Environmental Toxicant and Immune cells: A Review

2021 ◽  
Vol 2 (3) ◽  
pp. 11-34
Author(s):  
Aparajita Ray ◽  
Chiranjeeb Dey
Keyword(s):  
Immune System ◽  
Mast Cells ◽  
Nk Cells ◽  
Immune Cells ◽  
Defense Mechanism ◽  
Environmental Toxicology ◽  
Toxic Substances ◽  
Environmental Toxicants ◽  
Pathogenic Microorganisms ◽  
Environmental Toxicant

Immune system is the adaptive defense mechanism which is evolved in vertebrates to keep them from invading pathogenic microorganisms and cancer. In immune system consists of some specialized cells like: lymphocytes, neutrophils, NK cells, basophils, macrophages, eiosinophils, mast cells, etc.Ecotoxicology is a subdisicipline of environmental toxicology concerd with studing the damaging effects of toxicants at the population and nature. Environmental toxicants are simply toxic substances in the nature. Environmental toxicant which is effect on ecosystem very badly.In this paper we discuss that how environmental toxicant effect on immune system or immune cells.

scholarly journals Recognition of tumor cells by Dectin-1 orchestrates innate immune cells for anti-tumor responses

eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Shiho Chiba ◽  
Hiroaki Ikushima ◽  
Hiroshi Ueki ◽  
Hideyuki Yanai ◽  
Yoshitaka Kimura ◽  
...  
Keyword(s):  
Immune System ◽  
Nk Cells ◽  
Tumor Cells ◽  
Immune Cells ◽  
Innate Immune ◽  
Tumoricidal Activity ◽  
Effector Cells ◽  
Therapeutic Implications ◽  
Tumor Killing

The eradication of tumor cells requires communication to and signaling by cells of the immune system. Natural killer (NK) cells are essential tumor-killing effector cells of the innate immune system; however, little is known about whether or how other immune cells recognize tumor cells to assist NK cells. Here, we show that the innate immune receptor Dectin-1 expressed on dendritic cells and macrophages is critical to NK-mediated killing of tumor cells that express N-glycan structures at high levels. Receptor recognition of these tumor cells causes the activation of the IRF5 transcription factor and downstream gene induction for the full-blown tumoricidal activity of NK cells. Consistent with this, we show exacerbated in vivo tumor growth in mice genetically deficient in either Dectin-1 or IRF5. The critical contribution of Dectin-1 in the recognition of and signaling by tumor cells may offer new insight into the anti-tumor immune system with therapeutic implications.

scholarly journals Human Herpesvirus 6B Downregulates Expression of Activating Ligands during Lytic Infection To Escape Elimination by Natural Killer Cells

2016 ◽  
Vol 90 (21) ◽  
pp. 9608-9617 ◽  
Author(s):  
Dominik Schmiedel ◽  
Julie Tai ◽  
Francesca Levi-Schaffer ◽  
Sarah Dovrat ◽  
Ofer Mandelboim
Keyword(s):  
Immune System ◽  
Nk Cells ◽  
Natural Killer ◽  
Immune Cells ◽  
Human Herpesvirus ◽  
Innate Immune ◽  
Human Herpesvirus 6 ◽  
Content Type ◽  
Life Threatening ◽  
Infected Cells

ABSTRACT The Herpesviridae family consists of eight viruses, most of which infect a majority of the human population. One of the less-studied members is human herpesvirus 6 (HHV-6) ( Roseolovirus ), which causes a mild, well-characterized childhood disease. Primary HHV-6 infection is followed by lifelong latency. Reactivation frequently occurs in immunocompromised patients, such as those suffering from HIV infection or cancer or following transplantation, and causes potentially life-threatening complications. In this study, we investigated the mechanisms that HHV-6 utilizes to remain undetected by natural killer (NK) cells, which are key participants in the innate immune response to infections. We revealed viral mechanisms which downregulate ligands for two powerful activating NK cell receptors: ULBP1, ULBP3, and MICB, which trigger NKG2D, and B7-H6, which activates NKp30. Accordingly, this downregulation impaired the ability of NK cells to recognize HHV-6-infected cells. Thus, we describe for the first time immune evasion mechanisms of HHV-6 that protect lytically infected cells from NK elimination. IMPORTANCE Human herpesvirus 6 (HHV-6) latently infects a large portion of the human population and can reactivate in humans lacking a functional immune system, such as cancer or AIDS patients. Under these conditions, it can cause life-threatening diseases. To date, the actions and interplay of immune cells, and particularly cells of the innate immune system, during HHV-6 infection are poorly defined. In this study, we aimed to understand how cells undergoing lytic HHV-6 infection interact with natural killer (NK) cells, innate lymphocytes constituting the first line of defense against viral intruders. We show that HHV-6 suppresses the expression of surface proteins that alert the immune cells by triggering two major receptors on NK cells, NKG2D and NKp30. As a consequence, HHV-6 can replicate undetected by the innate immune system and potentially spread infection throughout the body. This study advances the understanding of HHV-6 biology and the measures it uses to successfully escape immune elimination.

scholarly journals The role of the immune system in tendon healing: a systematic review

2020 ◽  
Vol 133 (1) ◽  
pp. 49-64 ◽  
Author(s):  
Emanuele Chisari ◽  
Laura Rehak ◽  
Wasim S Khan ◽  
Nicola Maffulli
Keyword(s):  
Systematic Review ◽  
Immune Response ◽  
Immune System ◽  
Mast Cells ◽  
Immune Cells ◽  
Tendon Healing ◽  
Risk Of Bias ◽  
Cochrane Library ◽  
Healing Response

Abstract Introduction The role of the immune system in tendon healing relies on polymorphonucleocytes, mast cells, macrophages and lymphocytes, the ‘immune cells’ and their cytokine production. This systematic review reports how the immune system affects tendon healing. Sources of data We registered our protocol (registration number: CRD42019141838). After searching PubMed, Embase and Cochrane Library databases, we included studies of any level of evidence published in peer-reviewed journals reporting clinical or preclinical results. The PRISMA guidelines were applied, and risk of bias and the methodological quality of the included studies were assessed. We excluded all the articles with high risk of bias and/or low quality after the assessment. We included 62 articles assessed as medium or high quality. Areas of agreement Macrophages are major actors in the promotion of proper wound healing as well as the resolution of inflammation in response to pathogenic challenge or tissue damage. The immune cells secrete cytokines involving both pro-inflammatory and anti-inflammatory factors which could affect both healing and macrophage polarization. Areas of controversy The role of lymphocytes, mast cells and polymorphonucleocytes is still inconclusive. Growing points The immune system is a major actor in the complex mechanism behind the healing response occurring in tendons after an injury. A dysregulation of the immune response can ultimately lead to a failed healing response. Areas timely for developing research Further studies are needed to shed light on therapeutic targets to improve tendon healing and in managing new way to balance immune response.

scholarly journals Understanding the Role of Innate Immune Cells and Identifying Genes in Breast Cancer Microenvironment

Cancers ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2226
Author(s):  
Israa Shihab ◽  
Bariaa A. Khalil ◽  
Noha Mousaad Elemam ◽  
Ibrahim Y. Hachim ◽  
Mahmood Yaseen Hachim ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Immune System ◽  
Tumor Microenvironment ◽  
Nk Cells ◽  
Immune Cells ◽  
Innate Immune System ◽  
Adaptive Immune System ◽  
Innate Immune ◽  
Innate Immune Cells ◽  
Cancer Microenvironment

The innate immune system is the first line of defense against invading pathogens and has a major role in clearing transformed cells, besides its essential role in activating the adaptive immune system. Macrophages, dendritic cells, NK cells, and granulocytes are part of the innate immune system that accumulate in the tumor microenvironment such as breast cancer. These cells induce inflammation in situ by secreting cytokines and chemokines that promote tumor growth and progression, in addition to orchestrating the activities of other immune cells. In breast cancer microenvironment, innate immune cells are skewed towards immunosuppression that may lead to tumor evasion. However, the mechanisms by which immune cells could interact with breast cancer cells are complex and not fully understood. Therefore, the importance of the mammary tumor microenvironment in the development, growth, and progression of cancer is widely recognized. With the advances of using bioinformatics and analyzing data from gene banks, several genes involved in NK cells of breast cancer individuals have been identified. In this review, we discuss the activities of certain genes involved in the cross-talk among NK cells and breast cancer. Consequently, altering tumor immune microenvironment can make breast tumors more responsive to immunotherapy.

scholarly journals Age-related sexual dimorphism on the longitudinal progression of blood immune cells in BALB/cByJ mice

2021 ◽  
Author(s):  
Cláudia Serre-Miranda ◽  
Susana Roque ◽  
Palmira Barreira-Silva ◽  
Claudia Nobrega ◽  
Neide Vieira ◽  
...  
Keyword(s):  
T Cells ◽  
Immune System ◽  
Sexual Dimorphism ◽  
B Cells ◽  
Nk Cells ◽  
Mouse Models ◽  
Immune Cells ◽  
Age Related ◽  
The Impact ◽  
Over Time

Abstract The study of immune system aging is of relevance, considering its myriad of interactions and role in protecting and maintaining body homeostasis. While mouse models have been extensively used to study immune system aging, little is known on how the main immune populations progress over time and what is the impact of sex. To contribute to filling this gap, male and female BALB/cByJ mice were longitudinally evaluated, from 3 to 18 months old, for the main blood populations, assessed by flow cytometry. Using linear mixed-effect models, we observed that the percentages of neutrophils, monocytes, eosinophils and total natural killer (NK) cells increase with aging; while those of B cells, T cells (including CD4 + and CD8 + subsets) and Ly6C + NK cells, decrease. Males present higher percentages of neutrophils and classical monocytes Ly6C high over time, while females present higher percentages of total T cells, both CD4 + and CD8 +, eosinophils and NK cells. Males and females display similar percentages of B cells, even though with opposite accelerated progressions over time. This study revealed that mouse models recapitulate what is observed in humans during aging: an overall proportional decrease in the adaptive and an increase in the innate immune cells. Additionally, it uncovers an age-related sexual dimorphism in the proportion of immune cells in circulation, further strengthening the need to explore the impact of sex when addressing immune system aging using mouse models.

scholarly journals Influence of environmental stress on immunity of swine

2016 ◽  
Vol 72 (10) ◽  
pp. 595-599
Author(s):  
Zygmunt Pejsak ◽  
Marian Truszczyński
Keyword(s):  
Immune System ◽  
Inflammatory Cytokines ◽  
Immune Cells ◽  
Management Practices ◽  
Acute Phase Proteins ◽  
Pathogenic Microorganisms ◽  
Environmental Management Practices ◽  
Chain Link ◽  
Microbial Environment ◽  
Pro Inflammatory Cytokines

This paper deals with pigs kept in environments, where they are exposed to a high number of pathogenic microbes and have reduced feed intake and growth, even when no obvious acute illness exists. According to the presented article this chronic drain on production is called immunologic stress. Sentinel immune cells (e.g. macrophages) supervise the diverse microbial environment by detecting pathogen – associated molecular patterns (PAMPs), which are molecules associated with groups of pathogens. The immune sentinels detect PAMPs mainly with Toll – like receptors (TLRs). Stimulation of macrophages through their TLRs leads to the synthesis and secretion of pro-inflammatory cytokines and prostaglandins, initiating the inflammatory response that recruits both immune molecules and circulating immune cells. Pro-inflammatory cytokines enable the immune system to communicate with other physiological systems. They rearrange the animal’s metabolic priorities, resulting in re-partitioning of nutrients away from productive processes towards responses that support the immune system. Thus, the immune system, through detection of PAMPs and production of pro-inflammatory cytokines, is the critical chain link connecting the pathogenic environment to productivity. The evaluation indicates, that at maintenance a healthy animal uses about 0,5-2% of the body’s lysine for leucocytes, antibodies and acute phase proteins. In the situation of contamination by pathogens of the environment the immune response is estimated to account for about 9% of the body’s lysine. Providing additional lysine in the diet does not improve the reduced growth of the pig, caused by immunologic stress as the result of contamination of the pig environment by pathogenic or facultatively pathogenic microorganisms. Thus, minimizing exposure to pathogenic microorganisms and providing sound environmental management practices is a high priority.

scholarly journals Current Knowledge on the Biology of Lysophosphatidylserine as an Emerging Bioactive Lipid

2021 ◽  
Author(s):  
Jumpei Omi ◽  
Kuniyuki Kano ◽  
Junken Aoki
Keyword(s):  
Immune System ◽  
Mast Cells ◽  
G Protein ◽  
Lysophosphatidic Acid ◽  
Immune Cells ◽  
Current Knowledge ◽  
G Protein Coupled Receptors ◽  
Sphingosine 1 Phosphate ◽  
Recent Developments ◽  
G Protein Coupled

AbstractLysophosphatidylserine (LysoPS) is an emerging lysophospholipid (LPL) mediator, which acts through G protein-coupled receptors, like lysophosphatidic acid (LPA) and sphingosine 1-phosphate (S1P). LysoPS is detected in various tissues and cells and thought to be produced mainly by the deacylation of phosphatidylserine. LysoPS has been known to stimulate degranulation of mast cells. Recently, four LysoPS-specific G protein-coupled receptors (GPCRs) were identified. These GPCRs belong to the P2Y family which covers receptors for nucleotides and LPLs and are predominantly expressed in immune cells such as lymphocytes and macrophages. Studies on knockout mice of these GPCRs have revealed that LysoPS has immune-modulatory functions. Up-regulation of a LysoPS-producing enzyme, PS-specific phospholipase A1, was frequently observed in situations where the immune system is activated including autoimmune diseases and organ transplantations. Therefore, modulation of LysoPS signaling appears to be a promising method for providing therapies for the treatment of immune diseases. In this review, we summarize the biology of LysoPS-producing enzymes and receptors, recent developments in LysoPS signal modulators, and prospects for future therapeutic applications.

Mesenchymal Stromal Cells and Natural Killer Cells: A Complex Story of Love and Hate

2019 ◽  
Vol 14 (1) ◽  
pp. 14-21 ◽  
Author(s):  
Mehdi Najar ◽  
Mohammad Fayyad-Kazan ◽  
Makram Merimi ◽  
Arsène Burny ◽  
Dominique Bron ◽  
...  
Keyword(s):  
Immune System ◽  
Nk Cells ◽  
Natural Killer ◽  
Mesenchymal Stromal Cells ◽  
Immune Cells ◽  
Stromal Cells ◽  
Innate Immune System ◽  
Innate Immune ◽  
Complex Interactions ◽  
Cell Based Therapy

Mesenchymal stromal cells (MSCs), characterized by both multidifferentiation potential and potent immunomodulatory capacity, represent a promising, safe and powerful cell based-therapy for repairing tissue damage and/or treating diseases associated with aberrant immune responses. Natural killer (NK) cells are granular lymphocytes of the innate immune system that function alone or in combination with other immune cells to combat both tumors and virally infected cells. After their infusion, MSCs are guided by host inflammatory elements and can interact with different immune cells, particularly those of the innate immune system. Although some breakthroughs have been achieved in understanding these interactions, much remains to be determined. In this review, we discuss the complex interactions between NK cells and MSCs, particularly the importance of improving the therapeutic value of MSCs.

scholarly journals Regulation of the innate immune system by autophagy: neutrophils, eosinophils, mast cells, NK cells

2019 ◽  
Vol 26 (4) ◽  
pp. 703-714 ◽  
Author(s):  
Nina Germic ◽  
Ziva Frangez ◽  
Shida Yousefi ◽  
Hans-Uwe Simon
Keyword(s):  
Immune System ◽  
Mast Cells ◽  
Nk Cells ◽  
Innate Immune System ◽  
Innate Immune

scholarly journals AB0010 TRIPLE DMARD TREATMENT IN EARLY RHEUMATOID ARTHRITIS INCREASE SYNOVIAL ACTIVATED NATURAL KILLERS AND RESTING MAST CELLS BUT DECREASE PLASMA CELLS AND M1 MACROPHAGES

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 1308.2-1309
Author(s):  
M. Y. Hachim ◽  
N. M. Elemam ◽  
I. Hachim ◽  
S. Hannawi ◽  
R. Hamoudi ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Mast Cells ◽  
Nk Cells ◽  
Synovial Tissue ◽  
T Cell Activation ◽  
Immune Cells ◽  
Plasma Cells ◽  
Estrogen Metabolism ◽  
M1 Macrophages ◽  
Early Ra

Background:Rheumatoid arthritis (RA) is a chronic inflammatory joint disease with cartilage and bone damage as well as disability and its optimal therapeutic success depends on understanding the underlying pathophysiology[1]. Since RA is a heterogenous disease, there is an urge to characterize new molecular mechanisms to aid the development of more effective and personalized therapy [2]. Genome-wide transcriptional effects of tDMARD in early RA synovial tissues showed alterations in gene expression of T cell activation and plasmablast/plasma cell differentiation[3].Objectives:Using publicly available synovial tissue transcriptomic data to compare the immune cells infiltration at baseline and after 6 months of tDMARD to identify subgroups that might not respond well to tDMARD.Methods:RNAseq dataset (GSE97165) of synovial biopsies taken from 19 early RA patients at baseline and after 6 months of tDMARD treatment were retrieved and reanalyzed. The raw RNAseq data were used for in silico prediction of the immune cells’ infiltration the synovial tissue using CIBERSORT analytical tool to evaluate the pre versus post tDMARD changes in immune population and/or activation status. Then, patients were divided according to the level of alteration in immune cells percentage after the treatment. Differentially expressed genes between the subgroups were defined and gene set enrichment analysis was performed to identify the underlying pathways in each group using BioJupies tools.Results:4 immune cells populations showed significant changes after 6 months of tDMARD indicating their role in disease pathophysiology or in response to the therapy. Resting mast cells and activated natural killer (NK) cells were increased in 84% and 74% of patients, respectively. On the other hand, M1 macrophages and plasma cells were decreased after treatment in 68% and 58% of patients, respectively. GSEA of differentially expressed genes between patients who showed increased activated NK cells in comparison to those who showed decreased or no change in NK cells after treatment identify novel pathways that can explain the heterogeneity in response to treatment specifically genes related to WNT signaling, estrogen metabolism and IL17 signaling.Figure 1.Percentage of infiltrating immune cells in the synovial tissue at baseline and after 6 months of tDMARD therapy in 19 early RA patients using CIBERSORT tool.Figure 2.Top wikiPathways enriched in the patients with decreased percentage of synovial infiltrating activated NK after 6 months of tDMARD therapy compared to those who showed increased or unchanged percentage.Conclusion:Synovial tissue NK cells, resting mast cells, plasma cells and M1 macrophages play major role in response to tDMARD. Genes related to WNT signaling, estrogen metabolism and IL17 signaling can help stratification of patients for a more effective personalized medicine in RA.References:[1]Smolen, J.S., D. Aletaha, and I.B. McInnes,Rheumatoid arthritis.Lancet (London, England), 2016.388(10055): p. 2023-2038.[2]Safari, F., et al.,CRISPR and personalized Treg therapy: new insights into the treatment of rheumatoid arthritis.Immunopharmacology and immunotoxicology, 2018.40(3): p. 201-211.[3]Walsh, A.M., et al.,Triple DMARD treatment in early rheumatoid arthritis modulates synovial T cell activation and plasmablast/plasma cell differentiation pathways.PloS one, 2017.12(9): p. e0183928-e0183928.Disclosure of Interests:None declared

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