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Anthony John Swainson Davies 1932 – 2022

©Andrew Keat
©Andrew Keat

Anthony (Tony) John Swainson Davies, immunologist and mentor, died on 8 August at the age of 90. He was one of the visionaries that established the foundations of modern cellular immunology as the field developed in the 20-year period from 1960 to 1980. It is no exaggeration to state that once the thymus was identified as being critical for immune function in the mammal, Tony laid the path for discriminating the thymus as the origin of the T cells circulating in the periphery in addition to identifying their essential role providing help for B cell function. He never stopped working, never stopped thinking, about immunology. He continued publishing articles even in 2020 addressing the immune response to SARS-CoV-2 based on his more than 60 years of experience as an immunologist. 

Here, we integrate the memories and reflections of several of his students, mentees, and colleagues into a narrative of those heady days establishing the base elements of adaptive immunity. As you read, you may note some common strands weaved into the account including a universal recognition of his thirst for knowledge and understanding, a profound love of biological mechanism in all its manifestations, an irrepressible love for sharing and exchanging insights, all coupled with a responsibility to get the story right while gently and respectfully coaching and guiding all those around towards the truths he knew to be so. And all this was coupled with an irrepressible and sometimes edgy sense of humour.


Born in Chesterfield, Derbyshire on 12 March 1932, Tony earned a bachelor’s degree in Botany at the University of Manchester in 1952 and, following National Service in the Royal Air Force, returned to Manchester graduating with a PhD in plant cytogenetics in 1958. He was recruited to Prof. Peo Koller’s Department of Cytogenetics at the Chester Beatty Research Institute in London, a constituent of the Institute of Cancer Research (ICR) with strong ties to the adjacent Royal Marsden Hospital. This relationship was critical permitting discoveries at the ICR of the anti-proliferative agents busulphan, chlorambucil, and melphalan, for example, to move rapidly from bench to bedside. 

At that time, immunology as a discipline was realistically a subsidiary of pathology or clinical microbiology with focus upon viral diseases, vaccines, and antisera, a direct result of the effective poliovirus vaccines developed independently by Salk and Sabin. Browsing the Journal of Immunology for 1957 reveals that more than 80% of the published articles addressed some aspect of antibody responses to viral infection, or antibody responses to vaccines, or biophysical and biochemical properties of antisera.

It was into this environment that Tony entered as postdoctoral researcher. In Koller’s department, Jacques Miller, a PhD student, was working on the pathogenesis of lymphocytic leukaemia induced by Gross murine leukaemia virus. Although the leukaemia disseminated to several immune tissues, the tumours likely originated in the thymus as tumours did not develop in thymectomised adolescent mice even though the virus was introduced at birth. Miller reintroduced a neonatal thymus graft into the thymus-deficient, virus-infected animals and the mice developed leukaemic lymphomas from which he hypothesized that the virus replicated initially in the thymus and that this was a prerequisite for the malignant process1. If true, then injecting the virus after neonatal thymectomy, should prevent replication and transformation. The surprising result was that independent of viral introduction, thymectomised mice fared poorly and died several weeks after weaning. There was no such problem with mice thymectomised during adolescence or later – with the benefit of hindsight, we all now know why. The crucial experiments followed. Examination of the mice revealed minimal lymphocyte presence and abnormally small lymphoid organs. The mice couldn’t reject skin grafts. Miller had established that the thymus was essential for immunocompetence.

These results were published and, according to Miller’s recollection, “I concluded from all these data that the developing thymus was the source of lymphocytes that would mature to become fully immunocompetent”. This is absolutely true, but the other conclusion that Miller reached was that the results did not exclude “the production by the young thymus of a humoral factor necessary to the maturation or proliferation of lymphocytes elsewhere in the body”.2,3,4 There is an apocryphal story about a rail journey to a conference that Tony made with Jacques Miller, during which they argued about how the thymus acted: Miller espoused a humoral role, while Tony was for production of lymphocytes. 

Miller used the T6 chromosomal marker in an isogenic system, where host and transplanted cells could be differentiated by chromosomal morphology in mitotic spreads. Miller irradiated adult T6/T6 mice to inactivate endogenous haematopoiesis, and then reconstituted a near normal immune system through grafting wild-type bone marrow and neonatal thymus chromosomally distinguishable from the T6/T6 host. Published in 1962, although grafted cells were found in the host spleen, the proportion was disappointingly low and considered by both Miller and Tony to not be significant enough to attribute reconstitution of immunocompetence to thymic emigration and peripheral repopulation, at least in this model.4

In 1963, while still at the Chester Beatty, Jacques Miller published an article in Nature entitled ‘Evidence for a humoral thymus factor responsible for the maturation of immunological faculty’.5 A year later, also in Nature, also from the Chester Beatty, Tony published a short report entitled ‘A cellular component of thymic function’.6 In this latter article, the first real evidence for thymic emigrant cells restoring immunocompetency was presented. 

In the articles coming from Tony’s group from 1964 onwards to 1967, there is often a discussion giving room to the humoral hypothesis despite his results clearly supporting thymic lymphopoiesis. With hindsight, we can imagine that this was a prerequisite for publication, acknowledging the uncertainty in the field but, knowing Tony, one can sense his likely frustration of having to address what to him should now have been a footnote to canon. He was committed to the cellular hypothesis.

Two articles from Tony’s group stand out in this period, both in Transplantation. The first, in 1966, demonstrates unequivocally that cells from a neonatal thymic graft may form only a minor percentage of cells in the host peripheral immune organs but upon antigenic challenge or attachment of an allogeneic skin graft the cells responding by proliferation in the periphery were of thymic origin with the same observation upon secondary challenge.7 This report was a robust elaboration of the earlier 1964 article and provided incontrovertible evidence that antigen-responding immune cells were of thymic origin. The second article published in 1967 was a truly elegant approach designed to differentiate cells of differing origin in an age before monoclonal antibodies, molecularly defined cell surface antigens, FACS cell sorting and genome-encoded fluorescent labels.8 Simply, lethally irradiated mice were haematopoietically reconstituted with wild-type CBA bone marrow and neonatal CBA-T6/T6 thymus. Following antigenic challenge, splenocytes were transferred to secondary irradiated recipients which, before irradiation, had been rendered immune to the original bone marrow cells or to the T6/T6 thymocytes. This whole system was built on the CBA wild-type mice and CBA-T6/T6 mice being isogenic, not quite syngeneic, and differing in some minor H-2 specificities. Essentially, in mice with circulating antibody to T6/T6, the thymus-derived cells were killed; the remaining bone marrow-derived spleen cells could only mount a weak antibody response to sheep red blood cells (SRBC). In mice with circulating antibody to the bone marrow cells, no antibody to SRBC was produced by the surviving cells of thymic origin. In mice where both cell types survived, the antibody response to SRBC was robust.

In fact, as Tony relates, “These experiments were first completed and spoken of at an international conference at the Institute of Cancer Research in London in 1965.9 They were greeted with polite scepticism and had little impact at that time…Formal publication of these experiments was delayed partly, I suspect, because the contemporary referees were unable to deal with something that contradicted the monophyletic notion of lymphocytes in the immune response.”10

In one fell swoop, Tony and colleagues had demonstrated that lymphocytes of thymic origin (T cells, of course) cannot produce antibody, but they provide help for lymphocytes of bone marrow origin (B cells) thus identifying not only independent lymphocyte functionalities but also their necessary co-operativity. The following year, a series of three consecutive articles in the Journal of Experimental Medicine by Graham Mitchell and Jacques Miller demonstrated, using similar techniques, exactly the same phenomena. Remarkably, even in a review by Av Mitchison in 2004, multiple groups are given credit for demonstrating T–B cooperativity, with 1968 being described as the pivotal year for this functionality, but nowhere are the earlier results of Tony and his group given recognition or credit.11

Between 1967 and 1974, Mike Doenhoff joined Tony’s laboratory as a PhD student continuing as a fellow before leaving to take up a position at the London School of Hygiene and Tropical Medicine. Mike was the second student to have his PhD directly supervised by Tony, preceded by Elizabeth Leuchars, though he subsequently mentored many more. In a remarkable series of papers spanning a decade, Mike and Tony exploited the mouse T6/T6 marker chromosomes, and using a lymphocyte in vitro culture system developed by Hilliard Festenstein showed that the blood cells responding to phytohaemagglutinin (PHA) were thymus-derived, which in turn provided an opportune and incontrovertible marker for T cell identification prior to the routine use of Thy-1 and subsequent CD markers for cell characterisation. Mike recalls that “Tony knew Hilliard was trying to develop a method of culturing mouse blood lymphocytes, and when Hilliard reported success, he was immediately invited to spill the beans in the third floor lab. I remember having my face pressed up against the reinforced glass wall of the surgical room, wondering what Tony and Hilliard were up to. I was soon allowed to join that party and never looked back!” Using the T6/T6 markers and/or 3H-thymidine incorporation together with generation of mitotic T cell populations using PHA, Tony, Mike and colleagues were able to enumerate organ representation and kinetics of T cells during immune responses and during development and ageing. Tony referred to these articles as “the most satisfying of my career”.

Robert Kerbel, currently Professor of Medical Biophysics at the University of Toronto, Canada, joined Tony’s laboratory in 1971. As he recalls:

It was around 1971 when I made, in retrospect, one of the best decisions of my life – to undertake postdoctoral fellowship training in the lab of Tony Davies at the Chester Beatty Research Institute in London. I was completing my PhD thesis in cellular immunology at Queen’s University in Kingston Ontario, the main focus of my work being assessment of the relative thymus-derived (T) cell dependence of immune responses to defined antigens. During these studies I was intrigued by an unexpected finding: adult mice deprived of T cells actually had elevated antibody levels after injection of a synthetic antigen, polyvinyl pyrrolidone (PVP). This observation implicated the existence of what were called at the time ‘suppressor T cells’. Tony’s friend, the late American immunologist Richard Gershon, had just coined the term, and I consulted Richard about whether I should do my postdoc in London with Tony or with an immunologist in Australia. Richard was incredulous that I would actually consider anyone other than Tony, and predicted that a period of training with Tony would be one of the highlights of my life, both personally and professionally. He was right.

I was intrigued by Tony’s emphasis of using chromosome markers to trace the fate of transplanted T cells into irradiated adult thymectomised mice. In part this was because, by definition, detecting such cells meant they had to be dividing, and thus in all likelihood constituted being in an ‘activated’ state after challenge with a defined antigen. This approach facilitated Tony’s studies in the mid to late 1960s on thymus dependency of immune responses and led him to conclude that there must be two major lineages of lymphocytes constituting the immune response, one of course being T cells which did not make antibodies, and a second population derived from bone marrow (B cells), that did. His studies also showed that bone marrow-derived (B) cells were deficient in antibody production to most antigens without the assistance somehow provided by interacting T cells.
Of course, it was around the same period that other investigators, notably Jacques Miller and Max Cooper, came to similar conclusions for which they deservedly won many prestigious research awards and prizes. Tony’s contributions did not elicit anywhere near the same degree of recognition, but I think I know one reason why – his generosity.

One of the things about Tony that astonished me when I worked in his lab, is that many, if not most, of the papers submitted for publication by his trainees, myself included, did not include Tony as a co-author. This was Tony’s choice. He knew that the absence of his name would be important to show that a particular trainee was capable of being an independent researcher – a mandatory requirement for any young trainee applying for his or her first academic research position. In short, Tony did not promote himself, and never did; he was much more interested in promoting his trainees, as long as they were worthy of such praise. This was just one of many examples of his mentorship. He constantly challenged my research assumptions and cherished hypotheses. Tony really made you think. Based on my experience as a PhD student, I thought I was reasonably competent, when it came to writing a manuscript – until I gave him my first paper to edit summarising work in his lab. I think he used the entire contents of a new pen by the time he got to the last page.

After I left Tony’s lab in 1974, I kept in touch with him, visiting him in what seems like dozens of times. He always insisted that I stay with him and his wife, Agneta. Among my fondest memories of some of these visits, in addition to our long discussions about science, was going for long walks with him and Mango, his beloved pet dog. This was so despite the fact I could hardly keep up with him even when he was in his mid-80s. Another fond memory was Tony making bacon and egg breakfasts. He knew I loved English or Danish rashers, although I have to say he was rather stingy in the number he handed out. I think he did this on purpose. There was always a twinkle in his eye when I sadly looked down at my plate containing a single lonely rasher (or maybe it was two…).

It was during one of those visits to London that we had a lively discussion in which he made a comment that had a profound impact on the next stage of my career as a cancer researcher. I was still doing some immunological work, mostly involving immunotherapy of cancer, but my interest was waning somewhat as I had become intrigued with the concept of tumour angiogenesis and antiangiogenic therapy for cancer, pioneered by the late Judah Folkman. Thus, as a director of cancer biology research division in a new hospital research institute in Toronto, I wanted to recruit someone at a senior scientist level who had expertise in tumour angiogenesis. This was around 1988/89. However, other division leader colleagues and the director were not supportive. They were sceptical that antiangiogenic drugs would ever achieve any clinical success. I was complaining to Tony about this situation, when he cut me off, asking “if you are such a believer in the Folkman concept why not just work on it yourself?!” And so, I did. Looking back on his comment, it seems so obvious now. My decision, inspired by Tony, was followed by a 25–30-year span of great success working on many aspects of tumour angiogenesis and experimental therapeutic aspects of antiangiogenic drugs.


It was also during this period from the early-70s to ’80s that Tony’s concept of the immune system evolved. Specifically, that the immune system had not arisen simply as a means to reject that which was foreign but rather to permit some degree of discrimination between useful commensal organisms and those others that may not be so beneficial. Of course, our immune systems are sometimes fooled; we easily tolerate the harmless forms of E. coli that produce vitamins K and B in our lower intestines, but sometimes other more dangerous strains such as O157:H7 may establish themselves. Consequently, Tony began to take more than a passing interest in the role of the immune system in regulating the symbiotic relationship of parasites to mammals. This was nurtured further by maintaining a lifelong interaction with Mike Doenhoff whose research for more than 40 years has examined the interaction of the immune system with schistosome parasites.

Max Murray, Emeritus Professor of Veterinary Medicine at the University of Glasgow, was a close friend of Tony’s for nearly seven decades and recalls how he and Tony contributed to advancing the effort to understand the role of the immune system in the resistance of N’dama cattle of Central and West Africa to trypanosomiasis. An extracted summary of Max’s recollections is below.

I first met Tony Davies in 1966 at the Glasgow University Vet School where he was giving a lecture. The audience was huge with over a 150 people. Tony gave a truly masterful presentation; this event marked the initiation for me of a long and special friendship, both personal and scientific, which lasted till his sudden demise. 

In the early ’70s, I visited the Chester Beatty Research Institute several times where Tony and I addressed our parallel interests in African trypanosomiasis. In 1972, the Rockefeller Foundation at a meeting in Bellagio, Italy proposed building a research institute in Kenya. This proposal led to the renowned International Laboratory for Research in Animal Diseases (ILRAD) that opened in Kenya in 1973. 

My wife and I moved in 1976 to ILRAD, now a magnificent state-of-the-art research institute seven miles north of Nairobi. At the ‘official’ opening in 1978, Tony was one of the celebrated international speakers that also included Elvin Kabat and Martin Raff. In February 1981, Tony and I were both part of the strategy group that gathered once again at the Rockefeller Conference Centre at Bellagio to establish a major research effort to understand the genetic resistance of N’dama cattle and exploit the results for regional control of tsetse fly-transmitted African trypanosomiasis. The project was approved by the Gambian government and the International Trypanotolerance Centre (ITC) opened in The Gambia in 1983. In 1985, I had returned to Glasgow as Chair of Veterinary Medicine but Tony and I continued to travel regularly from the UK to Gambia to visit the ITC. By 1987 Tony had become the chairman of the ITC council, a position he undertook in his characteristically dynamic and insightful way.

Tony had an amazing mind which he never seemed able to switch off. Everything was of interest to him, be it teaching his son about the various fungi found on Wimbledon Common, to producing long chain fatty acids bound to silicon patches being developed as therapeutics.

He was a great and generous man, an exceptional and brilliant scientist and one of the international fathers of immunology. Most importantly, for 66 years he was my friend.

Towards the end of the 1970s, the laboratory maintained a constant research effort investigating T lymphocyte kinetics, primarily under the guidance of Val Wallis. At the same time, however, Tony was looking at how our growing knowledge of immune mechanism might be utilised to aid therapeutic options, particularly to control or eliminate malignant growth. He began collaborating with clinicians across the discipline of clinical oncology. In particular, the developing field of lineage-specific cell surface markers led to the idea that anti-lymphocyte antibodies could be used to target lymphomas and leukaemias. Further, conjugation of plant toxins such as abrin or ricin to the targeting antibody might offer a new avenue for specific tumour targeting. Tony coined the term Retiarian therapy to describe this approach, based on the Retiarius gladiator who wielded a weighted net to ensnare the opponent and a trident to then dispose of the trapped individual. This was an idea ahead of its time for its potential for cancer therapy and was developed under the insightful guidance and design of Phil Thorpe who later moved first to the Imperial Cancer Research Fund and then to Texas. Quietly working in the background was a senior biochemist, Caird Edwards, who turned his laboratory into a factory safely extracting ricin from castor beans and purifying it to homogeneity. Also in the background was Prof. Walter Ross, a giant of post-war development of anti-neoplastic alkylating agents and protagonist of their use for chemical conjugation. Tony marshalled all these brilliant minds and experimentalists to drive forward the field of targeted immunotherapy. 

Other clinical associations developed – Prof. Julian Bloom, one of the founders of radiotherapy in the new post-war field of nuclear medicine, and a consultant radiotherapist at the Royal Marsden, enjoyed a close personal relationship with Tony and together they directed successful studies in establishing human glioma xenografts in immunodeficient mice. Mark Pepys collaborated with Tony, as outlined below.

Prof. Sir Mark Pepys (University College, London) is overly modest in his narrative below – the “certain blood proteins that were not strictly ‘immunological’” include the discovery of circulating serum amyloid P-component, still of unknown function in the normal state but associating with amyloid fibrils in amyloidosis and also with αβ amyloid deposits in the brain and cerebral vasculature in Alzheimer's disease, rendering it a candidate for therapeutic targeting. Mark writes:

Tony Davies was a brilliantly creative and original immunologist whose discoveries and insights made a series of seminal contributions to understanding of the immune response and its regulation. They remain solid pillars of the canon of established knowledge and have long been universally accepted rather than closely associated with him personally. In one sense this is a great accolade. In other respects, it reflects that Tony, in my view unfairly, was not adequately recognised for his incisive and illuminating work at the time or subsequently.

As a young immunologist with my own original path opening up, I was vividly aware of Tony’s work and his eminent status as a leader in the field. When I serendipitously developed an interest in certain blood proteins that were not strictly ‘immunological’, I immediately thought of Tony as a potential collaborator. He always displayed an exceptionally broad interest in all areas of biology and he turned out to be the most open minded and generously helpful colleague and collaborator one could possibly imagine. Our swiftly conducted experiments together yielded exciting original observations that were promptly reported in a seminal Nature publication in 1979.

The topic was far outside Tony’s previous research interests but his contribution to the project was enormous. Through this and some subsequent minor collaborations, we developed a strong friendship and mutual respect, which included our strongly shared delight in socialising and joke telling. Tony’s sense of humour and generally optimistic view of life were legendary. More than 40 years on I still retell Tony’s ‘best’ joke and still burst out laughing when I think of it and recall the image of him acting it out – “just chewing a toffee”. That image will live with me for ever, and, I hope, also with at least some of those to whom I have retold it! This vignette illustrates one aspect of Tony’s unique character and attributes as clearly as his impeccable scientific record, which is well summarised by his amazing achievement of 24 papers published in Nature.

Our work and interests drifted apart in the 1980s but Tony approached me in the 2010s with exciting novel ideas related to our 1979 Nature paper. It was absolutely typical of his personality and the quality of his character, that our friendship took off again as if we had been working together throughout. Thereafter we continued to earnestly discuss and brainstorm together on several topics of mutual interest, though never quite putting our ideas into practice. This was no reflection on the quality of our plans but a direct result of the fact that both of us were also so extraordinarily busy with other research and development work. Indeed, Tony’s energy, drive, commitment, and still sparkling originality and intellectual creativity, were phenomenal for an 80+ year old. He showed no sign of slowing down, was always twinkling with good humour and instantly responsive when any work, including production of long documents, was required.

I find it impossible to imagine that he is still not there, ready to produce another thrilling new idea or tell a side-splitting joke. There are few who leave such a vivid personal impression on memory, as well as an indelible mark on their scientific field.

In 1978, Tony took on his next PhD student, Jonathan Duke-Cohan, with a very specific project in mind. It was apparent that haematopoietic stem cells (HSC) used for mouse reconstitution studies differed in their regenerative capacity depending upon their source. Based on the earlier results of Martin Rosendaal working at the Walter and Eliza Hall Institute in Melbourne, there arose the novel notion that each time a stem cell generated daughter cells to repopulate the blood, it lost some of its ‘stemness’. Martin had returned from Australia to take up a position at Queen Elizabeth College, London where he was a mentor for Jonathan’s final year physiology research project. Having been ‘primed’ by Martin, Jonathan sought out PhD studentships investigating HSC. Contemporaneously, Tony and Val Wallis had found that Melphalan eliminated in cell populations the ability to detect HSC by the CFU-S assay, the gold standard at the time for assay of HSC, despite strong haematopoietic repopulating remaining. Jonathan was recruited to investigate this phenomenon.  

They demonstrated that there were at least three levels of HSC, of which the CFU-S was the lowest in potential and developed in the spleen. A marrow-repopulating stem cell existed that could give rise to CFU-S, and a ‘reserve’ stem cell existed in foetal liver that could give rise to the marrow repopulating cell. This latter cell was maintained in the quiescent G0 cell cycle stage hence its resistance to melphalan. The resulting thesis is probably unique in history in discussing HSC and a Socratic school discourse on metempsychosis in adjacent sentences.12 The importance of words, their splendour, and proper use was an important theme in Tony’s environment. Jonathan remembers an extensive debate with Tony concerning the word ‘philoprogenitive’, how it was a mongrel word of Greek and Latin, what did it really mean (usually ‘prolific’), and did it deserve to be a word applied to early HSC? Possibly ‘yes’ if intended to mean happy in its state of being a progenitor; ‘no’ if it meant love of proliferation since that clearly wasn’t the case. Upon division, it was the committed daughter cells that loved to proliferate – the uncommitted daughter cell stayed quietly in its niche until required to produce further offspring.

Tony’s final PhD student, of only four directly supervised in total, was Deirdre McIntosh. Deirdre’s example provides the core reasons why Tony only had four directly supervised doctoral students. He guided Deirdre over more than 10 years through an intermediate graduate degree, her PhD, and seven refereed publications. For Tony, a student was a true apprentice, meant to carry on the craft to the next generation, and he took this responsibility very seriously. Further, after graduation, he was always available for wise advice and support maintaining friendship with all four. Sadly, Deirdre died of bowel cancer earlier in 2022, and her demise hit Tony hard.

Tony helped supervise a total of 22 PhD, MPhil, MD, and MS (Surgery) students, was an external examiner for 33 PhD students globally, and was a visiting examiner for BSc degrees at seven University of London Colleges and Medical Schools. 

In 1980, Prof. Robin Weiss was recruited to become the new ICR director, replacing Prof. Len Lamerton, a founder of nuclear medicine as a discipline after WWII. Robin Weiss recruited Tony to be Deputy Director of the ICR, a position he held from 1982 to 1991.

Robin Weiss (Emeritus Professor, University College London, and previous Director of the ICR) recalls Tony’s tenure as Deputy Director:

Tony masterminded the necessary… changes to the internal organisation of laboratories and services. Tony engaged in his new managerial duties with gusto and efficiency, but the extra workload inevitably took a toll on his personal research although it was of great benefit to the Institute as a whole. Nevertheless, during this period of his career, Tony not only maintained his insatiable curiosity about biology and immunology, but also championed its application to understanding and treating cancer. Throughout the 1980s Tony developed innovative research projects with the Royal Marsden Hospital, particularly with the Department of Surgery and the Breast Cancer Group of medical oncologists… [as well as mentoring the next generation of clinical oncologists]

Deciding upon retirement in 1991, Tony was appointed Emeritus Professor of the University of London whereupon he continued to challenge himself academically, becoming a consultant especially to groups needing help in navigating grant applications through successive cycles of the massive European Union Framework funding mechanism. He served on Scientific Advisory Committees including the Prostate Cancer Research Centre at King’s College (1999–2019) directed by Dr Aamir Ahmed, who became a close friend. He also became highly involved together with Prof. Max Murray in ventures aimed at using natural organic preparations designed to promote wellbeing in horses and later extended to other species.

As readers will have surmised from the text above, his colleagues, students, mentees, and collaborators feel as a group that Tony probably didn’t receive the proper recognition he deserved for his early work on defining the elements of adaptive immunity. He never really talked about it – for several reasons. First, he was generous; this is clear from his recollections of that critical time published in 1993.13 He respected his colleagues and was appreciative of their science and insight. He could be sharp and incisive with words, but never with malice. Usually, such words were delivered with a twinkle in his eye. He enjoyed life – he had much to do and didn’t have the time to mull over the past and harbour grudges. He has left a lasting impression on all who knew him, and he will be sorely missed.

Dr. Jonathan S. Duke-Cohan
Prof. Michael J. Doenhoff
Prof. Robert S. Kerbel
Prof. Mark B. Pepys
Prof. Maxwell Murray
Prof. Robin A. Weiss



1.    Miller JF. 1960 Studies on mouse leukaemia. The role of the thymus in leukaemogenesis by cell-free leukaemic filtrates. Br J Cancer. 14 93–8. doi: 10.1038/bjc.1960.11
2.    Miller JF. 2019 A Scientific Odyssey: Uncovering the secrets of thymus function. Cell 179 21–26. doi: 10.1016/j.cell.2019.08.023
3.    Miller JF. 1961 Immunological function of the thymus. Lancet 2 748–9. doi: 10.1016/s0140-6736(61)90693-6
4.    Miller JFAP. 1962 Effect of neonatal thymectomy on the immunological responsiveness of the mouse. Proc Roy Soc B. 156 415–28
5.    Osoba D, Miller JF. 1963 Evidence for a humoral thymus factor responsible for the maturation of immunological faculty. Nature 199 653–4. doi: 10.1038/199653a0
6.    Leuchars E, Cross AM, Davies AJ, Wallis VJ. 1964 A cellular component of thymic function. Nature 203 1189. doi: 10.1038/2031189a0. 
7.    Davies AJ, Leuchars E, Wallis V, Koller PC. 1966 The mitotic response of thymus-derived cells to antigenic stimulus. Transplantation. 4 438–51. doi: 10.1097/00007890-196607000-00008. 
8.    Davies AJS, Leuchars E, Wallis V, Marchant R, Elliott EV. 1967 The failure of thymus-derived cells to produce antibody. Transplantation 5 222–231.
9.    'A conference on radiation and the immune response'. Davies AJS and Micklem HS. Chester Beatty Research Institute, London, April 26–28, 1965.
10.    The 1967 Transplantation article was submitted on 17 June 1966 and published in March 1967. Henry Claman et al.’s article addressing in a less robust way the same issue (the system could not distinguish between antibody-producing source and helper cell) was submitted on 14 July 1966 and published in December 1966 in J. Immunol. (PMID:5333748).
11.    Mitchison NA. 2004 T-cell-B-cell cooperation. Nat Rev Immunol 4 308–12. doi: 10.1038/nri1334. 
12.    From: Duke-Cohan JS. Studies on a hierarchical organisation for murine haematopoietic stem cells. Ph.D. thesis, University of London 1982:
As Cebes surmised, while Socrates lay on his deathbed, the soul may survive through successive incarnations, and may be considered as immortal, but at each rebirth the soul may suffer some ill-effect which pushes it a little further towards its own death (Plato). This possible ill-effect of transplantation…
13.    Davies AJ. 1993 The tale of T cells. Immunol Today 14 137–9. doi: 10.1016/0167-5699(93)90216-8.