Immunology innate response

Parroche P, Lauw FN, Goutagny N, Latz E, Monks BG, Vis-intin A, Halmen KA, Lamphier M, Olivier M, Bartholomeu DC, GazzinelU RT, Golenbock DT. Malaria hemozoin is immunolog-ically inert but radically enhances innate responses by presenting malaria DNA to Toll-Uke receptor 9. Proc. Natl. Acad. Sci. U.S.A. 2007 104 1919-1924. 

Medzhitov, R. and Janeway, C.A. (1999) Innate immunity impact on the adaptive immune response. Current Opinion in Immunology 9, 4-9. 

The basal immunological mechanisms are complex but can now be analyzed with refined and more powerful laboratory methods, such as the microarray technique. With the help of this technique, additional information besides that concerning IgE and cytokine levels about the association between adaptive and innate immune response as well as other cellular responses can be gathered (6-8). 

Zaccone, P., Lehervari, Z., Jones, L.M., Sidobre, S., Kronenberg, M., Dunne, D.W. and Cooke, A. (2003) Schistosoma mansoni antigens modulate the activity of the innate immune response and prevent onset of type 1 diabetes. European Journal of Immunology 33, 1439-1449. 

Acquired immunity is antigen dependent and comprises all the specific immunological reactions associated with lymphocytes. In light of the existence of an antigen-specific defense system, a legitimate question arises as to why we have such an elaborate nonspecific immune system. One of the primary reasons may be that an acquired immune response takes time. For example, 5 days are needed to generate a primary antibody response, and the body must rely on the innate immune system to hold the infection in check during this time. As noted previously, acquired immunity can be subdivided into two effector arms, humoral immunity and cell-mediated immunity. The humor (i.e., a bodily fluid) associated with humoral immunity is the secreted form of Ig in the blood. The cells associated with cell-mediated immunity are the various subpopulations of T cells. 

Froicu, M. and Cantorna, M.T. (2007) Vitamin D and the vitamin D receptor are critical for control of the innate immune response to colonic injury. BMC Immunology, 8, 5. 

A number of experimental and clinical reports have suggested that a variety of factors unrelated to drug metabolism and direct hepatotoxicity may also influence susceptibility to DILL In addition, the nature of idiosyncratic liver injuries suggests that a majority of these reactions involve an immune mechanism. Hepatic cellular dysfunction and death have the ability to initiate immunological reactions, including both adaptive and innate immune responses. This inflammatory process has been implicated in the development of liver injury induced by such drugs as APAP, dihydralazine, and halothane (Laskin and Gardner 2003 Liu and Kaplowitz 2002 Luster et al. 2001). 

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