hyperacute rejection

[HiddenTruth]

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Sorry for the other thread. I am not sure what happened.

Anyways, is it type 2 HS, or type 2 and 3?

 

[ucbdancn00]

Sorry for the other thread. I am not sure what happened.

Anyways, is it type 2 HS, or type 2 and 3?

it's a type 3 HS; localized arthus reaction....Ab comes in and reacts with Ag with the recipient and causes deposition (probably skin)

occurs within minutes

ucb

 

[HiddenTruth]

it's a type 3 HS; localized arthus reaction....Ab comes in and reacts with Ag with the recipient and causes deposition (probably skin)

occurs within minutes

ucb

Yea that makes sense, robbins didn't separate hyperacute from acute--kinda confusin'. But, I think it can also be type 2 also--depending on what the cause of the rejection--if ABO incompat--> type 2, but if preformed ab--->then complement mediated type 3

And, acute would be type 2 (ADCC), and type 4. What do you think?

 

[ucbdancn00]

Yea that makes sense, robbins didn't separate hyperacute from acute--kinda confusin'. But, I think it can also be type 2 also--depending on what the cause of the rejection--if ABO incompat--> type 2, but if preformed ab--->then complement mediated type 3

And, acute would be type 2 (ADCC), and type 4. What do you think?

hyperacute: preformed Ab from the DONOR....so it's binding to Ag in the RECIPIENT......deposition in skin;

acute: CTL cells develop in RECIPIENT...and attack the foreign MHC containing cells of the donated tissue. Occurs weeks after transplant. Reversible.

chronic: fibrinoid vasculitis--> Ab mediated; probably a type 2 HS. months to years later. Irreversible.

hope this helps.

ucb

 

[Mumpu]

Your buzzword is "white graft." Organ gets attached, gets perfused, and immediately turns pale white and up-an'-dies.

 

[UCSBMed1]

hyperacute: preformed Ab from the DONOR....so it's binding to Ag in the RECIPIENT......deposition in skin;

acute: CTL cells develop in RECIPIENT...and attack the foreign MHC containing cells of the donated tissue. Occurs weeks after transplant. Reversible.

chronic: fibrinoid vasculitis--> Ab mediated; probably a type 2 HS. months to years later. Irreversible.

hope this helps.

ucb

Hmmm...

Just reading first aid, and it states that a hyperacute rejection is caused by anti-DONOR antibodies that are preformed and found in the RECIPIENT. These therefore cause a hyperacute rejection.

Because these abs are recognizing cells and not non-cellular antigens, I would think this would be a type II, ADCC response. Of course pathology could also be due to a type III, immune complex formation, but I don't think it is stated in any text which type of hypersensitivity reaction a hyperacute rejection is--I don't think it can be classified as one particular type (but is closest to type II and III). The main thing is that an immune response is elicited by pre-formed abs in the recipient recognizing antigen in the donor.

If I had to decide, I think I would go with type II because of the time of onset. It would only take minutes for complement to be recruited, PMNs to swarm in (C5a action, remember?) and release lysosomal inflammatory products. But it might take a little longer for the manifestations of an immune complex disease to present (all the diseases listed under type III take at least 24-48 hours to develop).

Anyone have insight from another source?

 

[HiddenTruth]

Hmmm...

Just reading first aid, and it states that a hyperacute rejection is caused by anti-DONOR antibodies that are preformed and found in the RECIPIENT. These therefore cause a hyperacute rejection.

Because these abs are recognizing cells and not non-cellular antigens, I would think this would be a type II, ADCC response. Of course pathology could also be due to a type III, immune complex formation, but I don't think it is stated in any text which type of hypersensitivity reaction a hyperacute rejection is--I don't think it can be classified as one particular type (but is closest to type II and III). The main thing is that an immune response is elicited by pre-formed abs in the recipient recognizing antigen in the donor.

If I had to decide, I think I would go with type II because of the time of onset. It would only take minutes for complement to be recruited, PMNs to swarm in (C5a action, remember?) and release lysosomal inflammatory products. But it might take a little longer for the manifestations of an immune complex disease to present (all the diseases listed under type III take at least 24-48 hours to develop).

Anyone have insight from another source?

Yea for sure the preformed antibodies are in the recipient against donor (otherwise it would be lik GVHD). The preformed Ab are usually there if a person has had multiple transfusions in the past, multiple pregnancies, or a previous transplant. And, hyperacute can also occur as a result of ABO incompatibility, which is definately type 2 as we know. In Robbins, it says, that it forms an Arthus type of reaction (so therefore it would mak sense that was type 3 in the case of preformed Ab)--but the timing is off. Goljan, however says it's a type 2.

In terms of acute, I'm pretty sure that's both 2 and 4. There is both humeral and CMI involved. T cells that become activated after recognizing donor MHC, further enhance CD8 activity and release IFNy, etc to activ MP to do their thing (CMI), and they also activate B cells to induce a humeral response. And B cells are mediated in C' activation and ADCC mediated destruction.

Hope this clarified things. Thanks for your input.

 

[me454555]

Acute is considered Type 4 hypersentivity b/c of CMI

 

[ucbdancn00]

yah mah bad...

hyperacute--> preformed Ab in the RECIPIENT against the DONOR Ag; sorry for the mistake

ucb