Dendritic cells and the immune cell network: DC:T cell interactions.
The key immunoregulatory pathways involve Toll-like Receptors (TLRs), cytokines and chemokines, which initiate and regulate immunity.
Imgenex is focused on the regulatory network of Dendritic Cell T cell interaction which leads to activation and polarization of responses from different T cell subsets.
T cells and T cell subsets comprise around 50% of the ongoing research being done in all of immunology today.
T cell responses are driven by interaction with Dendritic Cells (DCs) through DC activation upon recognition of antigens. TLRs comprise a main means for recognition of antigens by DCs which then process these antigens and activate T cells.
Activation of T cells occurs through the inflammatory/immune signaling cascade of which NF-kappa-B is a major pathway. Activation through the NF-kappa-B pathway leads to production of inflammatory mediators such as IL-1beta, IFNgamma, TNFalpha etc.
Imgenex is very strong in portfolio and reputation for Dendritic Cells, signaling pathways especially NF-kappa-B and Toll-like Receptors and Innate Immunity overall.
T helper (TH) cells have been categorized by different phenotypes often through their secretion of distinct effector molecules:
Th1 - Interferon- producing TH1 effect Cell Mediated Responses
Th2 - IL-4 producing TH2 cells effect Humoral or antibody mediated responses through activation of B Cells which produce antibodies
Tregs - Regulatory T cells suppress other T cell responses and IL-35 is thought to be one means in which this suppression occurs
Th17 cells appear to mediate and sustain inflammatory responses and are important for maintenance of autoimmunity type diseases.
Other T cell Subsets include
Imgenex has been building a solid portfolio for T cell subsets over the past several years and is now introducing key competitive and new products especially for Th17 and Tregs:
TH17 differentiation pathway. Naive cells can respond to IL-6, IL-21 and TGF-?. Initial stimulation results in STAT3 activation, which subsequently leads to induction of IRF-4, RORt, IL-23R, and IL-21.
An autocrine IL-21 feedback loop further promotes STAT3 activation and RORt expression, stabilizing the TH17 phenotype.
Additional known stimulatory and antagonistic molecules are listed as text in order to simplify the figure (Source: N. Ghilardi, W. Ouyang / Seminars in Immunology 19 (2007) 383–393).
Dendritic Cell: Th17 Polarization and the Inflammatory Response
ROR gamma Plasmids: