scholarly journals The intestinal immunoendocrine axis: novel cross-talk between enteroendocrine cells and the immune system during infection and inflammatory disease

2015 ◽  
Vol 43 (4) ◽  
pp. 727-733 ◽  
Author(s):  
John J Worthington
Keyword(s):  
Immune System ◽  
Cross Talk ◽  
Intestinal Epithelium ◽  
Immune Cells ◽  
Inflammatory Disease ◽  
Barrier Function ◽  
Crucial Role ◽  
Enteroendocrine Cells ◽  
Immune Homeostasis

The intestinal epithelium plays a crucial role in maintaining barrier function and immune homeostasis, a failure of which results in disease. This review focuses on the epithelial enteroendocrine cells and the crosstalk that exists with immune cells during inflammation.

scholarly journals Targeting neuro–immune communication in neurodegeneration: Challenges and opportunities

2018 ◽  
Vol 215 (11) ◽  
pp. 2702-2704 ◽  
Author(s):  
Aleksandra Deczkowska ◽  
Michal Schwartz
Keyword(s):  
Immune System ◽  
Cross Talk ◽  
Immune Cells ◽  
Therapeutic Approach ◽  
Neurological Diseases ◽  
Challenges And Opportunities ◽  
The Cross ◽  
The Brain

Immune cells patrol the brain and can support its function, but can we modulate brain–immune communication to fight neurological diseases? Here, we briefly discuss the mechanisms orchestrating the cross-talk between the brain and the immune system and describe how targeting this interaction in a well-controlled manner could be developed as a universal therapeutic approach to treat neurodegeneration.

scholarly journals Roles of Pro- and Anti-Inflammatory Cytokines in the Pathogenesis of SLE

2012 ◽  
Vol 2012 ◽  
pp. 1-15 ◽  
Author(s):  
Ding-Lei Su ◽  
Zhi-Min Lu ◽  
Min-Ning Shen ◽  
Xia Li ◽  
Ling-Yun Sun
Keyword(s):  
Complex Network ◽  
Inflammatory Cytokines ◽  
Immune Cells ◽  
Inflammatory Disease ◽  
Immune Homeostasis ◽  
Adaptive Immune ◽  
Adaptive Immune Cells ◽  
Autoimmune Inflammatory Disease ◽  
Anti Inflammatory

SLE is an autoimmune inflammatory disease in which various pro- and anti-inflammatory cytokines, including TGF-β, IL-10, BAFF, IL-6, IFN-α, IFN-γ, IL-17, and IL-23, play crucial pathogenic roles. Virtually, all these cytokines can be generated by both innate and adaptive immune cells and exert different effects depending on specific local microenvironment. They can also interact with each other, forming a complex network to maintain delicate immune homeostasis. In this paper, we elaborate on the abnormal secretion and functions of these cytokines in SLE, analyze their potential pathogenic roles, and probe into the possibility of them being utilized as targets for therapy.

scholarly journals The Vicious Cross-Talk between Tumor Cells with an EMT Phenotype and Cells of the Immune System

Cells ◽  
2019 ◽  
Vol 8 (5) ◽  
pp. 460 ◽  
Author(s):  
Elisabetta Romeo ◽  
Carmelo Antonio Caserta ◽  
Cristiano Rumio ◽  
Fabrizio Marcucci
Keyword(s):  
Immune System ◽  
Tumor Cells ◽  
Cross Talk ◽  
Immune Cells ◽  
Epithelial Mesenchymal Transition ◽  
Large Body ◽  
Adaptive Immune System ◽  
Migration And Invasion ◽  
Mesenchymal Transition ◽  
Immune Exclusion

Carcinoma cells that undergo an epithelial-mesenchymal transition (EMT) and display a predominantly mesenchymal phenotype (hereafter EMT tumor cells) are associated with immune exclusion and immune deviation in the tumor microenvironment (TME). A large body of evidence has shown that EMT tumor cells and immune cells can reciprocally influence each other, with EMT cells promoting immune exclusion and deviation and immune cells promoting, under certain circumstances, the induction of EMT in tumor cells. This cross-talk between EMT tumor cells and immune cells can occur both between EMT tumor cells and cells of either the native or adaptive immune system. In this article, we review this evidence and the functional consequences of it. We also discuss some recent evidence showing that tumor cells and cells of the immune system respond to similar stimuli, activate the expression of partially overlapping gene sets, and acquire, at least in part, identical functionalities such as migration and invasion. The possible significance of these symmetrical changes in the cross-talk between EMT tumor cells and immune cells is addressed. Eventually, we also discuss possible therapeutic opportunities that may derive from disrupting this cross-talk.

scholarly journals A primary human macrophage-enteroid co-culture model to investigate mucosal gut physiology and host-pathogen interactions

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Gaelle Noel ◽  
Nicholas W. Baetz ◽  
Janet F. Staab ◽  
Mark Donowitz ◽  
Olga Kovbasnjuk ◽  
...  
Keyword(s):  
Intestinal Epithelium ◽  
Immune Cells ◽  
Barrier Function ◽  
Morphological Changes ◽  
Human Monocyte ◽  
Human Macrophage ◽  
Primary Human Macrophage ◽  
Cell Height ◽  
Culture Model ◽  
Gut Physiology

Abstract Integration of the intestinal epithelium and the mucosal immune system is critical for gut homeostasis. The intestinal epithelium is a functional barrier that secludes luminal content, senses changes in the gut microenvironment, and releases immune regulators that signal underlying immune cells. However, interactions between epithelial and innate immune cells to maintain barrier integrity and prevent infection are complex and poorly understood. We developed and characterized a primary human macrophage-enteroid co-culture model for in-depth studies of epithelial and macrophage interactions. Human intestinal stem cell-derived enteroid monolayers co-cultured with human monocyte-derived macrophages were used to evaluate barrier function, cytokine secretion, and protein expression under basal conditions and following bacterial infection. Macrophages enhanced barrier function and maturity of enteroid monolayers as indicated by increased transepithelial electrical resistance and cell height. Communication between the epithelium and macrophages was demonstrated through morphological changes and cytokine production. Intraepithelial macrophage projections, efficient phagocytosis, and stabilized enteroid barrier function revealed a coordinated response to enterotoxigenic and enteropathogenic E. coli infections. In summary, we have established the first primary human macrophage-enteroid co-culture system, defined conditions that allow for a practical and reproducible culture model, and demonstrated its suitability to study gut physiology and host responses to enteric pathogens.

OSTEOIMMUNOLOGICAL IMPLICATIONS IN REGENERATIVE MEDICINE: CROSS-TALK BETWEEN MESENCHYMAL STEM CELLS AND IMMUNE CELLS

2021 ◽  
pp. 2140001
Author(s):  
Alden Davis ◽  
Robert E. Guldberg ◽  
Rebekah M. Samsonraj
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Immune System ◽  
T Cell ◽  
Regenerative Medicine ◽  
Cross Talk ◽  
Immune Cells ◽  
Bone Repair ◽  
Bone Fractures ◽  
Cell Types

Bone fractures are one of the most common orthopedic cases, yet strategies to resolve excessive inflammation and non-unions still lack satisfactory treatment methods owing to the complex fracture microenvironment, as well as the interactions between the plethora of cell types involved. Fracture is a highly inflammatory process which involves the recruitment of various immune cells which in turn release various cytokines and growth factors to perpetuate inflammation and eventually healing resolution. Osteoimmunology is an interdisciplinary field investigating the extensive interactions between the immune system and skeletal system. Mesenchymal stem cells (MSCs) are resident in almost every adult tissue and are responsible for initiating reparative cascades in the event of injury. A key aspect of MSCs is their role as trophic mediators, secreting a milieu of signaling as well as immunomodulatory cytokines that play important roles in tissue regeneration. This paracrine signaling polarizes macrophages into their anti-inflammatory M2 phenotype, activates osteoblasts, inhibits osteoclasts, as well as suppresses conventional T cell proliferation and promotes regulatory T cell (Treg) proliferation. MSCs have been shown to resolve inflammation whilst also supporting osteogenesis; for these reasons, they are considered promising candidates for cellular therapies to treat musculoskeletal pathologies. Through pretreatment and genetic modifications, MSCs can be predisposed to release specific molecules that can modulate the microenvironment and regulate the activity of the immune system towards enhancing bone repair. By understanding the cross-talk between MSCs and the immune system in bone physiology, more targeted therapies directed towards specific cells and discrete signaling molecules become possible that may allow for expedited healing and improved standard of care in orthopedics. In this review, we discuss the interplay between immune cells and MSCs and the potential ways to harness this cross-talk to improve regenerative medicine strategies.

scholarly journals Purinergic Signaling in Neutrophils During Inflammatory Diseases

2020 ◽  
Author(s):  
Hui Sun ◽  
Gang Xu ◽  
Pingsong Li ◽  
Yumei Li ◽  
Bingwei Sun
Keyword(s):  
Immune System ◽  
Immune Cells ◽  
Inflammatory Disease ◽  
Inflammatory Diseases ◽  
Purinergic Signaling ◽  
Regulatory Function ◽  
Potential Contribution ◽  
Complex Events ◽  
Inflammatory Molecules

Purinergic signaling is that nucleotides (especially ATP) and adenosine are utilized as transmitter molecules, which play an important role in the immune system. In the extracellular ventricle, ATP plays a significant role of pro-inflammatory molecules mainly through activating P2 receptors, while adenosine plays the role of anti-inflammatory molecules mainly through activating P1 receptors. As we know，neutrophils are the most abundant immune cells in our circulation and have become an essential part of coordinating a series of complex events during inflammatory diseases. However, due to the destruction of inflammatory substances from neutrophils, the activation of neutrophils is fine-tuned, and purinergic signaling is associated with this process. As a matter of fact, altering the balance between P2 and P1 signals is of great importance for neutrophils to exert immune activities properly. Here, we review the role of purinergic signaling in regulatory function of neutrophils during inflammatory disease, and then discuss the potential contribution of targeted purinergic signals in the treatment of the neutrophil during inflammatory diseases.

scholarly journals The cross talk between gastric cancer stem cells and the immune microenvironment: a tumor-promoting factor

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jared Becerril-Rico ◽  
Eduardo Alvarado-Ortiz ◽  
Mariel E. Toledo-Guzmán ◽  
Rosana Pelayo ◽  
Elizabeth Ortiz-Sánchez
Keyword(s):  
Gastric Cancer ◽  
Stem Cells ◽  
Immune System ◽  
Cancer Stem Cells ◽  
Cancer Cells ◽  
Immune Evasion ◽  
Cross Talk ◽  
Immune Cells ◽  
Immune Microenvironment ◽  
Gastric Cancer Stem Cells

AbstractCross talk between cancer cells and the immune system is determinant for cancer progression. Emerging evidence demonstrates that GC characteristics such as metastasis, treatment resistance, and disease recurrence are associated with a tumor subpopulation called gastric cancer stem cells (GCSCs). However, the specific interaction between GCSCs and the immune microenvironment is still under investigation. Although immune evasion has been well described for cancer stem cells (CSCs), recent studies show that GCSCs can also regulate the immune system and even benefit from it. This review will provide an overview of bidirectional interactions between CSCs and immune cells in GC, compiling relevant data about how CSCs can induce leukocyte reprogramming, resulting in pro-tumoral immune cells that orchestrate promotion of metastasis, chemoresistance, tumorigenicity, and even increase in number of cancer cells with stem properties. Some immune cells studied are tumor-associated macrophages (TAMs), neutrophils, Th17 and T regulatory (Treg) cells, mesenchymal stem cells (MSCs), and cancer-associated fibroblasts (CAFs), as well as the signaling pathways involved in these pro-tumoral activities. Conversely, although there are cytotoxic leukocytes that can potentially eliminate GCSCs, we describe mechanisms for immune evasion in GCSCs and their clinical implications. Furthermore, we describe current available immunotherapy targeting GCSC-related markers as possible treatment for GC, discussing how the CSC-modified immune microenvironment can mitigate or inactivate these immunotherapies, limiting their effectiveness. Finally, we summarize key concepts and relevant evidence to understand the cross talk between GCSCs and the immune microenvironment as an important process for effective design of therapies against GCSCs that improve the outcome of patients with GC.

Potential immunotherapy for Alzheimer disease and age-related dementia

2019 ◽  
Vol 21 (1) ◽  
pp. 21-25 ◽  
Keyword(s):  
Immune System ◽  
Alzheimer Disease ◽  
Cross Talk ◽  
Immune Checkpoint ◽  
Short Review ◽  
Immune Checkpoint Blockade ◽  
Checkpoint Blockade ◽  
New Approach ◽  
Age Related ◽  
The Brain

Emerging results support the concept that Alzheimer disease (AD) and age-related dementia are affected by the ability of the immune system to contain the brain's pathology. Accordingly, well-controlled boosting, rather than suppression of systemic immunity, has been suggested as a new approach to modify disease pathology without directly targeting any of the brain's disease hallmarks. Here, we provide a short review of the mechanisms orchestrating the cross-talk between the brain and the immune system. We then discuss how immune checkpoint blockade directed against the PD-1/PD-L1 pathways could be developed as an immunotherapeutic approach to combat this disease using a regimen that will address the needs to combat AD.

Potential immunotherapy for Alzheimer disease and age-related dementia

2019 ◽  
Vol 21 (1) ◽  
pp. 21-25 ◽  
Keyword(s):  
Immune System ◽  
Alzheimer Disease ◽  
Cross Talk ◽  
Immune Checkpoint ◽  
Short Review ◽  
Immune Checkpoint Blockade ◽  
Checkpoint Blockade ◽  
New Approach ◽  
Age Related ◽  
The Brain

Emerging results support the concept that Alzheimer disease (AD) and age-related dementia are affected by the ability of the immune system to contain the brain’s pathology. Accordingly, well-controlled boosting, rather than suppression of systemic immunity, has been suggested as a new approach to modify disease pathology without directly targeting any of the brain’s disease hallmarks. Here, we provide a short review of the mechanisms orchestrating the cross-talk between the brain and the immune system. We then discuss how immune checkpoint blockade directed against the PD-1/PD-L1 pathways could be developed as an immunotherapeutic approach to combat this disease using a regimen that will address the needs to combat AD.

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