The immune system has developed to respond specifically, quickly, and widely to protect host against foreign antigens (bacteria, viruses, toxins, etc.). Cytokines act as key mediators of immune events including innate immunity, antigen presentation, antibody production, bone marrow differentiation, and cellular recruitment. Chemotactic cytokines (Chemokines), a subfamily of cytokines, have a small molecular weight and are primarily responsible for the recruitment of cells, such as fibroblasts, keratinocytes, and immune cells, to localized areas (chemotaxis) (1-3).
To learn more about the complex biology of cytokines and chemokines, continue reading below.
Chondrex, Inc. provides both Human and Mouse Chemokine & Cytokine Detection ELISA Kits to study the complicated roles of cytokines in mediating physiological and pathological inflammatory reactions, including: arthritis, nephritis, allergies, IBD colitis, cancer, sepsis and COVID-19. The tables below list all of Chondrex, Inc.’s Mouse Cytokine/Chemokine Detection ELISA Kits currently available.
Chondrex, Inc. specializes in inflammatory research, including in-vitro and in-vivo inflammation models. For suggested models and kit pairings that can enable your inflammatory studies click here.
New Cytokine Detection ELISA Kits are constantly under development, please check back for new kits in the future. Additionally, if there is a cytokine/chemokine target you are interested in that we do not currently offer a kit for, please contact us about custom ELISA kit services at support@chondrex.com.
Human Chemokine & Cytokine Detection ELISA Kits
Mouse Chemokine & Cytokine Detection ELISA Kits
Rat Cytokine Detection ELISA Kits
| Product | Catalog # | Price (USD) |
| Rat Tumor Necrosis Factor Alpha (TNF-alpha) Detection ELISA Kit | 6901 | 357.00 |
Cytokines are small signaling proteins secreted by a wide variety of cell types (primarily immune cells) that regulate immune responses through autocrine signaling (signal to self), paracrine signaling (signal to nearby cells) or endocrine signaling (signal to distant cells through bloodstream). While the signaling pathways these mediators orchestrate are highly complex, cytokines are generally categorized as either pro-inflammatory or anti-inflammatory. During an inflammatory response, pro-inflammatory cytokines will potentiate inflammatory pathways, promote activation of cytotoxic T-cells and elicit antibody production by the humoral immune system (1-3). Pro-inflammatory cytokines are produced predominantly by activated macrophages and are involved in the up-regulation of inflammatory reactions. Interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α are all classified as pro-inflammatory cytokines (4). An example of a pro-inflammatory stimulus that elicits IL-1β up-regulation is a bacterial infection (Figure 1).
In contrast, anti-inflammatory cytokines ameliorate inflammatory responses by repressing the expression of specific cytokines and down-regulating expression of cytokine receptors. IL-10, the best studied anti-inflammatory cytokine, is primarily synthesized by CD4+ T-Cells (Th2) cells, monocytes, and B cells (Figure 2). Often, down-regulation of IL-10 is linked to aggressive pro-inflammatory responses and pathological inflammation. Decades of research have shown that IL-10 imbalance can affect the disease progression of rheumatoid arthritis, colitis, allergies, cancer, and viral infections, including corona viruses (4-6). Managing the balance and dynamics of pro-inflammatory and anti-inflammatory cytokines is crucial for overcoming immune challenges and maintaining homeostasis.
Interestingly, several cytokines, such as leukemia inhibitory factor, interferon-alpha, IL-6, and tumor growth factor-beta (TGF-β), have been categorized as both anti-inflammatory and pro-inflammatory (4,5). This indicates that some cytokines may play different, context-specific roles in healthy immune reactions and inflammatory diseases.
Chemokines are a sub-class of the cytokine family that have various effects in the immune system. Here we focus on their role as inflammatory mediators through their ability to influence cellular recruitment to sites of injury/damage. Chemokines are classified into four groups based on the location of their first two cysteine residues in N-terminal of the protein structure (7,8):
Chemokines induce inflammatory cell migration and activation by binding to specific G-protein-coupled cell-surface receptors (GPCR) expressed on different types of leukocytes. α-chemokines specifically attract neutrophils, but do not act on lymphocytes. Conversely, β-chemokines do not act on neutrophils, but selectively attract and activate monocytes and lymphocytes. Chemokine signaling attracts and accumulates leukocytes in injured or damaged tissues, initiating both acute and chronic inflammatory responses (Figure 3A). Therefore, elevated chemokine levels are observed in many inflammatory diseases (7-10).
The best studied chemokine is CXCL8, also known as IL-8. Once CXCL8 is bound to the GPCR located on the leukocytes cell surface, a complex intracellular signaling cascade is initiated. If the affected leukocyte is a neutrophil, CXCL8 promotes infection resolution by inducing phagocytosis and degranulation, which stimulates the release of antimicrobial extracellular fibers known as neutrophil extracellular traps (NETs) (11,12; Figure 3B). In addition, CXCL8 promotes angiogenesis by inducing endothelial cell proliferation, survival, and migration (11-14).
The differentiation of naïve T Cells (CD4+ cells) into specialized cell types are dependent on signaling by cytokines (i.e.IL-2, IL-4, IL-21, IL-12, TGF-β, IFN-γ) and several chemokines (i.e. CCL2-5). Naïve T Cells are differentiated into various T helper (Th) cell subsets through activation by co-stimulatory signaling molecules, including IL-2. The initial subsets of Th cells discovered were the Th1 (inflammation lineage) and Th2 (allergy lineage), however other Th cell subsets have subsequently been described (Th17, Th22, Th9 and Treg cells). The identification of these cell types is based on the unique cytokine profile each of them express (Figure 4). Recent studies have identified the role of chemokines (CCL2-5) in differentiation of Th1 and Th2 cells. Chemokines can influence the differentiation of these cells by acting directly on the Th1 and Th2 cell receptors and/or by manipulating the concentration of cytokines released by other cells, such as IL-12 and IL-4, which are necessary for Th1 and Th2 differentiation, respectively (15,16).
Rheumatoid Arthritis (RA)
Associated Cytokine(s): TNF-α, IL-1β, IL-4, IL-6, IL-10, IL-13, IL-17, and IL-23
Associated Chemokine(s): CCL2, CCL5, CCL28
Suggested inflammatory model(s): Adjuvant-Induced Arthritis, Collagen Antibody-Induced Arthritis, Collagen-Induced Arthritis
Inflammatory Bowel Disease (IBD)
Associated Cytokine(s): TNF-α, IL-17, IL-10, and IL-23
Associated Chemokine(s): CCL2, CCL5, CCL20, CCL25, CCL28
Suggested inflammatory model(s): Dextran Sulfate Sodium Colitis Model
Nephritis
Associated Cytokine(s): TNF-α, IL-4, IL-5 IL 10, IL-2, IFN γ, IL-17, and IL-6
Associated Chemokine(s): CCL2, CCL5
Suggested inflammatory model(s): Cationic BSA (cBSA) ICGN Model, Rat Anti-Glomerular Basement Membrane Nephritis Models
Allergens
Associated Cytokine(s): TNF-α, VEGF, TGF-β, IL-2, IL-4, IL-5, IL-6, IL-10, IL-13
Associated Chemokine(s): CCL2, CCL5, CCL17, CCL20
Suggested inflammatory model(s): Ovalbumin (OVA)-Induced Asthma, House Dust Mite (HDM)-Induced Asthma
Cancer
Associated Cytokine(s): TNF-α, IL-2, IL-6, IFN-γ
Associated Chemokine(s): CCL2, CCL5, CCL20, CCL25, CCL28, CXCL1, CXCL13, CXCL14
Cytokine Storm Related Diseases
Sepsis
Associated Cytokine(s): IL-1β, TNF-α, IL-6, IL-10, IL-17
Associated Chemokine(s): CXCL1, CCL2, CCL20, CCL28
Suggested inflammatory model(s): Sepsis/ Endotoxemia by LPS
COVID-19
Associated Cytokine(s): TNF-α, IL-1β, IL-6, IL-10, IL-13, IL-17
Associated Chemokine(s): CCL2
References