Move past autoimmune research challenges with our comprehensive 770 gene multiplex panel for human or mouse to evaluate the pathways, processes and cell types involved in autoimmune disease, chronic inflammatory disease, and aberrant immune response. Analyze autoimmune biomarkers rapidly without the need for qPCR or NGS.
- Therapeutic mechanism of action (MOA) studies
- Immuno-therapy induced adverse event investigations
- Discovery/validation of disease and therapeutic specific biomarkers
- Development of predictive signatures of drug response
- Compatible with challenging sample types such as PBMCs and FFPE
Recent publications1,2 from the Milieu Interieur project at Institut Pasteur have shown the utility of the Myriad RBM TruCulture whole blood collection and culture system paired with nCounter gene expression analysis to describe the human immune response to immunostimulatory agents including Toll-like receptor (TLR) agonists and microorganisms. The recent application note investigating the Human Immune Response with Myriad RBM’s TruCulture® System and the NanoString® nCounter Autoimmune Profiling Panel describes an easy to use, reproducible workflow for studying immune responses from whole blood. The results showed excellent technical reproducibility and correlation between levels of expressed mRNA and protein. With minimal hands-on time, whole blood can be collected, treated, and processed to identify immune signatures for different stimuli. Combining the TruCulture system with nCounter gene expression profiling enables the study of circulating immune responses through rapid and easy collection, stimulation, and subsequent profiling of leukocytes from healthy or diseased donors, with implications for the study of immunology, autoimmunity, and immuno-oncology.
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- Piasecka et al., (2018) Milieu Intérieur Consortium. Dissecting the Roles of Age, Sex and Genetics in Shaping Variation in the Human Immune Landscape, PNAS Jan 16;115(3)
- Urrutia et al. (2016) Milieu Intérieur Consortium. Standardized Whole-Blood Transcriptional Profiling Enables the Deconvolution of Complex Induced Immune Responses. Cell Reports. Sep 6;16(10):2777-2791
The 35 pathways and processes in this panel provide a comprehensive view into immune system dysfunction in autoimmune disease and treatment-induced adverse immune events.
|Autoimmune Profiling Pathways and Processes|
|Autoantigens||Apoptosis||Autophagy||B-Cell Receptor Signaling||Chemokine Signaling|
|Complement System||Cytosolic DNA Sensing||Cytotoxicity||Endothelial Activation||Epigenetics and Transcriptional Signaling|
|Fc Receptors and Phagocytosis||Growth Factor Signaling||Immunometabolism||Inflammasomes||Interleukin-12 Signaling|
|Other Interleukin Signaling||Lymphocyte Trafficking||MHC Class II Antigen Presentation||MHC Class II Antigen Presentation||mTOR|
|NF-kB Signaling||NLR Signaling||Oxidative Stress||T-cell Checkpoint Signaling||T-cell Receptor Signaling|
|TGF-Beta Signaling||Th1 Differentiation||Th2 Differentiation||Th17 Differentiation||Th17 Mediated Biology|
|TNF Family Signaling||Toll Like Receptor Signaling||Treg Differentiation||Type I Interferon Signaling||Type II Interferon Signaling|
Immune Cell Profiling
The Autoimmune Profiling Panels provide unique cell profiling data to measure the relative abundance of immune cell types1. The table below summarizes each cell type represented by gene content in the panel, as qualified through biostatistical approaches and selected literature in the field of immunology.
Relative Cell Type Abundance
|B Cells||B cells are the primary mediators of the humoral immune response, bearing antigen-specific B cell receptors and producing antibodies that can enable the immune system to respond to a broad variety of antigens. B cells can also function as MHC class II antigen presenting cells to stimulate T cell immunity.|
|T Cells||T-cells mediate cell-based immunity by recognizing primarily peptide antigens displayed on MHC class I or class II and either producing cytokines or directly killing the presenting cell.|
|TH1||CD4+ T cell subset that produces IL2 and Interferon-gamma to promote cellular immunity by acting on CD8+ T Cells, NK Cells and Macrophages|
|Regulatory T Cells (Tregs)||CD4+ T Cells that suppress effector B and T Cells and play a central role in suppression of the immune response and tolerance to self-antigens|
|CD8+ T Cells||A subset of T cells that are capable of binding cognate-antigen expressing cells via class I MHC and directly lysing them via perforin and granzymes.|
|Exhausted CD8+ T Cells||T-cells overstimulated by antigen can develop an "exhausted" phenotype, in which they are no longer effective in targeting antigen-bearing cells.|
|Cytotoxic Cells||All cells capable of cytotoxic activity, which can include T, NKT, and NK-cells.|
|Dendritic Cells||Professional antigen presenting cells that internalize, process, and present antigens to lymphocytes via MHC class I and class II along with costimulatory signals to initiate cellular immune responses.|
|Macrophages||Pluripotent cells with critical roles in initiating innate and adaptive immune responses, phagocytosing abnormal cells, and regulating wound healing and tissue repair.|
|Mast Cells||Mast cells release histamine containing granules and other signals in order to promote inflammation and regulate allergic responses.|
|Neutrophils||Neutrophils are highly abundant cells that respond early to sites of infection or inflammation, phagocytose cellular debris, and promote downstream immunity.|
|Natural Killer (NK) Cells||Cytotoxic cells of the innate immune system that are a significant source of interferon-gamma and are capable of directly killing targeted cells via detection of a loss in MHC surface expression.|
|NK CD56dim cells||The amount of CD56 present on an NK cell is indicative of its age and differentiation state; CD56dim cells are mature NK cells, more commonly found in peripheral blood than secondary lymphoid tissues, and have the greatest cytolytic activity.|
The Autoimmune Profiling Panel is designed to encompass adaptive and innate immune system dysfunction associated with six of the most common and debilitating autoimmune diseases. The table below describes the six conditions that were emphasized in creating this panel, along with induced adverse immune events. While this panel was designed around these 6 diseases, it will provide powerful immune system information for the research of any autoimmune or chronic inflammatory disease.
|Rheumatoid Arthritis||Chronic inflammatory disorder that impacts the lining of joints.|
|Inflammatory Bowel Disease||Chronic inflammation of the digestive tract.|
|Type 1 Diabetes||Autoimmune disease where the immune system mistakenly attacks the insulin-producing cells of the pancreas.|
|Multiple Sclerosis||Demyelinating disease that disrupts communication within the nervous system.|
|Systemic Lupus Erythematosus||Chronic inflammatory disease that manifests systemically throughout the body.|
|Psoriasis||Immune-mediated disease that causes skin cells to rapidly build up on the surface of the skin.|
|Induced Adverse Immune Events||Certain treatments and infections have been reported to interfere with the immune system and induce a series of autoimmune disease or adverse immune-related events.|
Targets for Approved and Investigational Therapies
Content in the Autoimmune Profiling Panel includes targets for more than 30 approved and investigational therapies for autoimmune and chronic inflammatory diseases.
|Therapeutic Target Categories|
|B-cell Targets||Immune Cell Signaling|
|Immune Checkpoint and Co-Stimulatory Targets||Innate and Adaptive Immune-Related Interleukins|
|Toll-like Receptors||Tumor Necrosis Factor (TNF)|
|Type I and II Interferons||Other Immunomodulatory Agents|
|Number of Targets||770 (Human), 770 (Mouse) including internal reference genes|
|Standard Input Material (No amplification required)||25 ng-300 ng|
|Sample Type(s)||FFPE-derived RNA, total RNA, fragmented RNA, cell lysates, PBMCs, whole blood/plasma|
|Customizable||Add up to 30 unique genes with Panel-Plus|
|Time to Results||Approximately 24 hours|
|Data Analysis||nSolver Analysis Software (RUO)|
Selected Panel References
Baranovski, B. M.,et al. T Helper Subsets, Peripheral Plasticity, and the Acute Phase Protein, α 1-Antitrypsin. BioMed Research International, 2015
Bolon, B. (2012). Cellular and Molecular Mechanisms of Autoimmune Disease. Toxicologic Pathology, 40(2), 216–229.
Guo Y, et al. CD40L-Dependent Pathway Is Active at Various Stages of Rheumatoid Arthritis Disease Progression. J Immunol 2017 Jun 1;198(11):4490-4501.
Li B, et al. Transcriptome analysis of psoriasis in a large case-control sample: RNA-seq provides insights into disease mechanisms. J Invest Dermatol 2014 Jul;134(7):1828-1838.
Kaizer EC, et al. Gene expression in peripheral blood mononuclear cells from children with diabetes. J Clin Endocrinol Metab 2007 Sep;92(9):3705-11.
Kemppinen AK, et al. Systematic review of genome-wide expression studies in multiple sclerosis. BMJ Open 2011 Jul 18;1(1):e000053.
Hung T, et al. The Ro60 autoantigen binds endogenous retroelements and regulates inflammatory gene expression. Science 2015 Oct 23;350(6259):455-9.
McGonagle, D., & McDermott, M. F. (2006). A proposed classification of the immunological diseases. PLoS Medicine, 3(8), 1242–1248.
Peters LA, et al. A functional genomics predictive network model identifies regulators of inflammatory bowel disease. Nat Genet2017 Oct;49(10):1437-1449.
Rosenblum, M. D., et al (2015). Mechanisms of human autoimmunity. Journal of Clinical Investigation, 125(6), 2228–2233.
Tabas, I., et al (2013). Anti-Inflammatory Therapy in Chronic Disease: Challenges and Opportunities. Science. 2013 January 11; 339(6116): 166–172.
Urrutia, A., et al. (2016). Standardized Whole-Blood Transcriptional Profiling Enables the Deconvolution of Complex Induced Immune Responses. Cell Reports, 16(10), 2777–2791.
For Research Use Only. Not for use in diagnostic procedures.