Risks of passive immunotherapy

[MudPhud20XX]

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So Kaplan immuno lists several risks of passive immunotherapy as below:

1. Introduction of antibodies from other species can generate IgE antibodies which may cause systemic anaphylaxis.
--> Why particularily IgE? I get that IgE is related to anaphylaxis with mast cells in hypersensitivity type I rxn and in order to get IgE, you would need TH2 cell's to stimulate B cells.

So is this saying that introduction of antibodies may stimulate TH2 and cause anaphylaxis just like there are million things out there that can lead to anaphylaxis to different people?

So this is probably beyond step 1, but we still don't know why certain people get anaphylaxis, right? Is this mainly related to genetics?

2. Introduction of antibodies from other species can generate IgG or IgM anti-isotype antibodies, which form complement-activating immune complexes, which can lead to type III hypersensitivity reaction
--> So this is through MHC Class II pathway where the foreign antibotides will be processed by APC (antigen presenting cells) which stimulates TH0 to become TH2, which stimulates B cells to produce IgG or IgM anti-isotype antibodies, did I get this right?

3. Introduction of antibodies from humans can elicit responses against minor immunoglobulin polymorphisms or allotypes.
--> How is this much different from #2?

Lastly, introduction of antibodies will not elicit cytotoxic T cells response which has to do with MHC class 1 since antibodies won't be residing inside cells where it can be processed by TAP and do all that MHC class 1 thing, right?

Sorry for bombarding with so many questions, but immuno is really a headache. It's never intuitive.

 

[ChessMaster3000]

So Kaplan immuno lists several risks of passive immunotherapy as below:

1. Introduction of antibodies from other species can generate IgE antibodies which may cause systemic anaphylaxis.
--> Why particularily IgE? I get that IgE is related to anaphylaxis with mast cells in hypersensitivity type I rxn and in order to get IgE, you would need TH2 cell's to stimulate B cells.


So is this saying that introduction of antibodies may stimulate TH2 and cause anaphylaxis just like there are million things out there that can lead to anaphylaxis to different people?
I believe so. When you are injecting foreign antibodies you are very clearly introducing foreign material into the body, so chances are >>>> that an immune response will be generated, compared to "regular" antigens.
So this is probably beyond step 1, but we still don't know why certain people get anaphylaxis, right? Is this mainly related to genetics?
If it were to ever be on step 1, the answer would probably be "multifactorial"--most likely genetics/epigenetic. But if you have ever heard of the "hygiene hypothesis" then environmental is an option.

2. Introduction of antibodies from other species can generate IgG or IgM anti-isotype antibodies, which form complement-activating immune complexes, which can lead to type III hypersensitivity reaction
--> So this is through MHC Class II pathway where the foreign antibotides will be processed by APC (antigen presenting cells) which stimulates TH0 to become TH2, which stimulates B cells to produce IgG or IgM anti-isotype antibodies, did I get this right?
yep
3. Introduction of antibodies from humans can elicit responses against minor immunoglobulin polymorphisms or allotypes.
--> How is this much different from #2?
it's not different, its simply not as important. this is probably because they are less frequently found on the surface of cells compared to MHC I/II, or perhaps for whatever reason they don't elicit as robust an immune response. that's just a guess.

Lastly, introduction of antibodies will not elicit cytotoxic T cells response which has to do with MHC class 1 since antibodies won't be residing inside cells where it can be processed by TAP and do all that MHC class 1 thing, right?
right on
Sorry for bombarding with so many questions, but immuno is really a headache. It's never intuitive.

 

[Transposony]

So Kaplan immuno lists several risks of passive immunotherapy as below:

1. Introduction of antibodies from other species can generate IgE antibodies which may cause systemic anaphylaxis.
--> Why particularily IgE? I get that IgE is related to anaphylaxis with mast cells in hypersensitivity type I rxn and in order to get IgE, you would need TH2 cell's to stimulate B cells.

So is this saying that introduction of antibodies may stimulate TH2 and cause anaphylaxis just like there are million things out there that can lead to anaphylaxis to different people?

Any form of foreign protein (antibodies are proteins) will have the same response as an allergen to induce Type 1 hypersensitivity reaction on subsequent exposure.
It is similar to why people with IgA deficiency develops anaphylaxis on transfusion of blood containing IgA.

By the way, Immuno is fun once you develop a basic understanding of the subject and can get a really good score just like Maths.

 

[MudPhud20XX]

Yup, Kaplan does talk about IgA deficiency and its correlation to increased atopy (atopic rxn form hypersensitivity type 1).

But now I don't understand how lacking IgA is assocaited with increased IgE? Again this has to do with the fact that IgA is considered as a foreign object that turns on TH2, which leads to class switching to IgE that upsets mast cell?

So I am assuming you may get IgG as a result of class switching, but this won't trigger hypersensitivity type 1 since IgG is not associated with mast cells, right?

Thanks for the encouragement. I hope so. I still feel lost completely lost : (

Now I'm trying to understand all these auto-antibodies/tests and their sensitivity/specificity. It's a mess LOL!

 

[sanj238]

Yup, Kaplan does talk about IgA deficiency and its correlation to increased atopy (atopic rxn form hypersensitivity type 1).

But now I don't understand how lacking IgA is assocaited with increased IgE? Again this has to do with the fact that IgA is considered as a foreign object that turns on TH2, which leads to class switching to IgE that upsets mast cell?

So I am assuming you may get IgG as a result of class switching, but this won't trigger hypersensitivity type 1 since IgG is not associated with mast cells, right?

Thanks for the encouragement. I hope so. I still feel lost completely lost : (

Now I'm trying to understand all these auto-antibodies/tests and their sensitivity/specificity. It's a mess LOL!

Lets say u get poison ivy. What type of immune response would you expect....looking this up online will ruin the fun. so just guess away

 

[sanj238]

Yup, Kaplan does talk about IgA deficiency and its correlation to increased atopy (atopic rxn form hypersensitivity type 1).

But now I don't understand how lacking IgA is assocaited with increased IgE? Again this has to do with the fact that IgA is considered as a foreign object that turns on TH2, which leads to class switching to IgE that upsets mast cell?

So I am assuming you may get IgG as a result of class switching, but this won't trigger hypersensitivity type 1 since IgG is not associated with mast cells, right?

Thanks for the encouragement. I hope so. I still feel lost completely lost : (

Now I'm trying to understand all these auto-antibodies/tests and their sensitivity/specificity. It's a mess LOL!

No, I doubt its IgG. its most likely an IgE. if its atopy of the general sort then it should be IgE. Kaplan does a good job of explaining this. basically you need multiple reactions with the foreign antigen. The first time it binds to the mast cells, this is like a primer, the second time is a cross reaction that leads to the IgE release.

IgG is different, as you know, igG is usually a secondary response to infections or it is used for opsonization....definitely not for atopy