Type 3 hypersensitivity is confusing?

In summary: This then activates the complement cascade leading to the attraction of neutrophils and the release of lysosomal enzymes which damage the vessel wall.In summary, Type 3 hypersensitivity is characterized by an excess of antigen and a deficiency of antibody, resulting in the formation of small immune complexes that are not properly phagocytosed and can deposit in tissues, causing damage. The Arthus reaction and serum sickness are examples of this type of reaction, with the former being an experimental way to demonstrate it and the latter occurring when large amounts of preformed antibodies are given to a patient. In both cases, the immune complexes can cause local inflammation and tissue damage, leading to symptoms such as rashes and vasculitis. In the Arthus reaction, the immune
  • #1
sameeralord
662
3
Hello guys,

I'm reading and trying to understand this and going no where. From what I gather in Type 3 hypersensitivity, there is too much antigen and small immune complexes are made, which are not phagocytosed and deposit in tissue causing tissue damage. Then what has Arthus reaction and serum sickness got to do with this concept (small immune complexes). I don't understand Arthus reaction and serum sickness, despite reading it for sometime now.
 
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  • #2
sameeralord said:
Hello guys,

I'm reading and trying to understand this and going no where. From what I gather in Type 3 hypersensitivity, there is too much antigen and small immune complexes are made, which are not phagocytosed and deposit in tissue causing tissue damage. Then what has Arthus reaction and serum sickness got to do with this concept (small immune complexes). I don't understand Arthus reaction and serum sickness, despite reading it for sometime now.

These are simply examples of the type III reaction. What exactly are you unable to understand?
 
  • #3
T3H is when you have excess antigen (Ag) and too little antibody (Ab) being formed. This results in small immune complexes being formed which aren't phagocytized and potential deposition along vasculature or basement membranes.

Arthus reaction is just an experimental way to demonstrate T3H. Its when you inject Ag into an individual with the specific Ab. At the injection site, there is excessive Ag which makes small immune complexes which deposit on the vasculature in the area leading to a red bump. Its not really relevant clinically.

In serum sickness, you have a patient being given large amounts of preformed antibodies hoping to give them passive immunity against the insulting substance. Such as antivenom or antitoxin. The host can make an immune response to these Ab's, but since you are giving such large amounts (as was often the case in WWII for soldiers being given anti-tetanus toxin) there is excess antigen. This results in the deposition along the vasculature and BM of glomeruli (glomerulinephritis).

The immune complexes cause local inflammation, histamine release, etc. That's why you get the red bump in Arthus, or the characteristic rashes of systemic lupus erythematosus.

Hope that helps
 
  • #4
bobze said:
T3H is when you have excess antigen (Ag) and too little antibody (Ab) being formed. This results in small immune complexes being formed which aren't phagocytized and potential deposition along vasculature or basement membranes.

Arthus reaction is just an experimental way to demonstrate T3H. Its when you inject Ag into an individual with the specific Ab. At the injection site, there is excessive Ag which makes small immune complexes which deposit on the vasculature in the area leading to a red bump. Its not really relevant clinically.

In serum sickness, you have a patient being given large amounts of preformed antibodies hoping to give them passive immunity against the insulting substance. Such as antivenom or antitoxin. The host can make an immune response to these Ab's, but since you are giving such large amounts (as was often the case in WWII for soldiers being given anti-tetanus toxin) there is excess antigen. This results in the deposition along the vasculature and BM of glomeruli (glomerulinephritis).

The immune complexes cause local inflammation, histamine release, etc. That's why you get the red bump in Arthus, or the characteristic rashes of systemic lupus erythematosus.

Hope that helps

Thanks Bobze :smile: I understand serum sickness now. However arthus reaction, why are we giving excess antigen for no reason. Is it as you said just to demonstrate this effect. Also in Arthus reaction immune complexes seem to precipate unlike serum sickness where they are soluble. Why is that?
 
  • #5
Correct, Arthus is just an experimental way to demonstrate a T3H. Like I said, its not useful clinically. Historically it was used to demonstrate the type 3 reaction. Around the turn of the 19th century I believe.

The immune complexes are still soluble. They are deposited in the small vasculature near the site of the injection, leading to vasculitis.

In serum sickness, you're giving the antivenom/toxin via IV administration. This circumvents the small vasculature that would lead to an Arthus reaction. However, your blood still passes through small vasculature which is why the effects are disseminated and the effects extend to areas like the glomeruli.
 
  • #6
As an afterthought, The actual way you get vasculitis or vascular damage is because after deposition the Ag-Ab complex is capable of fixing complement.
 

Related to Type 3 hypersensitivity is confusing?

1. What is Type 3 hypersensitivity?

Type 3 hypersensitivity is a type of immune reaction that occurs when the immune system mistakenly attacks its own tissues due to the formation and deposition of immune complexes. These immune complexes are formed when antibodies bind to antigens, and can cause inflammation and tissue damage.

2. How is Type 3 hypersensitivity different from other types of hypersensitivity?

Type 3 hypersensitivity is different from other types of hypersensitivity (such as Type 1 and Type 2) because it involves the formation and deposition of immune complexes, rather than direct attack by antibodies or immune cells. This can lead to a delayed reaction and a different pattern of tissue damage.

3. What are the symptoms of Type 3 hypersensitivity?

Symptoms of Type 3 hypersensitivity can vary depending on the affected tissues, but can include inflammation, swelling, rash, joint pain, and organ damage. These symptoms can range from mild to severe and can be acute or chronic.

4. What causes Type 3 hypersensitivity?

Type 3 hypersensitivity can be caused by a variety of factors, including infections, autoimmune disorders, and exposure to certain drugs or chemicals. It can also be triggered by genetic predisposition or environmental factors.

5. How is Type 3 hypersensitivity treated?

Treatment for Type 3 hypersensitivity focuses on managing the underlying cause and reducing inflammation and tissue damage. This may include medications to suppress the immune response, as well as therapies to address any underlying conditions. In severe cases, plasmapheresis (a procedure to remove immune complexes from the blood) may be necessary.

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