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Th1 / Th2 / Th17 Arrays

Th17 cells are a unique set of T helper cells characterized by the production of IL-17 (also known as IL-17A), IL-17F, and many other inflammatory cytokines. Th17 cells are pro-inflammatory and are thought to be involved in the immune response to fungal and certain bacterial infections, as well as being associated with inflammation and airway hyper-responsiveness in asthma and several autoimmune diseases, including inflammatory bowel disease, rheumatoid arthritis, multiple sclerosis, and asthma.

 

Quantibody® Multiplex ELISA Th17 Arrays

The Quantibody arrays are quantitative multiplex ELISA arrays featuring fluorescent detection. The antibodies are spotted on glass slide solid supports and require a laser scanner for data collection. Cytokine standards are provided with the array for calculation of target protein concentrations.

All Quantibody arrays feature the sandwich immunoassay principle, utilizing an immobilized capture antibody along with a corresponding biotinylated detection antibody.

Working sample volume: 50-100 µl

 
Quantibody Array Human Th1/Th2 Array Q1 (QAH-TH-1)
Detects 10 Human Th1 and Th2 Cytokines:
IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-13, GM-CSF, IFN-gamma, TNF alpha
Manual 

 

Quantibody Array Human Th1/Th2/Th17 Array Q1 (QAH-TH17-1)
Detects 20 Human Th1, Th2, and Th17 Cytokines:
GM-CSF, IL-1 beta, IL-2, IL-4, IL-5, IL-6, IL-10, IL-12 p70, IL-13, IL-17A, IL-17F, IL-21, IL-22, IL-23, IL-28, IFN-gamma, MIP-3 alpha, TGF beta 1, TNF alpha, TNF beta
Manual 

 

Quantibody Array

 Mouse Th1/Th2/Th17 Array Q1 (QAM-TH17-1)
Detects 18 Mouse Th1, Th2, Th17 Cytokines:
IL-1 beta, IL-2, IL-4, IL-5, IL-6, IL-10, IL-12 p70, IL-13, IL-17A, IL-17F, IL-21, IL-22, IL-23, IL-28, IFN-gamma, MIP-3 alpha, TGF beta 1, TNF alpha
Manual 

 

C-Series Membrane-based Th17 Array

The C-Series arrays are semi-quantitative, measuring the relative protein expression levels. C-Series features chemiluminescent signal detection. The antibodies are spotted on nitrocellulose membrane solid supports and are handled in a very similar manner to Western blots.

All C-Series arrays work on the sandwich ELISA principle, utilizing a matched pair of antibodies: an immobilized capture antibody and a corresponding biotinylated detection antibody.

Working sample volume: 1000 µl

 
Membrane Arrays Human T Cell Response Array C1 (AAH-TH-1)
Detects 10 Human proteins:
IL-2, IL-4, IL-5, IL-9, IL-10, IL-12 p70, IL-17A, IFN-gamma, TGF beta 1, TNF alpha
Manual 

 

Membrane Arrays Human T Cell Response Array C2 (AAH-TH-2)
Detects 20 Human Proteins:
IL-2, IL-4, IL-5, IL-6, IL-7, IL-10, IL-12 p70, IL-13, IFN-gamma, TGF beta 1, TNF alpha, IL-17A, IL-9, IL-22, IL-17F, IL-18, IL-23 p19, IL-21, IL-27, IL-33 (IL-1 F11)
Manual 

 

Membrane Arrays Human Th1/Th2/Th17 Array C1 (AAH-TH17-1)
Detects 34 Human TH1, Th2, & Th17 Cytokines:
CD30, CD40 Ligand, CD40, G-CSF, GITR, GM-CSF, IFN-gamma, IL-1 beta, IL-1 sRI, IL-1 sRII, IL-2, IL-4, IL-5, IL-6, IL-6 R, IL-10, IL-12 p40, IL-12 p70, IL-13, IL-17, IL-17F, IL-17 R, IL-21, IL-21R, IL-22, IL-23 (p19), IL-28A, MIP-3 alpha, spg130, TGF beta 1, TGF beta 3, TNF alpha, TNF beta, TRANCE
Manual 

 

G-Series Glass Slide-based Th17 Array

The G-Series arrays are semi-quantitative, measuring the relative protein expression levels. G-Series features fluorescent signal detection. The antibodies are spotted on glass slide solid supports and require a laser scanner for data collection.

All G-Series arrays work on the sandwich ELISA principle, utilizing a matched pair of antibodies: an immobilized capture antibody and a corresponding biotinylated detection antibody.

Working sample volume: 50-100 µl

 
Human Th1/Th2/Th17 Array G1 (AAH-TH17-G1)
Detects 34 Human Th1, Th2, & Th17 Cytokines:
CD30, CD40 Ligand, CD40, G-CSF, GITR, GM-CSF, IFN-gamma, IL-1 beta, IL-1 sRI, IL-1 sRII, IL-2, IL-4, IL-5, IL-6, IL-6 R, IL-10, IL-12 p40, IL-12 p70, IL-13, IL-17, IL-17F, IL-17 R, IL-21, IL-21R, IL-22, IL-23 (p19), IL-28A, MIP-3 alpha, spg130, TGF beta 1, TGF beta 3, TNF alpha, TNF beta, TRANCE
Manual 

 

Mini-Review: IL-17 and Th17 Arrays

T helper (Th) cells are involved in activating and directing other immune cells, and are particularly important in the immune system. It is this diversity in function and their role in influencing other cells that gives T helper cells their name.

Mature Th cells are believed to always express the surface protein CD4 (CD4+ T cells). Different T helper cells support unique effector functions via distinct cytokine expression profiles and share a common naive CD4+ T cell progenitor. Today, the most commonly studied T helper cells are Th1, Th2, Th17 and Treg. Th1 (Type 1) and Th2 (Type2),  were characterized  during the late 1980s. Th17 and Treg cells were discovered much more recently. 

Th1 cells express high levels of IFNγ and TGFβ1, enhancing cellular immune responses by increasing bacteriocidal activity in macrophages and the proliferation of cytotoxic CD8+ T cells. IFNγ, in turn, stimulates production of IL-12 by dendritic cells and macrophages, forming a positive feedback loop that reinforces IFNγ secretion by Th1 cells.

Th2 cells enhance humoral immune responses via expression of the proinflammatory cytokines IL-4, IL-5, IL-6, IL-10 and IL-13, which both proliferate B cells and induce B cell antibody class switching. In addition, IL-4 produced by Th2 cells creates an autocrine loop, reinforcing secretion of their pro-inflammatory signals. Th2 signals predominate in parasitic infections and physiologic allergic responses and contribute to the the hyper-allergic response in asthma.

The cytokines produced by Th2 cells inhibit release of IFNγ by Th1 cells and IL-12 in dendritic cells and macrophages. Conversely, IFNγ inhibits production of IL-4. Thus, Th1 and Th2 cells are both self-stimulating and inhibitory to the other cell type, meaning that once a population of naive T helper cells is pushed in the direction of differentiating into Th1 or Th2 cells, the relative ratio of Th1 to Th2 cytokine production can remain tipped in one direction.

This phenomenon is referred to as the Th1/Th2 balance, and imbalances of Th1/Th2 cell populations are associated with certain diseases: Th2 cytokine expression patterns tend to promote allergic hypersensitivities leading to asthma, hay fever, and eczema, while Th1 cytokine expression patterns are typically associate with chronic inflammation, tissue injury and auto-immune disorders such as lupus. The Th1/Th2 paradigm worked well for explaining many immune responses, but it was inadequate to model for many others.

In 2005 and 2006, a flurry of publications noted T helper cell responses that were mediated by IL-17 and not attributable to Th1 or Th2 cells. Among these, two publications appeared back-to-back in Nature Immunology (2005, Vol 6, issue 11),in which Harrington, et al., and Park, et al., both described a new type of T helper cell, characterized as producing large quantities of IL-17 and noted that maturation of these cells were inhibited by both IFNγ and IL-4 but the differentiated cells were resistant to regulation by these cytokines. The publication by Harrington is credited as the first to name these cells "Th17." 

Subsequent publications identified that differentiation of naive T helper cells into Th17 cells was driven by TGFβ1 (Veldhoen, Immunity 2006; Bettelli, Nature 2006; Mangan, Nature 2006), IL-6 (Veldhoen, ibid; Mangan, ibid; and IL-6 via IL-21 and IL-23 Zhou, Nat Immunol 2007), IL-21 (Korn, Nature 2007; Nurieva, Nature 2007) and IL-23 (Zhou, ibid). The latter had already been identified as contributing to IL-17 production by a group of T helper cells distinct from Th1 and Th2, ahead of Harrington and Park (Aggarwal, J Biol Chem 2003).

These findings, along with previous correlations of experimental autoimmune encephalomyelitis (EAE, a mouse model for multiple sclerosis) with induction of IL-17 by IL-23 helped to establish that Th17 cells play a crucial role in this disease (Langrish, J Exp Med 2005). Cytokines produced by Th17 cells have been associated with several human diseases, including psoriasis (via IL-23, Krueger, NEJM 2007), rheumatoid arthritis (Kirkham, Arthritis Rheum 2006), multiple sclerosis (Matusevicius, Mult Scler 1999), inflammatory bowel disease (via genome-wide association with IL23R, Duerr, Science 2006) asthma (Molet, J Allery Clin Immunol. 2001; Barczyk, Respir Med. 2003) and various bacterial and fungal infections.

As with Th1 and Th2, there appears to be a reciprocal, negative relationship between Th17 cells and regulatory T cells (Treg) via Foxp3 and retinoic acid receptors RARα and RARγt (Mucida, Science. 2007; Zhou, Nature. 2008; Du, J Immunol. 2008). TGFβ1 can induce differentiation of Treg cells, but IL-6 or IL-21 diverts differentiation of naive T cells to Th17 cells. Further evidence of this relationship is the increase in Tregs and defective generation of Th17 cells in IL-6 KO mice (Betteli, ibid; Korn, Nature. 2007).

The largest population of Th17 cells exist at epithelial and mucosal barrier surfaces, presumably as an additional layer of protection agains bacetrial and fungal penetration of these barriers. Tregs also reside primarily in these barriers, and both Treg and Th17 cells exist is large numbers in both the mucosa of the gut and gut-associated lymphoid tissue (GALT). A recent publication in Nature Reviews Immunology (Weaver & Hatton, 2009;9:883-889), the authors note that Th17 and Treg cells are not present in invertebrates, but appear early in the timeline of vertebrate speciation. They suggest that these two T helper cells co-evolved as an adaptation to accomodate a wider range of beneficial intestinal flora in early vertebrates.

For more information, see:

  • Korn T, Bettelli E, Oukaa M, Kuchroo VK. IL-17 and Th17 Cells. Ann Rev Immunol. 2009;27:485-517. Abstract

  • Rao A, Avni O.  Molecular aspects of T-cell differentiation. Br Med Bulletin. 2000;56(4):969-984. PDF

  • Mosmann TR, Coffman RL. Th1 and Th2 Cells: Different Patterns of Lymphokine Secretion Lead to Different Functional Properties. Ann Rev Immunol. 1989;7:145-73. PDF

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