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Natural Born Killers (Cells)

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Scott Feitell, DO
Drexel College of Medicine
Philadelphia, PA, USA

It's early, I hit the snooze, and didn't have time for coffee for this morning's Sunrise Symposium 10: Exploring Interactions Between Cellular and Humoral Immunity in Cardiac Allograft Rejection, but luckily this highly complex topic got the brain juices flowing faster then Woody Harrelson can pull a gun on Route 666.

Dr. Esmé Dijke opened the session with a great review of all the major players in innate immunity, and the role innate immunity plays in ACR and AMR. Macrophages and Neutrophils and NK cells, oh my! It became readily apparent from Dr. Dijke's talk that our well-balanced immune system provides both good and bad feature that aid and hinder transplant medicine. Unfortunately for every good these cells provide, like aiding wound healing and suppressing allogenic immune responses, these cells can also infiltrate graft tissue and co-stimulate allo-reactive T cells.

Next up, Dr. Annalisa Angelini reviewed the overlap between CMR and AMR, deemed the gray zone (though more like the Twilight Zone for us clinicians trying to help these patients), and reviewed histologic features that may help or hinder deciding which treatment pathway to follow. Staining for CD markers may be one tool that can help the pathologist and clinical team help decide what is going on. Particularly noteworthy, Dr. Angelini pointed out that most "mixed rejection" samples demonstrate a proclivity towards CD4 cells, while acute cellular rejection mostly demonstrates CD8 cells. She also interestingly pointed out varying degrees of inflammation in the endothelial layers of vessels, a capillary predominant vasculitis and a more diffuse vasculitis affecting all vessels, and proposed that perhaps differentiating which components of the vasculature are inflamed may help differentiate AMR, ACR and mixed rejection into more readily identifiable classes of rejection.

Dr. A. G. Kfoury then finished the session by outlining the ramifications of this "mixed rejection" picture and what it may really mean. He proposed several different pathways including the possibility that this mixed rejection is a unique pathophysiologic pathway of rejection, or that perhaps it is some combination of AMR and ACR or perhaps that each of these pathways may devolve into a mixed picture. In terms of treatment options, a confluence of factors including most importantly graft dysfunction, biopsy and antibody screening, donor antibody status and time from transplant should all play a role in deciding the aggressiveness of treatment.

Now I'm no Wayne Gale (another shameless Natural Born Killers movie reference, if you're not familiar with the movie), but that's some pretty good coverage of a 7:00 AM session without caffeine.

Disclosure Statement: the author has no conflicts of interest to report.

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