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Every kidney transplant today rests on a problem that once looked impossible: the body attacks tissue that is not its own. Joseph Murray, a Boston surgeon, got past it in 1954, first by sidestepping it and then by learning to hold it back. This post follows his Nobel Lecture, explains the biology, and ends with what a student can learn from how he worked.
Who was Joseph Murray?
The Nobel Prize facts page records that Murray was born on 1 April 1919 in Milford, Massachusetts, and died on 26 November 2012 in Boston. He shared the 1990 Nobel Prize in Physiology or Medicine with E. Donnall Thomas "for their discoveries concerning organ and cell transplantation in the treatment of human disease".
He did not take the usual route into science. In his Nobel autobiography he says he studied Latin, Greek, philosophy and English at the College of the Holy Cross: "Assuming I'd receive ample science in medical school, I took the minimum of chemistry, physics and biology." He then trained at Harvard Medical School.
How did a war hospital start his question?
During the Second World War, Murray was posted to Valley Forge General Hospital in Pennsylvania, a major plastic surgery centre. Many soldiers were so badly burned that there was not enough of their own skin to graft, so skin from other people was used as a temporary cover. That foreign skin was slowly rejected. Murray wrote that this fascinated him: "How could the host distinguish another person's skin from his own?"
His chief, Colonel James Barrett Brown, had a clue. In 1937 Brown had grafted skin between identical twins, and the grafts survived permanently in both.
Why were identical twins the key?
The 1990 Nobel press release explains that molecules on the surface of cells, called HLA antigens in humans, are recognised by the recipient's immune defence as foreign, and immune cells then try to reject the graft. Your NCERT Class 12 chapter Human Health and Disease says the same thing in exam language: the body tells "self" from "nonself", and the cell-mediated immune response is responsible for graft rejection, which is why tissue and blood group matching are needed and patients take immunosuppressants for life. Identical twins come from one fertilised egg, so their cells carry the same antigens. The immune system sees nothing foreign.
Peter Medawar's work showed that rejection is an immune response that can, in principle, be controlled. Our post on Medawar and immune tolerance covers that side of the story.
What happened in December 1954?
In his Nobel Lecture, Murray describes how, in the autumn of 1954, a Public Health Service doctor referred a patient with severe kidney disease who had a healthy twin brother. The team first exchanged small skin grafts between the twins. The grafts survived, which established that they were genetically identical.
Murray had already worked out the operation in dogs, placing the new kidney in the lower abdomen. He wrote that this "has become the universal renal transplant procedure since that time."
The harder question was ethical. Murray put it plainly: "For the first time in medical history a normal healthy person was to be subjected to a major surgical operation not for his own benefit." The team consulted doctors and clergy before offering the operation. According to a 2019 profile in the Singapore Medical Journal, surgery took place on 23 December 1954, with Murray leading the team for the recipient, Richard Herrick, and J. Hartwell Harrison leading the team for the donor, Ronald.
The kidney worked immediately. Murray was honest about what it meant: "we had achieved our long-term goal by bypassing, but not solving, the issue of biological incompatibility."
How did transplants between non-identical people become possible?
Murray's lecture describes the next steps. His team first tried total body X-rays followed by bone marrow infusion. In most patients the kidney worked for a few weeks, but only one of twelve kept working beyond three months. That one success, in 1959, was a non-identical twin given a lower X-ray dose, who lived a full life for 25 more years.
Drugs did better. In 1959 Schwartz and Dameshek showed that the drug 6-mercaptopurine could stop rabbits making antibodies. Roy Calne came to Boston in 1960, and George Hitchings and Gertrude Elion of Burroughs Wellcome supplied related compounds. One, BW-322, is now called azathioprine. The first patient given it, in March 1961, died of drug toxicity because the dose that suited dogs was toxic to people. A patient transplanted in April 1962 with a kidney from a person who had died, and treated with azathioprine, survived more than a year: the first successful transplant between unrelated people. Our post on Gertrude Elion and drug design explains where such drugs came from.
What do the numbers in his lecture show?
Murray gives figures you can read like a data question.
X-ray method: 1 success out of 12 patients is 1/12, about 8%.
By 1965: one-year survival of transplanted kidneys was approaching 80% from living related donors and 65% from deceased donors.
What that means: out of 100 kidneys from deceased donors, about 65 were still working after a year and about 35 were not.
A common slip is to read 65% as "65% of patients survived". The figure is for kidneys still working, which is not the same thing.
What can a student take from Murray's way of working?
Notice the odd detail. Slow rejection of skin grafts was routine on a burns ward. Murray asked why it happened at all.
Solve the part you can solve. The twin case removed the immune problem so the surgery could be tested on its own.
Report failures honestly. His lecture lists the patients who died and the doses that were wrong, and that record is what let others improve on them.
If antigens, antibodies and immune cells still blur together, the Fermi Concept Library covers every concept in physics, chemistry, biology, mathematics and computing, so you can review them one at a time.
Next step: find the paragraph on transplants in the NCERT chapter linked above, then explain in two sentences why the Herrick twins did not need immunosuppressants.
