Previous section Next section
IMMUNOLOGIC DYSFUNCTION
Body_ID: HC036075
Autoimmunity is normally avoided by thymic education; a breakdown in the processes involved leads to autoimmune disease
Body_ID: HC036078
While the immune system's activities are mostly beneficial, there are several situations in which they can have deleterious effects. These are best considered as aberrations of the quality, quantity or direction of the response (Table 36.3).
Body_ID: P036067
Body_ID: T036003
Table 36-3. Disorders of immune regulation.
Body_ID: None
Disorders of immune regulation
Body_ID: T036003.50
Antigen source Level of responsePolyclonal responseMonoclonal response
Body_ID: T036003.100
 ExogenousEndogenous
Body_ID: T036003.150
Decreased responseimmunodeficiency primary and secondary 
Body_ID: T036003.200
Increased responsetuberculosis, leprosy, immune complex diseaselymphoproliferative disease
Body_ID: T036003.250
Inappropriate responseallergic disease - IgE 
Body_ID: T036003.300
Increased and inappropriate responseallergic disease - EAAautoimmune disease
Body_ID: T036003.350
Body_ID: T036003
Body_ID: None
One particular aspect of these immunodysregulatory disorders, that of autoimmunity (self-reactivity), is avoided by the processes of thymic education. This is achieved via positive and negative selection and tolerance, which includes the processes of clonal deletion, clonal abortion and energy. These terms refer to the processes whereby self-reactive clones are eliminated or rendered impotent. These mechanisms can be seen as a multilayered fail-safe strategy. Should these processes breakdown or be circumvented, the resulting state of self-reactivity and the resulting inflammatory damage constitute autoimmune disease. The form of disease is determined by the target antigen and the form of the immune response. At its simplest, reactions against ubiquitous antigens lead to what are termed nonorgan-specific autoimmune diseases, whereas reactions to unique components of individual tissues, organs or systems lead to organ-specific disease. The former are best exemplified by systemic lupus erythematosus (SLE), in which the apparent target antigens are components common to all nuclei. Damage is seen in several tissues, including the skin, joints, kidneys, and nervous system. The latter are exemplified by autoimmune thyroiditis, where the apparent target is thyroid peroxidase enzyme. The use of the word 'apparent' should be noted here, as on more detailed investigation it becomes clear that these particular antigen systems, while acting as markers or indicators of autoimmune disease, are not pathogenically responsible for the damage being inflicted. The methods used to detect such autoantibodies include indirect and direct immunofluorescence, particle agglutination, electroimmunodiffusion and enzyme immunoassay.
Body_ID: P036068
These diseases, and the others mentioned in Table 36.3, are the focus of the discipline of clinical immunology and immunopathology. More information can be found by reading the books cited in the Further Reading list below.
Body_ID: P036069
Previous section
Bar end Bar end
Next section
Copyright © 2007 Elsevier Inc. All rights reserved. Read our Terms and Conditions of Use and our Privacy Policy.
For problems or suggestions concerning this service, please contact: studentconsult.help@elsevier.com