Immune Factors

In the last decades, postinfectious molecular mimicry has been postulated as the foremost putative mechanism underlying GBS. This implies that antigenic determinants are shared between an infectious agent and the peripheral nervous system. Thus the initial antigenic stimulation by the infectious agent results 

In any chronic autoimmune inflammatory concUdon, several andgens may be involved via epitope spreading (Lehmann et al., 1992), making it difficult to idendfy the culprit andgen in an individual padent. Moreover, andbodies display a variety of affinides and avicUdes and some may acdvate the complement cascade while others may not (Janeway et al., 

Yan et al., 2001 studied the sera of 21 CIDP padents for andmyelin acdvity using immunofluorescence and for binding to myelin proteins using Western blot analysis. Results showed that the sera of six padents (29%) contained and-P(, IgG andbodies, and four of these caused conducdon block and demyelinadon when injected ind aneurally into experimental animals. These results suggest that P is an autoandgen in 

Bnefly summarize the different experimental neuritis models in relation to the human diseases. 

Describe the key iimnunological factors contributing to axonal damage in GBS and CIDP. 

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The wide range of inflammatory and immune factors secreted by adipocytes has led to the view that there are many similarities between these cells and cells of the immune system. 

In addition, we discuss the most likely clinical consequences of mild-to moderate immunosuppression and potential confounders as well as non-immune factors that may modify these disease outcomes. Cases of profound immunosuppression, such as primary immunodeficiency diseases or HIV/AIDS, are not discussed, as these represent extreme examples of immunosuppression where neither the specific clinical diseases nor the eventual outcomes have much in common with events that occur in individuals with mild-to-moderate immunosuppression. 

The major gap in clarifying the shape of the dose-response curve (i.e., between immune response and disease) is a lack of large scale epidemiological studies in populations with mild-to moderate immunodeficiency that have been monitored simultaneously for immune system parameters and clinical disease. Attempts in conducting such studies will be complicated by many non-immune factors which can affect infectious disease incidences. 

Although both metabolic and immune factors may be involved in the aetiology of severe hepatitis after halothane the aetiology of postanaesthetic/postsurgical hepatitis is far from clear. A recent study revealed that paediatric anaesthesiologists had high titres of serum autoantibodies which react with specific hepatic proteins. Since the vast majority of these individuals have not developed hepatitis the pathological role of autoantibodies in volatile anaesthetic-induced hepatitis remains questionable (Njoku and co-workers 2002). 

Flatworm parasites are well recognized for their ability to live for decades in environments where they are in contact with potentially damaging immune factors. This adaptability reflects the fact that these parasites have evolved mechanisms to evade immune effector mechanisms, and more remarkably, to sense and utilize components of the host immune system for their own development. Schistosomes, digenetic trematodes, are undoubtedly the most well-studied parasitic flatworms. These parasites infect over 200 million people in tropical and subtropical zones, and cause severe disease in approximately 5% of those infected. Of immunological interest is the fact that pathology in schistosome-infected individuals is caused largely by the immune response... 

The evidence that schistosome biology is modulated by host-derived immune factors has fuelled interest in the actual parasite receptors that can interact with such molecules. The surface of schistosomes consists of a tegument,... 

Once schistosome cercariae penetrate the skin of their host, they can remain in this environment as schistosomula for up to 5 days before entering the vasculature and beginning their migration to the lungs and, subsequently, the hepatic portal vein (Wilson, 1987). During this journey, which may take 3 weeks (Wilson, 1987), and thereafter, schistosome parasites must contend with an assortment of host immune factors. Yet, as is well known, these parasites are able to complete the journey to their final destination and live for years. Research has shown that schistosomes have adapted a variety of mechanisms that enable them to evade a strong and potentially lethal host immune response. 

Gemmell, M.A. (1962) Natural and acquired immunity factors inhibiting penetration of some hexacanth embryos through the intestinal barrier. Nature 194, 701-702. 

LPS modifications play a role in CAMP resistance and virulence and also influence the host response to infection by altering cell signaling and the release of cytokines and other innate immune factors (Kawasaki et al., 2004b Lee et al., 2004). 

Oram 93 5x 106 Natural immunized (factor VII) PCR fd, PCR VL, V genes Mouse spleen Fab Phagemid 10 1 10-9... 

Resisting infection by producing immune factors and removing bacteria... 

The pH of the tears is approximately 7.4, and the tear layer contains small amounts of protein, including lysozymes, lactoferrins, gamma globulins, and other immune factors. The tears are primarily responsible for supplying the oxygen requirements of the corneal epithelium. 

Macrophages and all MP in general, are known to produce a plethora of immune factors that are secreted into the environment and can act in a paracrine and/or autocrine manner. The microenvironment affects timing, dosage, and the receptiveness of the target cells. Moreover, there are very few of these immune factors that are solely attributed to MP, and multiple other cell types express immune mediators. Nonetheless, several of these factors may w ork in concert with others and it is difficult to delineate individual versus combined effects. Thus, the varied biological effects of these factors are not mutually exclusive and thus the net effect of the response in the microenvironment may be unpredictable. Table 9.2 provides an overview of the major... 

Hadden RDM, Kai ch H, Hai tung HP, Zielasek J, Weissbrich B, Schubert J, Weishaupt A, Combladi DR, Swan AV, Hughes RAC, Toyka KV (2001) Preceding infecdons, immune factors, and outcome in Guillain-BaiTe syndrome. Neurology 56 758—765. 

Chapman, R.W. Role of immune factors in the pathogenesis of primary sclerosing cholangitis. Semin. Liver Dis. 1991 11 1-4... 

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