Immune response to self-antigens

One of the first cases of possible molecular mimicry was that of rheumatic fever, in which the symptoms were caused by antigens that mimic cardiac myosin.56-59 A simple rabbit study demonstrated how the administration of the key antigen induced strong inflammatory and myocardial changes as a result of host immune response to self antigens.59... 

The question regarding autoimmunity and a link with vaccine administration has been a common topic of debate for some years. Autoimmunity may be described as an inappropriate response of the immune system to self antigens that can lead to organ or tissue damage.47 The cause, although unknown, is likely to be multifactorial and may include hormonal, immunological, genetic, and environmental factors.47,48 In the past few years, there have been several reports of potential... 

Autoimmune diseases. Disorders that are characterized by (i) the production of autoantibodies or immune effector cells that are autoreactive to self-peptides and (ii) pathological changes (e.g. tissue infiltration, damage, and/or dysfunction) that resulted from these immune responses against self-antigens ( - autoantigens). 

The patient population targeted for therapeutic vaccination can be immunocompromised (e.g., cancer patients and elderly patients), hence various immunostimulation techniques need to be investigated in an effort to bolster the immune system and to overcome immune tolerance to self-antigens. Various strategies to stimulate antigen presentation are under investigation, including the use of novel adjuvants. The stimulation of the immune response needs to be carefully tempered to avoid overactivation of cytotoxic T cells that could be more destructive than intended. 

In autoimmunity, as with hypersensitivity, the immune system is stimulated by specific responses that are pathogenic, and both tend to have a genetic component that predisposes some individuals more than others. However, as is the case with hypersensitivity, the adverse immune response of drug-induced autoimmunity is not restricted to the drug itself but also involves a response to self antigens. 

T-Lymphocytes (4,5) and other cellular components of the immune system also have equally wide implications in regulation of the normal immune system. The T-lymphocytes play a central role in the body s response to harmful antigens and tumor—host interaction (4). Responses involve antigens derived from vimses, bacteria, parasites, and tumors. T-ceUs also participate in the immune surveillance response, where self-antigens are recognized, but usually sequestered within the cell and, when exposed, become markers of cellular damage. 

The mechanism most commonly invoked to explain the association of infection with autoimmune disease is molecular mimicry that is, the concept that antigens (or more properly, epitopes) of the microorganism closely resemble self-antigens.50 The induction of an immune response to the microbial antigen thus results in cross-reactivity with selfantigens and the induction of autoimmunity. Although epitope specific cross-reactivity has been shown in some animal models,48,51 53 molecular mimicry is clearly demonstrated to be the causative mechanism in few, if any, human diseases.3 54,55... 

Regulatory T (T ) cells represent a distinct T-cell lineage that plays a key role in tolerance to self antigen and prevention of autoimmune diseases, as well as in inappropriate immune responses involved in allergic diseases [1-3]. Tr cells are characterized by a set of phenotypic and functional... 

After an antigen (a non-self molecular entity) has entered the body, it is recognized by the cells of the immune system. An important step in eliciting an efficient immune response to an... 

Inject the neonates daily on d 1-5 after birth with 0.05 mL 0.5 mg/ mL of crossreacting antigen into the neck scruff. (The neonatal immune systems are maturing at this time and because the cross-reacting antigen is present they will adopt these proteins as self and lose the ability to mount an immune response to them.)... 

H2. Han, S., Zheng, B., Dao Porto, J., and Kelsoe, G., In situ studies of the primary immune response to (4-hydroxy-3-nitrophenyl) acetyl IV-affinity-dependent, antigen driven B cell apoptosis in germinal centers as a mechanism for maintaining self-tolerance. J. Exp. Med. 182, 1635-1644 (1995). 

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