Graft-versus-host disease historical perspective

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]Shyam Patel [2]


The history of GvHD dates back to the 1910s, when an immunologic reaction was observed in chick embryos. Since that time, many advances have been made throughout the decades with regards to our understanding of the disease and treatment options for the disease. A seminal discovery in the history of GvHD was made by Billingham in 1966, which paved the way for a deeper understanding of the pathophysiology of GvHD.

Historical Perspective

GvHD was recognized many years ago in the early 20th century.

  • In 1916, GvHD was first observed at the Rockefeller Institute in New York City. An immunologic reaction was noticed after engrafting adult chicken tissue containing T cells onto the chorioamnionic membrane of chick embryos.[1] At that time, the concept of T cells was in its infancy. Prior to that time, there was no suggestion of a link between GvHD and T cells.[1]
  • In 1957, Billingham and Brent noticed unexpected findings. They noticed that mice who were chimeric were becoming very sick and were termed "runts." It was eventually discovered that immunocompetent cells from neonatal inocula could migrate to areas of host lymphoid tissue and mount an attack.[1] In the same year, Morton Simonsen showed evidence of GvHD in chickens. He had injected allogeneic lymphoid cells into chick embryos.[1]
  • In 1959, the work done by Billingham and Brent work was published.
  • In 1962, Barnes and colleagues noted that mice who were lethally irradiated then treated with a bone marrow xenograft developed a secondary disease.[2] This article was called "Secondary disease of radiation chimeras: a syndrome due to lymphoid aplasia." This seminal paper helped to define what we know today about the pathophysiology of GvHD.[2]
  • In 1966, Billingham described 3 prerequisites for GvHD.[2] The first prerequisite is the existence of immunocompetent cells in the donor tissue. The second prerequisite is the presence of allelic disparities, or histocompatibility differences, between the donor and the recipient. The third prerequisite is the impaired ability of the recipient to reject the donor cells.[2] These findings paved the way for a better understanding of the pathophysiology of GvHD, and Billingham's principles still hold true today.
  • In 1978, Korngold and Sprent noted that the cellular mediators of GvHD are mature donor T cells.[2]
  • In 1990, Weisdorf and colleagues from the University of Minnesota made a seminal discovery after analyzing the long-term outcomes for patients with grades II-IV GvHD after stem cell transplant.[3] After treatment with steroids, it was noted that 41% of patients achieved a complete remission after 3 weeks of therapy.[3] There was a 5-year survival advantage (51% vs. 32%) in patients who had achieved complete remission from GvHD.[3]
  • In the 2000s, it was noted that multiple new classes of immunosuppressive medications could be used as an alternative to corticosteroids for treatment of GvHD.


  1. 1.0 1.1 1.2 1.3 Barker CF, Markmann JF (2013). "Historical overview of transplantation". Cold Spring Harb Perspect Med. 3 (4): a014977. doi:10.1101/cshperspect.a014977. PMC 3684003. PMID 23545575.
  2. 2.0 2.1 2.2 2.3 2.4 Villa NY, Rahman MM, McFadden G, Cogle CR (2016). "Therapeutics for Graft-versus-Host Disease: From Conventional Therapies to Novel Virotherapeutic Strategies". Viruses. 8 (3): 85. doi:10.3390/v8030085. PMC 4810275. PMID 27011200.
  3. 3.0 3.1 3.2 Weisdorf D, Haake R, Blazar B, Miller W, McGlave P, Ramsay N; et al. (1990). "Treatment of moderate/severe acute graft-versus-host disease after allogeneic bone marrow transplantation: an analysis of clinical risk features and outcome". Blood. 75 (4): 1024–30. PMID 2302454.

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