Great. Well, thank you so much. And I want to thank the organizers for inviting me to speak today on chronic AMR detection and treatment. Here are my disclosures. So fortunately, the we do have criteria for chronic antibody-mediated rejection that were published by the BAMF group and include both histologic features that are required, specifically, at least mild mononuclear portal and or perivanular inflammation with interface and or perivanular necroinflammatory activity. So this is an atypical type of inflammation. And then at least moderate periportal, portal sinusoidal, or and or perivanular fibrosis, indicating that you have to have at least some scar somewhere. Then you have to have DSA in serum. They did not specify an MFI appropriately. And then at least some C4D staining focally with a greater than 10% of portal tracts being positive and then the reasonable exclusion of other insults. And you can have a possible diagnosis of chronic AMR if the C4D staining is negative. And has been highlighted previously, one of the hallmark features of chronic antibody-mediated rejection is finding interface activity present, which are these fingers of can everybody... Does the pointer show up? It doesn't seem to. The fingers of inflammatory cells going into the lobule. And at higher power, you can see it here. And we're really not focusing on lymphocytes because that's more indicative of standard TCMR or T-cell-mediated rejection. When we're focusing on the type of fibrosis that we need in order to make the definition, this is not the standard type of fibrosis that you would find in a patient with viral hepatitis. And so here is a classic case looking at the central vein. And so many investigators have found the predominance of fibrosis being around the central vein or the pericellular fibrosis, which in the NASH world we would sort of call the chicken wire fibrosis, except without the fat. Turning to C4D staining, I think this was an extreme difficulty in liver for some time, but fortunately the BAMF group, three BAMF meetings ago, got together and really did a great job helping to improve the situation markedly. 31 centers collaborated and most donated tissue that was, in their opinion, C4D positive or should be C4D positive. And then they made a micro array of formalin-fixed paraffin-embedded tissue. And then everyone in the group actually stained it at their center. And then different pathologists around the world scored them. And what they found, which has now been published by Desley Neal in Human Pathology in 2018, was a specific protocol that can stain simultaneously the livers, hearts, and kidneys with the same staining protocol, which has been very useful in many centers, especially large transplant programs that offer more than one organ. This was very specific to have a high pH antigen retrieval, and in most programs the kidney dominant programs, they have a low pH antigen retrieval, which definitely will decrease your C4D sensitivity in liver. The antibody that you use matters as well as the type of detection matters. So if this is not something that you've implemented at your center, I strongly recommend it. When looking specifically for C4D positivity in the liver, under the best of circumstances in the chronic situation is often difficult to find, and the most sensitive areas that stain most frequently are going to be the periportal capillaries, which are shown here. We're not used to looking at capillaries in the liver, and so I think it's oftentimes overlooked, but they do exist, and they are a target for antibodies and destruction. So C4D there will be positive earlier. Some other findings that have been put out in the literature that are histopathologic and associated with chronic AMR are portal venopathy. Desi Neal was nice enough to let me use this photo. It's basically a fibrosis of the portal venules, and our group and others did show an association between that and chronic AMR. There was also a retrospective review of 67 liver biopsies in 45 pediatric patients by the UCLA group and found that all four patients diagnosed with chronic AMR in that group did also have portal venopathy, so maybe something that's specific but not as sensitive. And then Dr. Stevenson, in collaboration with Dr. Dimitris, did find that V lesions in the liver, something that pathologists have been evaluating in the kidney for some time, are also associated with TCMR as well as chronic antibody-mediated rejection. Certainly, liver doctors don't ever on purpose biopsy large arteries, and when we do, we usually have tachycardia. But certainly, if you ever do see it, you hope the patient is okay, and then you have to worry because it is a fibroinflammatory process that is usually indicative of antibodies being present as well. In collaboration with Jake, we developed the CAMR score, which was looking specifically at histopathologic features that were indicative of not just antibodies, but also poor outcome with antibodies. And so this was back in the era when hepatitis C existed, although the reviewers did ask me to put this in. Fortunately, there was no statistically significant difference whether it was part of the group or not. And the reason for that is because many of the features that are found in patients with chronic antibody-mediated rejection don't have any bearing on what you see in a biopsy with active viral hepatitis. So we found lobular inflammation, interface hepatitis, portal collagenization, which is this densification of the portal tract that should normally be much more fine in a reticulin, and then portal venopathy and subsinusoidal fibrosis. Of note, all of the patients used in this cohort to develop the score did have a protocol liver biopsy. And so their aminotransferases as well as their alkaline phosphatases were either normal or near normal and had been stable. So these were not patients that had indication biopsies. They were all either year one or year two after transplant biopsies. And you can see here in the red box that not the CAMR scores in all of these patients had class 2 DSA in their serum with an MFI greater than 10,000. There was a marked difference between those graphs at year one or two that went on to lose their graft many years later versus those who went on to do well long term despite continuing to have serum DSA present. And not only was that predictive on the initial biopsy, but it seemed quite stable to the second protocol biopsy that they received indicating that people tend to parcel into one or the other groups. I've been asked in the past did anybody switch groups meaning that they were had a good biopsy with a low score on the first biopsy and a potentially high score on a follow-up biopsy or vice versa and the answer was is yes, but usually some major thing occurred like a viral infection. This score did parcel patients out into their outcomes and do remember that all the patients in this group had DSA with MFI of greater than 10,000 that remained present long term and yet a significant number of them had excellent long-term outcomes, although those with the highest scores had a 50 percent 10-year risk for graft loss. In a separate group of patients with similar characteristics of DSA and serum being present, although in this group the MFIs could be considerably lower of 1,000 all the way up to over 10,000, that the patients with the lowest CAMR scores regardless of the MFI had excellent long-term outcomes, but in the cohort with high CAMR scores there was an incremental improvement if their MFI was lower, although that certainly would not necessarily be on a case-by-case basis. But generally when we look throughout the literature at people who have looked at DSA in serum by single antigen beads and evaluated histopathology, there's always been an association with both inflammation and fibrosis. The vast majority of these studies were performed before the BAMF criteria were put out. And so when we look at how fibrosis was assessed, most of the time it was just measured by either Metavir or Eshach and therefore shown to be increased in those patients with DSA present as a cohort. And some of the histologic characteristics were finding a late TCMR present on protocol biopsies as well as lobular or interface hepatitis, V lesions, portal venopathy, and interface hepatitis tends to come up more frequently. But I do want to highlight that this of course does not happen in all patients. And so there are many patients with a DSA in serum that do well long term, including some children who have been weaned off immunosuppression successfully without complications even on biopsy. So the question becomes is there any mechanism that we can propose for antibodies being causing any type of injury or is this simply an association and something else is causing the injuries like PBC patients with an AMA that's positive? And so we're going to go through a little bit of data in order to hypothesize about why my opinion is that we may be able to start to think about this as potentially causing injury. But it could either be causing injury by direct antibody binding or simply through ADCC or antibody-dependent cellular cytotoxicity, i.e. the antibodies recruit in the cells and the cells do all of the injuring or is this both? And so certainly we don't have data enough to make a definitive conclusion, but hopefully this will stimulate discussion. So antibodies always need a target to bind to and we know that the vast majority of antibodies in livers that persist after transplant or develop de novo are against class 2. 80% are against DQ. And so you can see in this panel here, which is kind of busy, that we measured class 2 antigen expression in kidney that is constitutively expressed. However, in liver and or quiescent conditions, there is minimal class 2 expression. However, certain factors like viral infection do upregulate class 2 expression quite a lot. And so you can see here that in areas with high level of class 2, which would be number 3, that there is more portal inflammation when there's higher levels of class 2 in the inlet venules as well as the portal capillaries, possibly indicating that antibodies may be able to recruit cells to that area. And similarly, if you look at the central veins, when you have high level class 2 expression there, there is more cellularity or central perivenulitis in that specific location. We also looked at class 2 expression and whether or not it correlated with a long-term outcome in these DSA positive patients. And you can see that those who lost their allograft did have higher levels of class 2 expression in the portal veins and portal capillaries than those patients who did not lose their allografts. Secondly, we looked at a different group, one that developed non-HLA DSAs after transplant, specifically de novo AT1R antibodies, and showed that through SMA staining, and Dr. Demetrius did all of this evaluation and staining, and the pink here is smooth muscle actin, which indicates activated stellate cells, and then in the panel on your right, you can see C4D staining, and the asterisk does highlight what I'm trying to focus on, which is an area absent of cells, and in the area absent of cells, C4D is staining, indicating antibody binding, and in that same area, indicating antibody binding, and in that same location, you'll see activated stellate cells, and so we hypothesize, but don't prove, that antibodies may be able to stimulate stellate cells into producing fibrosis. This has now been referred to several times, but Dr. Fang's lovely weaning study of 157 stable pediatric liver transplant patients did undergo eligibility biopsies, and all of them had to have normal or near-normal LFTs with ALT less than 50, and as you've heard, they clustered into three different groups. I think it was surprising that so many patients that so many people thought were doing perfectly well, actually about half of them had abnormalities found on routine protocol biopsy, but of note, the Cluster 1 group that had interfaced hepatitis was associated with overexpression of TCMR and gene expression, which you just heard about, and so those patients did actually have more often Class 2 antibodies present, and that was one of the biggest risk factors for being in Cluster 1, as well as the ALT level, even within the normal range, once again highlighting the potential for ADCC or antibody-dependent cellular toxicity as a potential mechanism for graft injury in these patients. And they did find that C4D staining did follow both HLA Class 2 antigen expression as well as blood flow, once again indicating that you need antigen expression in order to have antibody binding. And so this importance of ADCC may be further highlighted in Abhi Shikhed's beautiful weaning study as well, and 275 adult patients this time who were consented pre-transplant. However, post-transplant were only eligible if they were on stable monotherapy with trachromis and had 95 of those patients were actually randomized to withdrawal. This was once again in the hep C era, so they had to have less than Stage 2 fibrosis. And 69 patients did have serum available for de novo DSA analysis, and acute rejection and biopsy-proven findings disqualifying patients from withdrawal were more likely to be associated with having developed de novo DSA. And de novo DSA development was an additional risk factor for rejection during immunosuppression minimization, leading them to conclude two things. One was that de novo DSA should be considered for immunosuppression withdrawal eligibility. And secondly, I think maybe more importantly is that patients, two-thirds of patients were actually able to reduce immunosuppression to greater than 50%. And so I think we are all potentially looking at DSA as a positive biomarker of injury, but actually it may be more useful as a negative marker predicting who may be eligible to have lower doses of immunosuppression than our standard protocols. And so this data does highlight the two-hit hypothesis, whereby under quiescent conditions patients have minimal to negligible Class 2 antigen expression throughout the liver, which one injury can then up-regulate the Class 2 expression, most commonly non-compliance with immunosuppression, T-cell mediated rejection, viral infections, autoimmune hepatitis. Those types of injuries will up-regulate it that allow this antibody binding and then the final recruitment of cells into the allograft. So when we're thinking about defining liver transplant success, you know, I was thinking this is a pediatric symposium. And so I think it depends a lot on who you ask, right? If you ask the transplant professional, I think a lot of surgeons especially, but hepatologists as well, are graded very much on their one-year outcomes. And so everybody wants, you know, 95% one-year survival, the liver injury tests looking good, and comorbid conditions controlled. And if that's how you define success, then we're doing extremely well in most patients. But actually of late, I've started to ask patients what they actually would like. And most of them actually want to live to over 80 years of age, never have a single medical problem, and maybe they might be interested in taking one pill, especially if it was magic to make everything go away. And so if we're using their standard, then we have a very long way to go. And so, you know, I think in general chronic antibody-mediated rejection is best prevented, and so I think the most critical part of that is actually adherence, and I think we as providers overestimate how much people are willing to do for us as far as come to clinic, get labs, do tests, and take pills. And so I think we need to focus more on what the HIV community has done, which is co-formulate things into one pill and simplify regimens down to one pill a day. And what has been previously determined is the risk for de novo DSA, which is certainly going to be a risk for chronic antibody-mediated rejection, is using cyclosporine as opposed to tocrolimus-based immunosuppression. And so that certainly, I have no conflicts with either company that makes single tablets for tocrolimus, but that may be an option to enhance compliance. And then low CNI levels, which was a measure of noncompliance, was certainly the biggest predictors of those developing de novo DSA. We certainly can't change our age or our MELD score at transplant, although I know we're all trying to. And then we need to focus, as far as therapeutics are concerned, in order to optimize outcomes to change the target antigen expression, specifically class 2, and I think that will be the future as far as therapeutics for chronic AMR is concerned. So in conclusion, chronic AMR does exist. It's unclear if the injury is mediated by antibody cells or both, but I hypothesize that it is being mediated by both, but we need more data in order to know that. DSA is strongly associated with liver allograft fibrosis progression, although not in all patients. And I can't overemphasize enough the utility of a one-year protocol biopsy in those patients who have a significant life expectancy. Making the diagnosis, I think, is important. We're never going to actually improve things if we don't look for it and try to intervene. And then treatment really is best done through prevention, through simplifying our patients' immunosuppression protocols and management, and then enhancing compliance with the Tercolimus-based immunosuppression scheme. At least that's our knowledge for now. And then antibodies do need a target antigen to bind to, and so there's evolving data on that, and I think that's hopefully where we're going to learn the most on how to mitigate this. Thank you very much. Thanks, Jackie. 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chronic antibody-mediated rejection

liver transplant patients

histologic features

DSA in serum

C4D staining

CAMR score

immunosuppression regimens

Class 2 antigen expression