Patients may also respond differently to therapies based on their deconvolution results. We have proposed that there is a regulation of the maximum Lomitapide Mesylate activation of lymphocytes. Drugs targeting positive or negative regulators of the activation of different lymphocytes may show an effect on the slope or percent of the maximum activation state we observe. In summary, deconvolution can provide a powerful insight into the immune response in patients with autoimmune disease. The kidney is the principal target organ for infection in the mouse IV challenge model and, while sepsis has been evidenced as the major cause of death in the mouse model, the extent of kidney damage in animals showing severe symptoms is considerable and is likely to contribute to the overall pathology of the disease. It has been recognized for many years that the disease processes in C. albicans-infected kidneys result in heavy host leukocyte infiltrates and micro-abscess formation. This process suggests a contribution of host immune responses to tissue damage in the kidney, a contribution long recognized and well accepted for many bacterial infections. Hence we set out to explain the pathological basis for kidney damage following C. albicans infection. The kidney is not the only organ affected in the mouse C. albicans challenge model. Invasion of the brain by C. albicans occurs in animals receiving high challenge doses. In the spleen, lungs and liver, viable fungi are gradually cleared even while infection damage progresses in the kidneys. Detailed studies of pathological events in the mouse model indicate that changes associated with disease become measurable within 3 days of challenge with C. albicans, including body weight, systolic blood pressure, blood glucose, urea, chloride and creatinine levels. The mouse IV challenge model is a highly reproducible, longstanding, and widely used test for investigations into host-fungus interactions andefficacyof antifungal agents.However,evaluation of virulence effects solely in terms of kidney burdens and survival times seems a rather crude and unsophisticated approach against which to examine host immune responses when compared to current technologies which permit determination of levels of individual cytokines, enumeration of leukocytes of different receptor types and generation of RNA 
expression profile data for host and fungal cells. Consistent experimental evidence indicates that early innate immune responses, rather than adaptive responses, are essential for protection of mice against IV C. albicans challenge and progress has been made ex vivo and in vivo towards identification of specific interactions between leukocyte receptors involved in innate responses and different surface polysaccharides in C. albicans �� the so-called ��pathogen-associated molecular patterns��. Spellberg and colleagues concluded that failure of the kidney to halt progression of C. albicans infection correlates with cytokines produced locally in the infected organ, rather than with Folinic acid calcium salt pentahydrate systemic immune responses, as represented by cytokine production in splenic cells. The long-standing view has been that overall protective vs. nonprotective immunity to C. albicans challenge depends on a response dominated by Th1 rather than Th2 cells. However, recent work by Romani��s group suggests that IL-17-producing cells, induced subsequent to the immediate innate responses to C. albicans, promote damaging inflammation and impair the anti-Candida effects of neutrophils at sites of gastric infection. C. albicans yeast cells that have been transported from the bloodstream into visceral organs in experimentally.