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Chapter 18 Lecture 4 (Type III (Immune Complex–Mediated) Hypersensitivity…
Chapter 18 Lecture 4
Type III (Immune Complex–Mediated) Hypersensitivity Systemic lupus erythematosus (SLE)
Patients make autoantibodies against numerous self-antigens found in normal organs and tissues
Immune system ends up attacking its own organs
Many different lesions and therefore many different clinical manifestations
One constant feature of SLE, is the development of the self-reactive antibodies against the nucleic acids
Many other autoantibodies can also occur
Against red blood cells, platelets, lymphocytes, and muscle cells
Bleeding disorders, hemolytic anemia, muscle inflammation, damage to heart.
Easy to misdiagnose.
Name Systemic Lupus erythematosus comes from two features of the disease
Systemic affects different organs throughout the body
Lupus is Latin for wolf
Erythematosus- redness of skin
Rash is caused by the deposits of nucleic acid antibody complexes in the skin (sun makes it worse)
Trigger unknown although some drugs can induce a lupus like disease
Treatment with immunosuppressive drugs reduces autoantibody formation
Treatment with corticosteroids reduces inflammation
Type IV (Delayed or Cell-Mediated) Hypersensitivity
When we encounter antigens and we are sensitized people we could have a delayed hypersensitivity which means….
Inflammation 12–24 hours after contact
Results from the interactions with the antigen, antigen-presenting cells, and T cells
Delay reflects the time it takes for macrophages and T cells to migrate to and divide at the site of the antigen
Two common examples of this is the
Tuberculin response and allergic contact dermatitis then we discuss
Interactions between body and tissue grafted
Type IV (Delayed or Cell-Mediated) Hypersensitivity Allergic contact dermatitis
The oil of poison ivy(urushiol) and related plants is a small molecule that becomes antigenic when it binds to almost any protein in contacts. (this includes proteins in our skin)
Our body looks these chemically modified skin proteins as foreign, so our body begins its Cell-mediated immune response resulting in an intensely irritating skin rash
In severe cases, acellular, fluid-filled blisters develop
Can be caused by formaldehyde, cosmetics, dyes, drugs, metal ions and chemicals used to produce latex
Treated with corticosteroids, and we can use epi
Good to wash area with soap and water
Type IV (Delayed or Cell-Mediated) Hypersensitivity Tuberculin response
Skin exposed to tuberculosis or tuberculosis vaccine reacts to an injection of tuberculin beneath the skin
Mantoux test used to diagnose contact with antigens of M. tuberculosis
When tuberculin is injected into the skin of a healthy individual who has never been infected or vaccinated you should see
No response
The response of red, hard swelling(10mm or greater) develops in individuals previously infected or immunized
It is not possible to determine if the test is positive that it is due to current infection, previous infection or immunization.
Response facilitated by memory T cells that cause a slowly developing inflammation