metainflammation
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JCI - Inflammatory links between obesity and metabolic disease - 0 views
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The chronic nature of obesity produces a tonic low-grade activation of the innate immune system that affects steady-state measures of metabolic homeostasis over time
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Multiple inflammatory inputs contribute to metabolic dysfunction, including increases in circulating cytokines (10), decreases in protective factors (e.g., adiponectin; ref. 11), and communication between inflammatory and metabolic cells
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increasing adiposity results in a shift in the inflammatory profile of ATMs as a whole from an M2 state to one in which classical M1 proinflammatory signals predominate (21–23).
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Physiologic enhancement of the M2 pathways (e.g., eosinophil recruitment in parasitic infection) also appears to be capable of reducing metainflammation and improving insulin sensitivity (27).
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Independent of obesity, hypothalamic inflammation can impair insulin release from β cells, impair peripheral insulin action, and potentiate hypertension (63–65).
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inflammation in pancreatic islets can reduce insulin secretion and trigger β cell apoptosis leading to decreased islet mass, critical events in the progression to diabetes (33, 34)
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Since an estimated excess of 20–30 million macrophages accumulate with each kilogram of excess fat in humans, one could argue that increased adipose tissue mass is de facto a state of increased inflammatory mass
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Lipid infusion and a high-fat diet (HFD) activate hypothalamic inflammatory signaling pathways, resulting in increased food intake and nutrient storage (57)
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DIO, metabolites such as diacylglycerols and ceramides accumulate in the hypothalamus and induce leptin and insulin resistance in the CNS (58, 59)
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saturated FAs, which activate neuronal JNK and NF-κB signaling pathways with direct effects on leptin and insulin signaling (60)
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Upon stimulation by LPS and IFN-γ, macrophages assume a classical proinflammatory activation state (M1) that generates bactericidal or Th1 responses typically associated with obesity
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Maternal obesity is associated with endotoxemia and ATM accumulation that may affect the developing fetus (73)
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a risk factor for obesity in offspring, and involves inflammatory macrophage infiltration that can alter the maternal-fetal circulation (74
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Of these PRRs, TLR4 has received the most attention, as this receptor can be activated by free FAs to generate proinflammatory signals and activate NF-κB
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The adipokine adiponectin has long been recognized to have positive benefits on multiple cell types to promote insulin sensitivity and deactivate proinflammatory pathways.
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adiponectin stimulates ceramidase activity and modulates the balance between ceramides and sphingosine-1-phosphate
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Inhibition of ceramide production blocks the ability of saturated FAs to induce insulin resistance (101)
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Epigallocatechin-3-gallate ameliorates experimental autoimmune encephalomyelitis by alt... - 0 views
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EGCG epigallocatechin-3-gallate autoimmune disease MS cytokine cytokines inflammation
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IL-17 and Th17 Cells. [Annu Rev Immunol. 2009] - PubMed result - 0 views
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Vinegar Treatment Prevents the Development of Murine Experimental Colitis via Inhibitio... - 0 views
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Early-onset pediatric atopic dermatitis is TH2 but also TH17 polarized in skin - Journa... - 0 views
www.jacionline.org/...fulltext
dermatitis atopic dermatitis eczema Th2 Th17 immunology immune system
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The Role of Macrophage Polarization in Infectious and Inflammatory Diseases - 0 views
www.ncbi.nlm.nih.gov/...PMC4012075
immune system M1 M2 macrophages inflammation cancer "autoimmune disease"
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The significance of proinflammatory cytokines and Th1/ Th2 balance in depression and ac... - 1 views
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Artesunate promotes Th1 differentiation from CD4+ T cells to enhance cell apoptosis in ... - 0 views
Tumor Regression and Cure Depends on Sustained Th1 Responses : Journal of Immunotherapy - 0 views
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Progesterone inhibits mature rat dendritic cells in a receptor-mediated fashion - 0 views
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progesterone inflammation dendritic cells T cell Th1 hormone hormones
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Helper T Cells and Lymphocyte Activation - Molecular Biology of the Cell - NCBI Bookshelf - 0 views
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Regulatory effects of estriol on T cell migra... [J Neuroimmunol. 2002] - PubMed - NCBI - 0 views
www.ncbi.nlm.nih.gov/...11958828
Estriol E3 inflammation NF-kappaB Th2 T-cells rheumatoid arthritis RA MS multiple
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The Complex Role of Estrogens in Inflammation - 0 views
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up-regulation of ERβ relative to ERα under hypoxic conditions, which might lead to a preponderance of signaling through ERβ pathways
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it seems that E2 at periovulatory to pregnancy levels inhibited proinflammatory cytokines from PBMCs
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it is clear that E2 can stimulate antibody production by B cells, probably by inhibiting T cell suppression of B cells
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E2 at periovulatory to pregnancy serum levels is able to stimulate antibody secretion under healthy conditions but also in autoimmune diseases, whereas similar serum levels of E2 lead to a suppression of bone marrow B cell lineage precursors
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In chronic inflammatory disorders, where B cells play a decisive role, E2 would promote the disease when autoaggressive B cells are already present, whereas chronically elevated E2 would inhibit initiation of an autoimmune disease when no such B cells are available. This might be a good reason why particularly B cell-dependent diseases such as SLE, mixed connective tissue disease (Sharp syndrome), IgA nephropathy, dermatitis herpetiformis, gluten sensitive enteropathy, myasthenia gravis, and thyroiditis appear in women in the reproductive years, predominantly, in the third or fourth decades of life
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Th17 cells are thought to be the main responsible cells for chronic inflammatory tissue destruction in autoimmune diseases
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antiinflammatory T regulatory cells producing TGF-β and proinflammatory T helper type 17 cells (Th17) producing IL-17
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Because IFN-γ has been allocated a Th17-inhibiting role (Fig. 1⇑), its increase by E2 at pregnancy doses and the E2-mediated inhibition of TNF must be viewed as a favorable effect in chronic inflammation
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in humans and mice, E2 at periovulatory to pregnancy levels stimulates IL-4, IL-10, and IFN-γ but inhibits TNF from CD4+ T cells
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In humans and mice, E3 and E2, respectively, at pregnancy levels inhibit T cell-dependent delayed type hypersensitivity
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increased IL-4, IL-10, and IFN-γ in the presence of low TNF support an antiaggressive immune response
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secretion of IL-1β is increased at periovulatory/proestrus to early pregnancy levels, whereas IL-1 secretion is inhibited at high pregnancy levels
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The dichotomous effect of E2 on IL-1β and TNF at high and low concentrations is most probably due to inhibition of NF-κB at high concentrations
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experiments with mouse and rat macroglial and microglial cells demonstrate that E2 at proestrus to pregnancy levels exerts neuroprotective effects by increasing TGF-β and by inhibiting iNOS and NO release, and reducing expression of proinflammatory cytokines and prostaglandin E2 production.
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E2 at periovulatory to pregnancy levels inhibits NF-κB activation, which must be viewed as an antiinflammatory signal
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It was shown that E2 concentrations equal to or above 10−10 m are necessary to inhibit NF-κB activation
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important proinflammatory cytokines are typically inhibited at periovulatory (proestrus) to pregnancy levels of E2, which is evident for IL-6, IL-8, and TNF
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most in vitro studies demonstrated a stimulatory effect of E2 on secretion of IL-4, IL-10, and TGF-β typically at periovulatory to pregnancy levels
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E2 at periovulatory to pregnancy levels has an ameliorating effect on chronic inflammatory diseases as long as B cell-dependent immunity or an overshooting fibrotic tissue repair process do not play a crucial pathogenic role. However, when the B cell plays an important role, E2 might even stimulate the disease process as substantiated by flare-ups in SLE during pregnancy
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Short-term administration of E2 at pregnancy levels was shown to induce an inflammatory response specific to the lateral prostate of the castrated male rat
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http://www.integratedhealthclinic.com/assets/byCancerType/Pancreatic/4-LDN%20and%20IV%2... - 0 views
www.integratedhealthclinic.com/...IV%20Alpha%20Lipoic%20Acid.pdf
alpha lipoic acid ALA cancer pancreatic LDN low dose naltrexone selenium milk thistle silymarin IV intravenous
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The psychoneuroendocrine-immunotherapy of cancer: Historical evolution and clinical res... - 0 views
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It is known that immune system-induced destruction of cancer cells is mainly mediated by T cytotoxic lymphocytes (CD8+) and NK cells (CD16+), respectively, through an antigen-specific and an antigen nonspecific cytotoxicity
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NK cells are mainly stimulated by IL-2 released by T helper-1 (TH1) lymphocytes (CD4+) while T cytotoxic lymphocytes (CD8+) are namely under a stimulatory control released by IL-12 produced by the dendritic cells
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On the other hand, the anticancer immunity is inhibited by the activation of the macrophage system through the production of suppressive cytokines, such as IL-6 and T regulatory (T reg) lymphocytes (CD4+CD25+), which counteract the anticancer immunity by producing immunosuppressive cytokines inhibiting the secretion of both IL-2 and IL-12, including TGF-beta and IL-10, or by a direct cell-cell contact
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How is the Immune System Suppressed by Cancer - 1 views
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Excellent work by Prof de Groot of Essen, indicated by adding exogenous xanthine oxidase ( XO) in hepatoma cells, hydrogen peroxide was produced to destroy the hepatoma cells
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The other important influence of NO is in its inhibition of the proapoptoic caspases cascade. This in turn protects the cells from intracellular preprogrammed death.
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nitric oxide in immune suppression in relation to oxygen radicals is its inhibitory effect on the binding of leukocytes (PMN) at the endothelial surface
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NO from the tumor cells actually suppresses the iNOS, and in addition it reduces oxygen radicals to stop the formation of peroxynitrite in these cells. But NO is not the only inhibitor of iNOS in cancer.
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Prostaglandin E2, released from tumor cells is also an inhibitor of iNOS, as well as suppressing the immune system
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Th-1 subset of T-cells. These cells are responsible for anti-viral and anti-cancer activities, via their cytokine production including Interleukin-2, (IL-2), and Interleukin-12 which stimulates T-killer cell replication and further activation and release of tumor fighting cytokines.
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Th1 cells stimulate NK and other tumor fighting macrophages via IL-2 and IL-12; In contrast, Th2, which is stimulated in allergies and parasitic infections, produce IL-4 and IL-10. IL-4 and IL-10 inhibit TH-1 activation and the histamine released from mast cell degranulation upregulates T suppressor cells to further immune suppression.
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Th-2 subset of lymphocytes, on the other hand are activated in allergies and parasitic infections to release Interleukin-4 and Interleukin-10
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Mast cells contain histamine which when released increases the T suppressor cells, to lower the immune system and also acts directly on many tumor Histamine receptors to stimulate tumor growth
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Tumor cells release IL-10, and this is thought to be one of the important areas of Th-1 suppression in cancer patients
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IL-10 is also a central regulator of cyclooxygenase-2 expression and prostaglandin production in tumor cells stimulating their angiogenesis and NO production
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nitric oxide in tumor cells even prevents the activation of caspases responsible for apoptosis
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early stages of carcinogenesis, which we call tumor promotion, one needs a strong immune system, and fewer oxygen radicals to prevent mutations but still enough to destroy the tumor cells should they develop
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later stages of cancer development, the oxygen radicals are decreased around the tumors and in the tumor cells themselves, and the entire cancer fighting Th-1 cell replication and movement are suppressed. The results are a decrease in direct toxicity and apoptosis, which is prevented by NO, a suppression of the macrophage and leukocyte toxicity and finally, a suppression of the T-cell induced tumor toxicity
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elevated lactic acid which neutralizes the toxicity and activity of Lymphocyte immune response and mobility
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The lactic acid is also feeding fungi around tumors and that leads to elevated histamine which increases T-suppressor cells. Histamine alone stimulates many tumor cells.
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last but not least, the Lactic acid from tumor cells and acidic diets shifts the lymphocyte activity to reduce its efficacy against cancer cells and pathogens in addition to altering the bacteria of the intestinal tract.
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intestinal tract bacteria in cancer cells release sterols that suppress the immune system and down regulate anticancer activity from lymphocytes.
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In addition to the lactic acid, adenosine is also released from tumors. Through IL-10, adenosine and other molecules secreted by regulatory T cells, the CD8+ cells can be inactivated to an anergic state
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Adenosine is a purine nucleoside found within the interstitial fluid of solid tumors at concentrations that are able to inhibit cell-mediated immune responses to tumor cells
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Adenosine appears to up-regulate the PD1 receptor in T-1 Lymphocytes and inhibits the immune system further
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Mast cells with their release of histamine lower the immune system and also stimulate tumor growth and activate the metalloproteinases involved in angiogenesis and metastases
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Cimetidine, an antihistamine has been actually shown to increase in apoptosis in MDSC via a separate mechanism than the antihistamine effect
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In vitro analyses revealed a striking induction of IL-8 expression in CAFs and LFs by tumor necrosis factor-alpha (TNF-alpha)
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these data raise the possibility that the majority of CAFs in CLM originate from resident LFs. TNF-alpha-induced up-regulation of IL-8 via nuclear factor-kappaB in CAFs is an inflammatory pathway, potentially permissive for cancer invasion that may represent a novel therapeutic target
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Role of IL-2 in cancer immunotherapy: OncoImmunology: Vol 5, No 6 - 1 views
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approved for the treatment of metastatic renal cell carcinoma (1992) and later for metastatic melanoma (1998) by FDA
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It is produced predominately by antigen-simulated CD4+ T cells, while it can also be produced by CD8+ cells, natural killer (NK) cells, and activated dendritic cells (DC)
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It can promote CD8+ T-cell and NK cell cytotoxicity activity, and modulate T-cell differentiation programs in response to antigen, promoting naive CD4+ T-cell differentiation into T helper-1 (Th1) and T helper-2 (Th2) cells while inhibiting T helper-17 (Th17) differentiation
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Of note, Tregs, which act to dampen the immune response, constitutively express high levels of α chain
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IL-2Rα is unique to IL-2 and is expressed by a number of immune cells including T regulatory cells (Treg), activated CD4+ and CD8+T cells, B cells, mature DCs, endothelial cells
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Unfortunately, not all of patients would benefit from targeted therapy and nearly all patients who initially respond to targeted inhibitors inevitably develop acquired resistance to the treatment
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IL-2 also stimulates T-regulatory cells that constitutively express CTLA-4 and can suppress immune reactions. Hence, IL-2 might enhance antitumor reactivity in the presence of CTLA-4 blockade
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both HD and low-dose IL-2 therapy preferentially induce the expansion of CD4+CD25+Foxp3+ Treg and the Treg level remains elevated after each cycle of HD IL-2 therapy
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Due to rapid elimination and metabolism via the kidney, IL-2 has a short serum half-life of several minutes
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HD IL-2-induced severe toxicities including vascular leak syndrome (VLS), pulmonary edema, hypotension, and heart toxicities
Frontiers | Elevated Exhaustion Levels of NK and CD8+ T Cells as Indicators for Progres... - 0 views
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COVID natural killer cells Th1 covid19 COVID-19 Th2 SARS-CoV-2 NK-cells CD8
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