Richard Batchelor was a pioneer in transplant immunology and a past president of the TTS. He was born in Woking, England, but had much of his earlier education in India, both in Chennai and Madras, where his father had been posted on business. On return to the United Kingdom, he completed his education in Marlborough College and then entered Emmanuel College at Cambridge to start his medical studies. He graduated from Cambridge with a BA, but it was interesting that in his final year, his choice was pathology, which probably determined his subsequent career to a great extent.
He then moved to Guy's Hospital in London for his clinical training and graduated in medicine in 1955. After a year as a house officer (intern), he was drafted for National Service in the Royal Army Military Corp, where he spent 2 years, but this was spent in pathology at in the military hospital in Aldershot. Toward the end of that time, he was invited by Professor Peter Gorer FRS to join his laboratory as an MRC graduate student. Peter Gorer was an extremely distinguished tumor immunologist but also played a major role in defining the major histocompatibility system in the mouse known as H-2. Unfortunately, Peter Gorer died at a relatively young age in 1961 which left Richard somewhat up in the air but he was appointed as a lecturer and later a senior lecturer in pathology at Guy's Hospital.
However, in 1967, he became Director of the Blond McIndoe Research Centre at the Queen Victoria Hospital in East Grinstead, and an Honorary Professor at the Royal College of Surgeons of England. The Queen Victoria Hospital was a major plastic surgery center particularly for the management of burns, and so much of his work moved into transplant immunology. Indeed, he created a powerhouse in transplant immunology at East Grinstead with major interest in HLA, the major histocompatibility system in man, a natural follow-on to the H2 system in the mouse. He became interested in the possibility of passive enhancement of allografts a phenomenon with which he was familiar with from his tumor immunology days. While there, he had a young surgical Research Fellow, Michael French, working with him who developed the technique of transplanting kidneys in the rat, a new technique at that time. They were able to show that the administration of donor-specific antibody would result in prolongation of the donor renal allograft.
He was one of the pioneers in the genetics of HLA and, indeed, called for volunteers to be skin grafted with a view to developing cytotoxic antibodies as a result of the skin grafts which could be used for tissue typing purposes. Richard, himself, was a recipient of skin grafts which he proudly used to demonstrate, and there are quite a number of these ex-volunteers still around with the healed skin grafts which, needless to say, were all rejected in due course.
In 1979, he moved to the Royal Postgraduate Medical School at Hammersmith as Professor of Tissue Transplantation, and 3 years later, he was appointed as Head of the Department of Immunology, a position he held until he retired in 1994, to become Emeritus Professor of Pathology. His research interests ranged from the use of matching for HLA in renal transplantation and also in corneal grafts. Later, the association between HLA and disease became a major interest, and he was particularly involved with the autoimmune disorders, multiple sclerosis, systemic lupus erythematosus, and rheumatoid arthritis, as well as developing a major interest in the immune response to bone marrow transplants.
In 1970, he asked whether he could come and do a sabbatical with me as we were by then friends and colleagues, and we had also developed renal transplantation in the rat as an experimental model through the persistence of John Fabre, and during his stay there, he and John Fabre did some interesting further experiments with passive enhancement, showing that the effect was augmented by induction with antilymphocyte serum in strong models of incompatibility in the rat.
However, as part of the international histocompatibility workshop in 1970, which was to concentrate on the study of HLA in nonwhite populations. I was responsible for South East Asia and Oceania, and I had already arranged to go to the New Guinea Highlands because these were relatively isolated population that had been, as far as we knew, untouched by other populations for some ten thousand years, having moved down from Southeast Asia during the second Ice Age. Richard, on his way to Melbourne, had arranged to bleed the native population in Fiji and send the samples to my laboratory in Melbourne for HLA typing. Richard came with me, and we had a fascinating 2 months in the Highlands of New Guinea. Originally, we intended to do the tissue typing in the laboratories of the Research Institute at Goroka (this had been set up by sir McFarlane Burnet to study the recently discovered neurological disease, Kuru, which was considered by Burnet to be an autoimmune disease), but this was not proving very satisfactory, and my senior technician back in Melbourne, Wendy Schlesinger, said that we were past doing that sort of laboratory work and could we ship the blood samples down to my laboratory in Melbourne. This proved to be quite a challenge for you could spend the best part of the day going 30 to 40 miles in the Highlands but it worked pretty well because we would bleed in the villages we were visiting as the sun came up, and indeed that was necessary because the women did all the work in the fields and the bleeding had to be done very early. We would then race back in the old Land Rover with our trusty guide, Sandy McPherson, to Goroka, put the blood on a plane down to Port Moresby, then to Brisbane and from there to Melbourne, and amazingly, most of the time, the samples got there in a satisfactory condition and my team back in Melbourne could isolate the lymphocytes for HLA typing. As perhaps expected, the results of these studies proved to be quite unique as the HLA system (only class 1 at that time) was indeed very restricted, for example, no HLA-1 or HLA-2 but a high prevalence of HLA-9. This relative lack of polymorphism may have resulted from their genetic isolation and perhaps because of the lack of exposure to the usual viral and bacterial infections that were uncommon before white man came into the area during and after the Second World War.
Richard had an incredibly distinguished career and was president of the TTS in 1988, was the second President of the British Transplant Society in 1975, and President of the British Society of Histocompatibility and Immunogenetics in 1992. Richard will be sadly missed in the international transplant community for no other reason than from his very wise words arising from his enormous experience in the field.
After his retirement from the Chair of Immunology, he became a member of Council of the Arthritis Foundation and then a trustee of the Kennedy Institute. He oversaw the move of the Kennedy Institute to the Charing Cross Hospital in London and later to the Oxford Medical School to a new building on the Old Road Campus.
He also was a kind and considerate man, and I regarded myself fortunate as being able to consider him not only a colleague, but also a good friend.
Sadly, his wife, Moira, died 6 months earlier, and he leaves 4 children, Andrew, Simon, Annabel, and Lucinda and several grandchildren.