| The mammalian Toll-like receptors (TLRs) are homologues of Drosophila Toll which are considered as pattern recognition receptors related to innte immunity and linking to acquired immunity. TLRs are characterized by extracellular leucine-rich repeat domains and intracellular signaling domain that shares homology with cytoplasmic sequences of the mammalian IL-1 receptor. Activation of most TLRs leads to recruitment of MyD88 which interacts with IL-1 receptor-associated kinase, and following by initiation of a signal transduction cascade culminating in nuclear translocation of NF-kB family members, and production of cytokines. So far there have been 12 members, i.e.Toll 1-11 and 18-wheeler in TLR family since the first TLR molecular was identified in 1997. Not only do TLRs involve in infection immunity and innate immunity, but also non-infection immunity or adaptive immunity, such as antigen presenting, immune tolerance, and cell apoptosis. TLRs also play an important role in autoimmune disease, allergic disease, transplantation rejection and tumor. Some TLRs binding with corresponding ligand can induce effector cells to produce related cytokine, such as IL-10, IL-4, IL-5 and IL-13 which play key role in inflammation process. At present allergic disease is considered to be correlated closely with Th2 cells, for example Th2-cytokine IL-4 can stimulate production of IgE and IL-5 can collect chemotactic eosinophilia; and some cytokine correlated such as IL-12 and IFN-γ can inhibit allergic inflammation. Just as deduction of hygiene hypothesis, bacterial and viral infections during early life direct the maturing immune system toward Th1, which counterbalance proallergic responses of Th2 cells. Thus, a reduction in the overall microbial burden will result in weak Th1 imprinting and unrestrained Th2 responses that allow an increase in allergy. Many...
|
PDF Full Text Request