Human Reactive Inflammatory Cytokine Antibody Sampler Kit

The Human Reactive Inflammatory Cytokine Antibody Sampler Kit provides an economical means of detecting inflammation-associated cytokine expression. The kit includes enough antibodies to perform two western blot experiments with each primary antibody.

Interleukin-1 alpha (IL-1α) and interleukin-1 beta (IL-1β) are pro-inflammatory cytokines (1). IL-1α is produced by many cell types, including epithelial cells, monocytes, and macrophages (1,2). It is typically sequestered but can be released during necroptosis or inflammasome activation (3-5). IL-1α is active in both its uncleaved (pro-IL-1α) and cleaved forms and thus acts as an alarmin, initiating signaling through IL-1R1 (6). IL-1β is not active until it is cleaved (7,8). IL-1β expression is induced by inflammatory stimuli, including TLR ligands, IL-1β itself, and tumor necrosis factor-alpha (TNF-α) (1,9,10). IL-1β is primarily synthesized by activated monocytes and macrophages. It activates innate immune cells and polarizes CD4⁺ T cells toward T helper (Th) 1 and Th17 cells (10).

IL-2 is mainly produced by activated CD4⁺ and CD8⁺ T cells (11). IL-2 is a pro-inflammatory cytokine, promoting proliferation and activation of CD4+ and CD8+ T cells, B cells, and NK cells through binding the IL-2 receptor complex (11). At low doses, however, IL-2 can have anti-inflammatory effects (12).

IL-4, a cytokine produced by mast cells, basophils, and activated T cells, is an anti-inflammatory cytokine that promotes differentiation of naive T cells into Th2 lineage cells (13-15). In autoimmune conditions, IL-4 can play pro-inflammatory roles and is a therapeutic target (16).

IL-6, when interacting with soluble IL-6R and binding to gp130, has pro-inflammatory effects, but when interacting with membrane-bound IL-6R, it exerts anti-inflammatory effects (17). IL-6 regulates the acute phase response and is produced by T cells, macrophages, and endothelial cells (18,19). IL-6 can also prime macrophages for M2, or anti-inflammatory, states by upregulating IL-4R (20).

IL-8 is a neutrophil chemoattractant and is able to activate degranulation and respiratory burst (21-23). IL-8 is produced by T cells, monocytes, neutrophils, fibroblasts, endothelial cells, and others in response to inflammatory stimuli such as IL-1α/β and TNF-α (24). Beyond its chemotactic effects, IL-8 can play roles in cancer by promoting tumor angiogenesis and stimulating proliferation by activating NF-kB signaling (25,26).

IL-10 is an anti-inflammatory cytokine produced by various immune cells (27,28). IL-10 is often produced alongside pro-inflammatory cytokines in response to pathogens and limits damage to the host that can be caused by strong inflammatory responses (29). After binding to IL-10Rα, which complexes with IL-10Rβ, IL-10 activates Stat3, suppresses gp130 activity, and induces expression of transcriptional repressors of the inflammatory response (30).

Interferon-gamma (IFN-γ) is produced by T, B, NK, and antigen-presenting cells and has diverse pro- and anti-inflammatory functions (31). Its expression is induced by type I IFNs, IL-12, IL-15, and IL-18, and it acts through IFNγR1 and IFNγR2 to activate signaling through Stat1 (31). IFN-γ upregulates expression of major histocompatibility complex (MHC) class I and II, which help to activate cytotoxic CD8⁺ and CD4⁺ T cells, respectively (31-33). IFN-γ can also suppress pro-inflammatory cytokine expression and promote tumor cell apoptosis by upregulating expression of several caspases (31,34).

TNF-α is a pro-inflammatory mediator secreted by various subsets of immune cells, including T cells, B cells, NK cells, and macrophages (35). In the context of certain autoimmune diseases, and in antigen presentation, however, TNF-α can be immunosuppressive (36,37). TNF-α expression is induced by various stimuli, including IL-1β, IFN-γ, and microbial infections. Depending on downstream signaling checkpoints through MAPK, NF-kB, and caspase-8, it can promote both inflammatory gene expression and apoptosis, necroptosis, and pyroptosis (38-41).