您好,聚研生物科技敬请您关注以下信息:   [登录] [ 注册]

购物车



芯片及抗体专区

抗体芯片Th17 arrays

 

NEW! Quantibody® Th17 Arrays

 

Quantibody® Th17 Arrays Product Info

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. (For more details, see mini-review below)

 

Quantibody® Human Th17 Array kits detects the following 20 Human Cytokines expressed by Th1, Th2 and/or Th17 cells: 

GM-CSF, IL-1β, IL-2, IL-4, IL-5, IL-6, IL-10, IL-12 (p70), IL-13, IL-17 (IL-17A), IL-17F, IL-21, IL-22, IL-23, IL-28, IFNγ, MIP-3α, TGFβ1, TNFα and TNFβ

 

QAH-TH17-1-1 (1 slide) can test 8-10 samples quantitatively

QAH-TH17-1-2 (2 slides) can test 16-24 samples quantitatively

QAH-TH17-1-4 (4 slides) can test 48-56 samples quantitatively

 

Quantibody® Mouse Th17 Array kits detects the following 20 Mouse Cytokines expressed by Th1, Th2 and/or Th17 cells:

IL-1β, IL-2, IL-4, IL-5, IL-6, IL-10, IL-12 (p70), IL-13, IL-17, IL-17F, IL-21, IL-22, IL-23, IL-28, IFNγ, MIP-3α, TGFβ1, TNFα

 

QAM-TH17-1-1 (1 slide) can test 8-10 samples quantitatively

QAM-TH17-1-2 (2 slides) can test 16-24 samples quantitatively

QAM-TH17-1-4 (4 slides) can test 48-56 samples quantitatively

 

Mini-Review IL-17 and Th17 Cells

 

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 (Type 2), were characterized during the late 1980s. Th17 and Treg cells were discovered much more recently

T helper maturation

Exposure of a common naive T helper cell (Th0) to different cytokine signals can result in differentiation to Th1, Th2, Th17 or Treg cells. These differentiated cells secrete distinct cytokine profiles and have discrete effector roles in immune response. Some Th cells inhibit the function or maturation of other Th cell types. Depicted In this example is the negative influence of Th1 and Th2 cells on Th17.

Th1 cells express high levels of Interferon gamma (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 Interferon gamma 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

 

更多产品信息请联系:

 

广州聚研生物科技有限公司

Tel:020-87322722 87328692

fax:020-87328692

不仅是产品供应商,更是您的研究伙伴

Web: www.asbio.com.cn

  址:广州市中山一路51号拓业大厦506室(510600
E-mailinfo@asbio.com.cn


发布日期:2010-9-7 【返回】