions by associative learning. Taking a well-established paradigm employing a conditioned taste aversion model in rats with the immunosuppressive drug cyclosporine A (CsA) as an unconditioned stimulus (US) as an example, we will then summarize the efferent and afferent communication pathways as well as central processes activated during a learned immunosuppression. In addition, the potential clinical relevance of learned placebo effects on the outcome of immune-related diseases has been demonstrated in a number of different clinical conditions in rodents. More importantly, the learned immunosuppression is not restricted to experimental animals but can be also induced in humans. These data so far show that (i) behavioral conditioned immunosuppression is not limited to a single event but can be reproduced over time, (ii) immunosuppression cannot be induced by mere expectation, (iii) psychological and biological variables can be identified as predictors for this learned immunosuppression. Together with experimental approaches employing a placebo-controlled dose reduction these data provide a basis for new therapeutic approaches to the treatment of diseases where a suppression of immune functions is required via modulation of nervous system-immune system communication by learned placebo effects.

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The Therapeutic Potential of Chemokines in the Treatment of Chemotherapy- Induced Peripheral Neuropathy

Current Drug Targets ◽

10.2174/1389450120666190906153652 ◽

2020 ◽

Vol 21 (3) ◽

pp. 288-301 ◽

Cited By ~ 5

Author(s):

Lin Zhou ◽

Luyao Ao ◽

Yunyi Yan ◽

Wanting Li ◽

Anqi Ye ◽

...

Keyword(s):

Nervous System ◽

Neuropathic Pain ◽

Immune System ◽

Peripheral Neuropathy ◽

Immune Cell ◽

Therapeutic Potential ◽

Chemotherapeutic Agents ◽

Cell Trafficking ◽

Mediated Communication ◽

Novel Therapeutic Strategies

Background: Some of the current challenges and complications of cancer therapy are chemotherapy- induced peripheral neuropathy (CIPN) and the neuropathic pain that are associated with this condition. Many major chemotherapeutic agents can cause neurotoxicity, significantly modulate the immune system and are always accompanied by various adverse effects. Recent evidence suggests that cross-talk occurs between the nervous system and the immune system during treatment with chemotherapeutic agents; thus, an emerging concept is that neuroinflammation is one of the major mechanisms underlying CIPN, as demonstrated by the upregulation of chemokines. Chemokines were originally identified as regulators of peripheral immune cell trafficking, and chemokines are also expressed on neurons and glial cells in the central nervous system. Objective: In this review, we collected evidence demonstrating that chemokines are potential mediators and contributors to pain signalling in CIPN. The expression of chemokines and their receptors, such as CX3CL1/CX3CR1, CCL2/CCR2, CXCL1/CXCR2, CXCL12/CXCR4 and CCL3/CCR5, is altered in the pathological conditions of CIPN, and chemokine receptor antagonists attenuate neuropathic pain behaviour. Conclusion: By understanding the mechanisms of chemokine-mediated communication, we may reveal chemokine targets that can be used as novel therapeutic strategies for the treatment of CIPN.

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Secondary haemophagocytic lymphohistiocytosis in COVID-19: correlation of the autopsy findings of bone marrow haemophagocytosis with HScore

Journal of Clinical Pathology ◽

10.1136/jclinpath-2020-207337 ◽

2021 ◽

pp. jclinpath-2020-207337

Author(s):

Claudia Núñez-Torrón ◽

Ana Ferrer-Gómez ◽

Esther Moreno Moreno ◽

Belen Pérez-Mies ◽

Jesús Villarrubia ◽

...

Keyword(s):

Bone Marrow ◽

Immune Response ◽

Immune System ◽

Multiorgan Failure ◽

Histological Findings ◽

Haemophagocytic Lymphohistiocytosis ◽

Bone Marrow Tissue ◽

Autopsy Findings ◽

Specific Finding ◽

Clinical Records

BackgroundSecondary haemophagocytic lymphohistiocytosis (sHLH) is characterised by a hyper activation of immune system that leads to multiorgan failure. It is suggested that excessive immune response in patients with COVID-19 could mimic this syndrome. Some COVID-19 autopsy studies have revealed the presence of haemophagocytosis images in bone marrow, raising the possibility, along with HScore parameters, of sHLH.AimOur objective is to ascertain the existence of sHLH in some patients with severe COVID-19.MethodsWe report the autopsy histological findings of 16 patients with COVID-19, focusing on the presence of haemophagocytosis in bone marrow, obtained from rib squeeze and integrating these findings with HScore parameters. CD68 immunohistochemical stains were used to highlight histiocytes and haemophagocytic cells. Clinical evolution and laboratory parameters of patients were collected from electronic clinical records.ResultsEleven patients (68.7%) displayed moderate histiocytic hyperplasia with haemophagocytosis (HHH) in bone marrow, three patients (18.7%) displayed severe HHH and the remainder were mild. All HScore parameters were collected in 10 patients (62.5%). Among the patients in which all parameters were evaluable, eight patients (80%) had an HScore >169. sHLH was not clinically suspected in any case.ConclusionsOur results support the recommendation of some authors to use the HScore in patients with severe COVID-19 in order to identify those who could benefit from immunosuppressive therapies. The presence of haemophagocytosis in bone marrow tissue, despite not being a specific finding, has proved to be a very useful tool in our study to identify these patients.

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The immune response of T cells and therapeutic targets related to regulating the levels of T helper cells after ischaemic stroke

Journal of Neuroinflammation ◽

10.1186/s12974-020-02057-z ◽

2021 ◽

Vol 18 (1) ◽

Author(s):

Tian-Yu Lei ◽

Ying-Ze Ye ◽

Xi-Qun Zhu ◽

Daniel Smerin ◽

Li-Juan Gu ◽

...

Keyword(s):

Immune Response ◽

T Cells ◽

Immune System ◽

Immune Responses ◽

Ischaemic Stroke ◽

Immune Cells ◽

Tissue Injury ◽

Recovery Period ◽

Vital Functions ◽

Anti Inflammatory

AbstractThrough considerable effort in research and clinical studies, the immune system has been identified as a participant in the onset and progression of brain injury after ischaemic stroke. Due to the involvement of all types of immune cells, the roles of the immune system in stroke pathology and associated effects are complicated. Past research concentrated on the functions of monocytes and neutrophils in the pathogenesis of ischaemic stroke and tried to demonstrate the mechanisms of tissue injury and protection involving these immune cells. Within the past several years, an increasing number of studies have elucidated the vital functions of T cells in the innate and adaptive immune responses in both the acute and chronic phases of ischaemic stroke. Recently, the phenotypes of T cells with proinflammatory or anti-inflammatory function have been demonstrated in detail. T cells with distinctive phenotypes can also influence cerebral inflammation through various pathways, such as regulating the immune response, interacting with brain-resident immune cells and modulating neurogenesis and angiogenesis during different phases following stroke. In view of the limited treatment options available following stroke other than tissue plasminogen activator therapy, understanding the function of immune responses, especially T cell responses, in the post-stroke recovery period can provide a new therapeutic direction. Here, we discuss the different functions and temporal evolution of T cells with different phenotypes during the acute and chronic phases of ischaemic stroke. We suggest that modulating the balance between the proinflammatory and anti-inflammatory functions of T cells with distinct phenotypes may become a potential therapeutic approach that reduces the mortality and improves the functional outcomes and prognosis of patients suffering from ischaemic stroke.

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