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PDP - Template Name: Antibody Sampler Kit
PDP - Template ID: *******4a3ef3a
  1. Products /
  2. Primary Antibodies /
  3. Human Reactive Inflammatory Cytokine Antibody Sampler Kit

Human Reactive Inflammatory Cytokine Antibody Sampler Kit #83636

    Product Information

    Kit Usage Information

    Protocols

    Product Description

    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.

    Background

    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).
    1. Garlanda, C. et al. (2013) Immunity 39, 1003-18.
    2. Palomo, J. et al. (2015) Cytokine 76, 25-37.
    3. Dinarello, C.A. (2018) Immunol Rev 281, 8-27.
    4. Cohen, I. et al. (2010) Proc Natl Acad Sci USA 107, 2574-9.
    5. Tsuchiya, K. et al. (2021) Cell Rep 34, 108887.
    6. Malik, A. and Kanneganti, T.D. (2018) Immunol Rev 281, 124-137.
    7. Thornberry, N.A. et al. (1992) Nature 356, 768-74.
    8. Cerretti, D.P. et al. (1992) Science 256, 97-100.
    9. Dinarello, C.A. (2011) Blood 117, 3720-32.
    10. Bent, R. et al. (2018) Int J Mol Sci 19, 2155.
    11. Liao, W. et al. (2011) Curr Opin Immunol 23, 598-604.
    12. Zhang, J.Y. et al. (2022) Nat Commun 13, 7324.
    13. Yokota, T. et al. (1986) Proc Natl Acad Sci USA 83, 5894-8.
    14. Grabstein, K. et al. (1986) J Exp Med 163, 1405-14.
    15. Kopf, M. et al. (1993) Nature 362, 245-8.
    16. Gärtner, Y. et al. (2023) Pharmacol Ther 242, 108348.
    17. Scheller, J. et al. (2011) Biochim Biophys Acta 1813, 878-88.
    18. Heinrich, P.C. et al. (1998) Biochem J 334 (Pt 2), 297-314.
    19. Heinrich, P.C. et al. (1998) Z Ernahrungswiss 37 Suppl 1, 43-9.
    20. Mauer, J. et al. (2014) Nat Immunol 15, 423-30.
    21. Payne, A.S. and Cornelius, L.A. (2002) J Invest Dermatol 118, 915-22.
    22. Brat, D.J. et al. (2005) Neuro Oncol 7, 122-33.
    23. Mukaida, N. (2003) Am J Physiol Lung Cell Mol Physiol 284, L566-77.
    24. Baggiolini, M. and Clark-Lewis, I. (1992) FEBS Lett 307, 97-101.
    25. Zhang, B. et al. (2015) Cancer Biol Ther 16, 898-911.
    26. Fousek, K. et al. (2021) Pharmacol Ther 219, 107692.
    27. Moore, K.W. et al. (2001) Annu Rev Immunol 19, 683-765.
    28. Gabryšová, L. et al. (2014) Curr Top Microbiol Immunol 380, 157-90.
    29. Saraiva, M. and O'Garra, A. (2010) Nat Rev Immunol 10, 170-81.
    30. Saraiva, M. et al. (2020) J Exp Med 217, e20190418.
    31. Castro, F. et al. (2018) Front Immunol 9, 847.
    32. Curtsinger, J.M. et al. (2012) J Immunol 189, 659-68.
    33. Akbar, S.M. et al. (1996) Immunology 87, 519-27.
    34. Mühl, H. and Pfeilschifter, J. (2003) Int Immunopharmacol 3, 1247-55.
    35. Aggarwal, B.B. (2003) Nat Rev Immunol 3, 745-56.
    36. Kassiotis, G. and Kollias, G. (2001) J Exp Med 193, 427-34.
    37. Masli, S. and Turpie, B. (2009) Immunology 127, 62-72.
    38. Bethea, J.R. et al. (1992) J Neuroimmunol 36, 179-91.
    39. Vila-del Sol, V. et al. (2008) J Immunol 181, 4461-70.
    40. Rahman, M.M. and McFadden, G. (2006) PLoS Pathog 2, e4.
    41. van Loo, G. and Bertrand, M.J.M. (2023) Nat Rev Immunol 23, 289-303.

    Database Links

    UniProt ID: P01584 , P01583 , P01579 , P22301 , P05112 , P05231 , P60568 , P10145 , P01375


    Entrez-Gene Id: 3553 , 3552 , 3458 , 3586 , 3565 , 3569 , 3558 , 3576 , 7124


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