mdeast

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I've always been a little iffy on understanding these completely.

One example I can't get around is Hashimoto's Thyroiditis. It's classified as a Delayed Type IV hypersensitivity reaction, yet it involves both T helper and antibody mediated destruction of tissues (i.e. there are also antibodies that are targeted against thyroid self-antigens (i.e. thyroid peroxidase present in the disease...yet the definition of Type IV reactions is that they are not anti-body mediated). To me, this seems more of a mixed Type IV/Type II reaction- but it's never classified as that anywhere.

Am I missing something here about classification? Would rather learn these conceptually than just memorize which fall under each category.
 

MrBigglesworth

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The actual destruction is by T-cells.

The 'anti-bodies' are more like markers/traces of the disease. Ie, the antibodies in hashimoto's are a result of sequestered proteins being released and the B-cells making antibodies against it. The damage is t-cell mediated.

Does that make sense... ?
 

Kaputt

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Yeah, what MrBigglesworth said. A lot of Type IV hypersensitivity reactions will also end up generating antibodies, but it's the T cells that do the killing. Hashimoto's has measurable antibodies, as does Type I diabetes and Rheumatoid arthritis.

It's analogous to TB infection too, which can be considered Type IV hypersensitivity. You generate antibodies against TB, but they're not the main way the body fights TB.

It's likely that the antibody generation is secondary to tissue destruction.
 

DOMan79

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I've always been a little iffy on understanding these completely.

One example I can't get around is Hashimoto's Thyroiditis. It's classified as a Delayed Type IV hypersensitivity reaction, yet it involves both T helper and antibody mediated destruction of tissues (i.e. there are also antibodies that are targeted against thyroid self-antigens (i.e. thyroid peroxidase present in the disease...yet the definition of Type IV reactions is that they are not anti-body mediated). To me, this seems more of a mixed Type IV/Type II reaction- but it's never classified as that anywhere.

Am I missing something here about classification? Would rather learn these conceptually than just memorize which fall under each category.

best way i use to differentiate between type 2 and 3 is that type 2 is antibodies against self...type 3 is antibodies against non-self

for type IV..even if there are ab's...it's the T-cell that is doing the destroying
 
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mdeast

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best way i use to differentiate between type 2 and 3 is that type 2 is antibodies against self...type 3 is antibodies against non-self

for type IV..even if there are ab's...it's the T-cell that is doing the destroying

Wait. I don't think that Type 2/3 difference is correct. SLE is antibodies against self (i.e. dsDNA, etc.)...but it's a Type 3 reaction. Type 2 just means antibody mediated vs. Type 3 which is complement mediated damage usually with antibodies.

And thanks to the other people for the responses. That definitely makes more sense....I guess I wasn't understanding the Hashimoto mechanism well enough.
 

Morsetlis

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That classification of Type II and Type III would be incorrect when you think about Transfusion reactions (Ab against non-self, Type II) and obviously SLE (Ab against self dsDNA, Type III).

In Hashimoto's, the mediation of damage is mostly through T-Cell's, and the generation of antibodies does not primarily destroy the thyroid tissue through complements / phagocytosis, as it would be in Type II reactions.
 

DOMan79

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Wait. I don't think that Type 2/3 difference is correct. SLE is antibodies against self (i.e. dsDNA, etc.)...but it's a Type 3 reaction. Type 2 just means antibody mediated vs. Type 3 which is complement mediated damage usually with antibodies.

And thanks to the other people for the responses. That definitely makes more sense....I guess I wasn't understanding the Hashimoto mechanism well enough.

ah..you're right..i was quoting from DIT...that's the best way to quickly differentiate them with some exceptions...thanks for reminding me of the exceptions
 

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I guess I have a similar question. FA talks about Guillain-Barre being due to moleculary mimicry, e.g. Campylobacter, in the neuro section. But in the immuno chapter it's listed as a Type IV HS reaction. I always assumed that "molecular mimicry" implied Ab-mediated recognition and destruction (as in rheumatic fever). So in this case, are the T-cells the ones being sensitized to Camp antigens, and then mediating the destruction of Schwann cells?

Also, as a follow-up to the OP's question, when you see autoantibodies in these Type IV reactions (hashimoto, Type I DM, etc.) I always assumed they were being created SECONDARILY to the cellular destruction by T cells. Is this right?

Thanks guys
 

Morsetlis

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I guess I have a similar question. FA talks about Guillain-Barre being due to moleculary mimicry, e.g. Campylobacter, in the neuro section. But in the immuno chapter it's listed as a Type IV HS reaction. I always assumed that "molecular mimicry" implied Ab-mediated recognition and destruction (as in rheumatic fever). So in this case, are the T-cells the ones being sensitized to Camp antigens, and then mediating the destruction of Schwann cells?

Also, as a follow-up to the OP's question, when you see autoantibodies in these Type IV reactions (hashimoto, Type I DM, etc.) I always assumed they were being created SECONDARILY to the cellular destruction by T cells. Is this right?

Thanks guys

Well, Type II HSR involve Ab, and then pathology because of complements, or phagocytosis.

Since the Schwann cells are being destroyed by T-cell mediated processes, even though antibodies started it, it is T-cells that finish the job, so thus it is Type IV.

In Rheumatic Fever, the Ab recruits mostly granulocytes. Thus it is Type II.
 
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