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Artykuły w czasopismach na temat „Epigentics”

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Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 29 stycznia 2023

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1

Ren, Jun, i Yingmei Zhang. "Emerging Therapeutic Potential Targeting Genetics and Epigentics in Heart Failure". Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1863, nr 8 (sierpień 2017): 1867–69. http://dx.doi.org/10.1016/j.bbadis.2017.05.023.

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Pisarska, M. D., G. M. Barlow, N. Xu, M. O. Goodarzi, V. Funari i J. Williams. "Special research presentation: epigentic profiles in ART pregnancies". Fertility and Sterility 102, nr 3 (wrzesień 2014): e105-e106. http://dx.doi.org/10.1016/j.fertnstert.2014.07.362.

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Khan, Muhammad Babar, Julia R. Schneider, Kevin Kwan i John A. Boockvar. "Epigentic Regulators of Glioma Stem Cells are Potential Therapeutic Targets". Neurosurgery 82, nr 5 (16.04.2018): E104—E105. http://dx.doi.org/10.1093/neuros/nyy039.

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Mehboob, Riffat. "Role of Epigenetic alterations in the development of cancers". Pakistan BioMedical Journal 5, nr 2 (28.02.2022): 01. http://dx.doi.org/10.54393/pbmj.v5i2.346.

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Many different factors are involved in the progression of cancers. Genes mutations and chromosomal abnormalities are normally considered main cause of cancers but there are some other reason for the development of cancers. Other cancer causing factors are known as epigenetic alterations [1,2]. Epigentic modification of genome is known as epigenetic alterations, lead toward cancer cells production. Epigentic modification does not cause change in sequences of nucleotide. Similar to genetic alteration epigenetic alteration can’t be ignored [3]. Basically mechanisms behind epigenetic modifications are deregulation of DNA proteins, change in CpG island methylation, change in histone, oncogenes activation and deactivation of tumor suppressor [4]. Epigenetic alterations is directly linked with functional alterations of genome. Alteration in DNA methylation, histone degeneration and functional and structural abnormalities of chromosomes are the major examples of epigenetic modifications [5]. The main function of all epigenetic alterations is to modulate gene expression with same DNA sequences. Means these changes never effect main basal sequence oF DNA [6], which remain same in cell division [7]. Many different types of cancers contains large number of epigenetic alterations, the most important of these are epigenetic alterations that occurs in DNA repair genes. These DNA repair genes drive slow expression of DNA proteins. These abnormalities cause genetic unreliability, which is mainly considered as characteristic of various cancers [8,9].

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5

Mu, Shengyu, Tatsuo Shimosawa, Sayoko Ogura, Hong Wang, Yuzaburo Uetake, Fumiko Mori i Toshiro Fujita. "36 SALT-SENSITIVE HYPERTENSION AND RENAL-SYMPATHETIC TONE, EPIGENTIC MODULATION OF WNK4". Journal of Hypertension 30 (wrzesień 2012): e11. http://dx.doi.org/10.1097/01.hjh.0000419862.52153.c4.

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6

Medley, T., R. Idrizi, J. Jowett, H. Sumer, P. Verma i D. Kaye. "Cell of Origin Influence Transcriptional Epigentic and Functional Profiles of iPS Cell Derived Cardiomyocytes". Heart, Lung and Circulation 21 (styczeń 2012): S75. http://dx.doi.org/10.1016/j.hlc.2012.05.189.

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7

Kim, K. J., Y. D. Min, T. B. Lee i C. H. Choi. "Epigentic mechanisms involved in the differential expression of MDR1 between gastric and colon cancer cells". Journal of Clinical Oncology 23, nr 16_suppl (czerwiec 2005): 9708. http://dx.doi.org/10.1200/jco.2005.23.16_suppl.9708.

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8

Takaro, Tim K., Meaghan Jones, Michael Kobor, Jeffrey Brook, Kathleen Mclean, Yayuk Joffres, Ryan Allen, Michael Brauer i Malcolm Sears. "Epigentic Markers Of Early Life Exposures In The Canadian Healthy Infant Longitudinal Development (Child) Birth Cohort". ISEE Conference Abstracts 2015, nr 1 (20.08.2015): 2608. http://dx.doi.org/10.1289/isee.2015.2015-2608.

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9

Lecamwasam, A., B. Novakovic, B. Meyer, E. Ekinci, K. Dwyer i R. Saffery. "SAT-183 DNA METHYLATION PROFILING IDENTIFIES EPIGENTIC DIFFERENCES BETWEEN EARLY VERSUS LATE STAGES OF DIABETIC CHRONIC KIDNEY DISEASE". Kidney International Reports 5, nr 3 (marzec 2020): S78. http://dx.doi.org/10.1016/j.ekir.2020.02.195.

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Thakur, Vikram, Brian R. Davis, Irene Sarosiek, Richard W. McCallum i Munmun Chattopadhyay. "Tu1310 ALTERATIONS IN EPIGENTIC MODIFIERS IN GASTRIC ANTRAL SMOOTH MUSCLE OF PATIENTS WITH DIABETIC GASTROPARESIS COMPARED TO IDIOPATHIC ETIOLOGY". Gastroenterology 158, nr 6 (maj 2020): S—1052. http://dx.doi.org/10.1016/s0016-5085(20)33317-5.

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11

Mullur, Rashmi, Yan-Yun Liu i Gregory A. Brent. "Thyroid Hormone Regulation of Metabolism". Physiological Reviews 94, nr 2 (kwiecień 2014): 355–82. http://dx.doi.org/10.1152/physrev.00030.2013.

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Thyroid hormone (TH) is required for normal development as well as regulating metabolism in the adult. The thyroid hormone receptor (TR) isoforms, α and β, are differentially expressed in tissues and have distinct roles in TH signaling. Local activation of thyroxine (T4), to the active form, triiodothyronine (T3), by 5′-deiodinase type 2 (D2) is a key mechanism of TH regulation of metabolism. D2 is expressed in the hypothalamus, white fat, brown adipose tissue (BAT), and skeletal muscle and is required for adaptive thermogenesis. The thyroid gland is regulated by thyrotropin releasing hormone (TRH) and thyroid stimulating hormone (TSH). In addition to TRH/TSH regulation by TH feedback, there is central modulation by nutritional signals, such as leptin, as well as peptides regulating appetite. The nutrient status of the cell provides feedback on TH signaling pathways through epigentic modification of histones. Integration of TH signaling with the adrenergic nervous system occurs peripherally, in liver, white fat, and BAT, but also centrally, in the hypothalamus. TR regulates cholesterol and carbohydrate metabolism through direct actions on gene expression as well as cross-talk with other nuclear receptors, including peroxisome proliferator-activated receptor (PPAR), liver X receptor (LXR), and bile acid signaling pathways. TH modulates hepatic insulin sensitivity, especially important for the suppression of hepatic gluconeogenesis. The role of TH in regulating metabolic pathways has led to several new therapeutic targets for metabolic disorders. Understanding the mechanisms and interactions of the various TH signaling pathways in metabolism will improve our likelihood of identifying effective and selective targets.

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12

Levine, Arnold J. "The p53 protein plays a central role in the mechanism of action of epigentic drugs that alter the methylation of cytosine residues in DNA". Oncotarget 8, nr 5 (24.01.2017): 7228–30. http://dx.doi.org/10.18632/oncotarget.14805.

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13

Bellmunt, Joaquim, Guangwu Guo, Stephanie A. Mullane, Anna Orsola, Lillian Werner, Paul Van Hummelen, Aaron Thorner i in. "Genomic landscape of high-grade T1 micropapillary bladder tumors." Journal of Clinical Oncology 33, nr 7_suppl (1.03.2015): 299. http://dx.doi.org/10.1200/jco.2015.33.7_suppl.299.

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299 Background: The genomic landscape of high-grade T1 micropapillary bladder tumors (HGT1micropap) is unknown. Clinically, micropapillary bladder cancer is an aggressive and possibly lethal disease. Our main objective was to assess the genomic landscape of HGT1micropap through identifying mutations, insertions/deletions (indels), translocations, and copy number variations (CNVs). Methods: We prospectively identified nine HGT1micropap with 45.4 months of median follow up. Patients were treated in a uniform manner using TUR, BCG, and appropriate follow up. We performed whole exome sequencing using Ilumina Exome _v5 plus translocation. Mutations and indels were called using the Firehose pipeline. CNVs were called using ExomeCNV. We examined the mutational landscape and compared the genomic alterations to TCGA (>T2, n=131)2 and publicly available data on non-muscle invasive bladder tumors (Ta/T1, n=37)1. Results: Within the HGT1micropap, mutations on TP53, KMT2D, TSC1, and ATM were suggested to occur more frequently compared to the NMIBC control group1. FGFR3 was seen at the expected frequency for NMIBC. The mutations of interest are presented in Table 1 with the percentage seen in the other cohorts. Of interest, TSC1 was seen in higher frequency in micropapillary than in the NMIBC or the TCGA cohort2. We did not see any patterns between CNVs and mutations. We also saw two patients with severe chromothripsis. 3 patients had loss of chromosome 9 or 9q without any other severe chromosome alterations. CNV alterations will be presented and compared to MIBC. Conclusions: In this preliminary analysis, our HGT1micropap, showed a mutational landscape more similar to MIBC compared to NMIBC bladder landscape. We did not find any clear driver of the micropapillary histology at the exome level in this limited sample of patient, which may indicate that tumor heterogeneity or epigentic changes may be driving this aggressive phenotype. [Table: see text]

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14

Orlacchio, Arturo, Daniel Weissinger, Catherine Do, Benjamin Tycko, Diane M. Simeone i Tamas Gonda. "Abstract C041: Hypomethylating therapy induces a potential immuno-suppressive myeloid phenotype by altering cancer cell cytokine secretion in PDAC". Cancer Research 82, nr 22_Supplement (15.11.2022): C041. http://dx.doi.org/10.1158/1538-7445.panca22-c041.

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Abstract Introduction: We have previously shown using the KPC (KrasLSL G12D/+; p53 r172H/+; Pdx1-Cre) mouse model of PDAC that sequential treatment with the DNA hypomethylating agents (HMA) followed by anti-PD-1 led to increased tumor necrosis, slowed tumor growth, increased tumor-infiltrating CD8+ cells, and significantly increased mean survival. However, acquired treatment resistance occurred, with emergence of a specific subtype of M2-polarized putatively immunosuppressive Chi3l3+ macrophages. In this study, we characterize the mechanism of polarization of these cells, define their function, and identify a potential therapeutic strategy to combine with epigentic therapy to prevent unfavourable macrophage polarization and improve the efficacy of epigenetic priming of immunotherapy against PDAC. Methods: Studies were conducted with primary macrophages (PM)e isolated from bone marrow (BMDM) or the peritoneum of 6-8 weeks mice and RAW264.7 cells were also used and exposed to conditioned media from primary KPC cell lines with and without previous treatment with the HMAs decitabine or azacytidine. The effect was compared with polarization by direct HMA, IFN-γ and IL-4. Gene set enrichment analysis was done on RNASeq data from myeloid cells and validated by RT-PCR. We used cytokine arrays and Western blot validation to identify secreted cytokines from KPC cells. Results: We profiled expression of RAW264.7 cells, BMDM and PMs following exposure to IL-4 or IFN-γ and identified a signature associated with each treatment (CD206, Fizz1, Tlr8, IGF1, Mgl2 associated with IL-4 and TNFα, CD86, CD64, CD40, NOS2 associated with IFN-γ). Direct exposure of myeloid cells to hypomethylating agents did not result in a significant polarization. We next used conditioned media of KPC cells to identify a hypomethylation specific effect and found a significant IL-4 like enrichment (Chi3l3, Arg1, Il4i1, Raet1a, Lgals4) and a HMA-specific myeloid signature (CD137, IL1a, Ccl2, Ccl7, Spp1) with treatment. To assess which cytokines might trigger this polarization, we employed cytokine arrays and identified a small number of candidate cytokines that are specific to hypomethylation induced polarization of myeloid cells, including CXCL1/2, CCL2, GM-CSF, FGF-21, IGFBP-6 and ICAM-1. Conclusions: Our results show that paracrine secretion of cytokines from cancer cells treated with HMA drugs, rather than direct effect of hypomethylating therapy on macrophages, is responsible for polarizing macrophages into an immunosuppressive subtype. We further identified several candidate cytokines secreted by cancer cells following hypomethylating therapy that may be relevant for this immunosuppressive polarization of macrophages and might be specific therapeutic targets in combination with hypomethylating therapy. Citation Format: Arturo Orlacchio, Daniel Weissinger, Catherine Do, Benjamin Tycko, Diane M. Simeone, Tamas Gonda. Hypomethylating therapy induces a potential immuno-suppressive myeloid phenotype by altering cancer cell cytokine secretion in PDAC [abstract]. In: Proceedings of the AACR Special Conference on Pancreatic Cancer; 2022 Sep 13-16; Boston, MA. Philadelphia (PA): AACR; Cancer Res 2022;82(22 Suppl):Abstract nr C041.

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15

Daw, Jennifer, Devin Saunders, Adria Vasquez i Celina Valencia. "Abstract B013: Epigenetic clocks and breast cancer outcomes: A scoping review. [R]". Cancer Research 83, nr 2_Supplement_1 (15.01.2023): B013. http://dx.doi.org/10.1158/1538-7445.agca22-b013.

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Abstract Introduction: Age is a strong predictor for breast cancer (BCa) risk. The median age at diagnosis varies by race/ethnicity. In the United States (U.S.), non-White women are more likely to be diagnosed at a younger age than non-Hispanic White (NHW) women. Epigenetic age, measured as changes to DNA via methylation (DNAm) using epigentic clocks, is highly accurate at estimating cellular age using several tissues and cell types may differ from chronological age. Epigenetic age is more robust than other molecular markers of aging, such as telomere length. Differences between epigenetic age and chronological age, termed epigenetic age acceleration, may be the driver of age and race/ethnicity discrepancies when estimating BCa risk. Age-related methylation between disease-free and tumor breast tissue is significantly differentially methylated. For example, aberrant methylation of promoter regions of polycomb group protein target genes and CpG islands associated with BCa risk and progression. Therefore, the purpose of this scoping review is to gather data on epigenetic clocks as a predictor for BCa incidence. Study objective: Synthesize the existing evidence on epigenetic accelerated aging measured with epigenetic clocks and breast cancer risk in the U.S. Methods: The PROSPERO Scoping Review Protocol was used for this project. We performed multiple PubMed searches utilizing search language developed by an experienced search librarian. The searches were conducted from January 2022 to April 2022. The searches yielded a total of 2,908 studies in the search process. The eligibility for inclusion applied during article review was: 1) the study must have used an epigenetic clock to assess epigenetic accelerated age in their sample, 2) the study’s primary outcome needed to be breast cancer risk, 3) the study needed to use a U.S. based study sample 3) the study needed to be published in a peer-reviewed PubMed indexed journal, 4) the study must have been published by April 30, 2022. Results: A total of seven articles from the 2,908 were determined eligible for inclusion. Data extraction from these seven articles demonstrated epigenetic accelerated age measured with epigenetic clocks does have an associative relationship with the development of breast cancer. Discussion: BCa risk is also known to drastically increase after menopause, although there are significant differences of menopausal transition in race/ethnicity. On average, African American, Asian, and Latina women begin menopause earlier than non-Hispanic White women. Emerging evidence suggests that earlier menopause in these populations may be a result of structural factors experienced by historically disadvantaged communities. The studies included in this review focused primarily on NHW women. More research is needed to better understand the role of DNAm and accelerated epigenetic age in diverse populations. Citation Format: Jennifer Daw, Devin Saunders, Adria Vasquez, Celina Valencia. Epigenetic clocks and breast cancer outcomes: A scoping review. [R] [abstract]. In: Proceedings of the AACR Special Conference: Aging and Cancer; 2022 Nov 17-20; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2022;83(2 Suppl_1):Abstract nr B013.

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16

Hemmerich, Peter, Stefanie Weidtkamp-Peters, Christian Hoischen, Lars Schmiedeberg, Indri Erliandri i Stephan Diekmann. "CENP-I as a new epigentic mark at centromere chromatin". GBM Annual Spring meeting Mosbach 2008 2008, Spring (marzec 2008). http://dx.doi.org/10.1240/sav_gbm_2008_m_002212.

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17

Lemche, Erwin, Oleg S. Chaban i Alexandra V. Lemche. "Neuroendorine and Epigentic Mechanisms Subserving Autonomic Imbalance and HPA Dysfunction in the Metabolic Syndrome". Frontiers in Neuroscience 10 (14.04.2016). http://dx.doi.org/10.3389/fnins.2016.00142.

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18

Knestrick, M., D. Demers, R. Fleeman, B. Vesely, A. Azhari, DE Kyle, LN Shaw i BJ Baker. "An epigentic-based fungal metabolite screening protocol for discovery of potential lead compounds for drug treatments". Planta Medica 80, nr 10 (14.07.2014). http://dx.doi.org/10.1055/s-0034-1382618.

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Beaver, Mariah, Akanksha Bhatnagar, Priyalakshmi Panikker, Haolin Zhang, Renee Snook, Visha Parmar, Gayathri Vijayakumar, Niteesha Betini, Sunya Akhter i Felice Elefant. "Disruption of Tip60 HAT mediated neural histone acetylation homeostasis is an early common event in neurodegenerative diseases". Scientific Reports 10, nr 1 (26.10.2020). http://dx.doi.org/10.1038/s41598-020-75035-3.

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AbstractEpigenetic dysregulation is a common mechanism shared by molecularly and clinically heterogenous neurodegenerative diseases (NDs). Histone acetylation homeostasis, maintained by the antagonistic activity of histone acetyltransferases (HATs) and histone deacetylases (HDACs), is necessary for appropriate gene expression and neuronal function. Disruption of neural acetylation homeostasis has been implicated in multiple types of NDs including Alzheimer’s disease (AD), yet mechanisms underlying alterations remain unclear. We show that like AD, disruption of Tip60 HAT/HDAC2 balance with concomitant epigenetic repression of common Tip60 target neuroplasticity genes occurs early in multiple types of Drosophila ND models such as Parkinson’s Disease (PD), Huntington’s Disease (HD) and Amyotrophic Lateral Sclerosis (ALS). Repressed neuroplasticity genes show reduced enrichment of Tip60 and epigentic acetylation signatures at all gene loci examined with certain genes showing inappropriate HDAC2 repressor enrichment. Functional neuronal consequences for these disease conditions are reminiscent of human pathology and include locomotion, synapse morphology, and short-term memory deficits. Increasing Tip60 HAT levels specifically in the mushroom body learning and memory center in the Drosophila brain protects against locomotion and short-term memory function deficits in multiple NDs. Together, our results support a model by which Tip60 protects against neurological impairments in different NDs via similar modes of action.

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20

Pangeni, Rajendra P., Ivonne Olivaries, David Huen, Vannessa C. Buzatto, Timothy P. Dawson, Katherine M. Ashton, Charles Davis i in. "Genome-wide methylation analyses identifies Non-coding RNA genes dysregulated in breast tumours that metastasise to the brain". Scientific Reports 12, nr 1 (20.01.2022). http://dx.doi.org/10.1038/s41598-022-05050-z.

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AbstractBrain metastases comprise 40% of all metastatic tumours and breast tumours are among the tumours that most commonly metastasise to the brain, the role that epigenetic gene dysregulation plays in this process is not well understood. We carried out 450 K methylation array analysis to investigate epigenetically dysregulated genes in breast to brain metastases (BBM) compared to normal breast tissues (BN) and primary breast tumours (BP). For this, we referenced 450 K methylation data for BBM tumours prepared in our laboratory with BN and BP from The Cancer Genome Atlas. Experimental validation on our initially identified genes, in an independent cohort of BP and in BBM and their originating primary breast tumours using Combined Bisulphite and Restriction Analysis (CoBRA) and Methylation Specific PCR identified three genes (RP11-713P17.4, MIR124-2, NUS1P3) that are hypermethylated and three genes (MIR3193, CTD-2023M8.1 and MTND6P4) that are hypomethylated in breast to brain metastases. In addition, methylation differences in candidate genes between BBM tumours and originating primary tumours shows dysregulation of DNA methylation occurs either at an early stage of tumour evolution (in the primary tumour) or at a later evolutionary stage (where the epigenetic change is only observed in the brain metastasis). Epigentic changes identified could also be found when analysing tumour free circulating DNA (tfcDNA) in patient’s serum taken during BBM biopsies. Epigenetic dysregulation of RP11-713P17.4, MIR3193, MTND6P4 are early events suggesting a potential use for these genes as prognostic markers.

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Liu, Zhi-ping, i Qing-Jun Zhang. "Abstract 118: Role Of Histone Trimethyl Demethylase Jmjd2A In Cardiac Hypertrophy And Heart Development". Circulation Research 113, suppl_1 (sierpień 2013). http://dx.doi.org/10.1161/res.113.suppl_1.a118.

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Epigentic regulation via histone memethylation has been shown to play important role in embryonic development and pathogenesis of adult diseases. Methylation of histone H3 lysine 9 (H3K9) mediates heterochromatin formation and also participates in inhibition of gene transcription at euchromatic sites. Methylation of H3K9 is required for proper embryonic development as shown by various genetic studies of H3K9 methyltransferases in mice. Histone demethylases for methylated H3K9 have been shown to play important role in tumorigenesis. However, their roles in development and in adult cardiovascular diseases remain elusive. Jmjd2A is H3K9me3 specific demethylase. To study its biological functions, we generated mouse with conditional alleles of Jmjd2A. Our studies with post-natal heart specific Jmjd2A deletion and overexpression mouse lines indicated that Jmjd2A is required for pathological cardiac hypertrophy and the demethylase activity of Jmjd2A is required for its transcriptional activity. Jmjd2A also plays an important role during embryonic development. Mice with homozygous deletion of Jmjd2A exhibit partial embryonic lethality depending on the genetic background. In C57Bl6 (N>5) mouse strain, some of the Jmjd2A-null embryos die between embryonic day E10-E12 with heart failure phenotype. Deletion of Jmjd2A appears to have no effect on formation of linear heart tube and subsequent looping at E9.5. However, while WT or Jmjd2A het hearts continue to grow with appearance of ventricular and atrial septum and formation of trabeculae, Jmjd2A-null embryonic hearts have pericardial effusion, thin myocardium, lack of atrial and ventricular septation, and under-developed trabaculae. These failing hearts show reduced cardiomyocyte proliferation. Gene expression profiling suggests potential downstream effectors of Jmjd2A including cell cycle and “immediate early” genes. Our data demonstrate that Jmjd2A plays important roles during heart development and functions as a hypertrophic determinant in response to pathological stimuli in adult hearts.

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Malherbe, Delphine C., i Ilhem Messaoudi. "Transcriptional and Epigenetic Regulation of Monocyte and Macrophage Dysfunction by Chronic Alcohol Consumption". Frontiers in Immunology 13 (29.06.2022). http://dx.doi.org/10.3389/fimmu.2022.911951.

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Drinking alcohol, even in moderation, can affect the immune system. Studies have shown disproportionate effects of alcohol on circulating and tissue-resident myeloid cells (granulocytes, monocytes, macrophages, dendritic cells). These cells orchestrate the body’s first line of defense against microbial challenges as well as maintain tissue homeostasis and repair. Alcohol’s effects on these cells are dependent on exposure pattern, with acute drinking dampening but chronic drinking enhancing production of inflammatory mediators. Although chronic drinking is associated with heightened systemic inflammation, studies on tissue resident macrophage populations in several organs including the spleen, liver, brain, and lung have also shown compromised functional and metabolic capacities of these cells. Many of these effects are thought to be mediated by oxidative stress caused by alcohol and its metabolites which can directly impact the cellular epigenetic landscapes. In addition, since myeloid cells are relatively short-lived in circulation and are under constant repopulation from the bone marrow compartment, alcohol’s effects on bone marrow progenitors and hematopoiesis are important for understanding the impact of alcohol systemically on these myeloid populations. Alcohol-induced disruption of progenitor, circulating, and tissue resident myeloid populations contribute to the increased susceptibility of patients with alcohol use disorders to viral and bacterial infections. In this review, we provide an overview of the impact of chronic alcohol consumption on the function of monocytes and macrophages in host defense, tissue repair and inflammation. We then summarize our current understanding of the mechanisms underlying alcohol-induced disruption and examine changes in transcriptome and epigenome of monocytes and mcrophages. Overall, chronic alcohol consumption leads to hyper-inflammation concomitant with decreased microbial and wound healing responses by monocytes/macrophages due to a rewiring of the epigentic and transcriptional landscape. However, in advanced alcoholic liver disease, myeloid cells become immunosuppressed as a response to the surrounding hyper-inflammatory milieu. Therefore, the effect of chronic alcohol on the inflammatory response depends on disease state and the immune cell population.

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