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Sir Andrew McMichael

MB, PhD, FRCP, FMedSci., FRS


Group Leader


I qualified in Medicine from Cambridge University and St Marys Hospital Medical School  in 1968 and spent three years as a junior hospital doctor in London hospitals. A chance meeting with Professor Sir Stanley Peart connected me to Ita Askonas FRS at the MRC National institute of Medical Research (Mill Hill) leading to three years working with her and Alan Williamson for a PhD, studying the clonality of B lymphocytes. From there I moved to Stanford  California to work with Hugh McDevitt on the role of HLA in the immune response. I returned to Oxford in 1977 and started to study human T cell responses, discovering some T cell surface molecules such as CD1 (with Cesar Milstein). I focused on cytotoxic T cell (CTL) responses to influenza virus, and Frances Gotch and I showed that CTL responses give protection against this virus infection in humans. Alain Townsend then joined my laboratory  to study virus specificity of CTL and discovered that they recognised peptides bound to class I MHC molecules, different MHC allotypes binding different peptides. 

In the early 1980s AIDS appeared we started to study CTL responses to HIV-1. We identified several peptide epitopes and showed that sequence variation in the peptides could result in immune escape and that such escape was selected by the CTL response. This  was very common and  became clear that immune control of HIV infection is undermined by such escape. HLA types that bound more conserved peptide epitopes were associated with better immune control of this infection. This gave us a possible route to a vaccine which we are exploring as part of the CHAVI/CHAID.CHAD consortium.  .

In the 1990s a collaboration with  John Altmann and Mark Davis enable us  to apply MHC tetramer technology to the identification and quantitation antigen specific  human T cells. Then my postdoc Veronique Braud, having identified an HLA signal sequence peptide (|VL9) as a major ligand for HLA-E.  showed that HLA-E-VL9 tetramers  bound to the NKG2-CD94 receptors on NK cells (and some T cells) to help regulate innate immunity.

I returned to HLA-E in 2016 when Louis Picker and colleagues (OHSU) showed that a rhesus CMV vectored SIV vaccine could protect monkeys from SIV by enabling early clearance of the infecting virus. These T cells were restricted by Mamu-E, an HLA-E homologue. We then showed that humans can make similar T cell responses, in vitro, and that such T cells suppress HIV infection of CD4 T cells in vitro. Together with Geraldine Gillespie and our current team we have characterised the structural and peptide binding properties of HLA-E and how it traffics within cells. We have identified HLA-E presented peptide epitopes in HIV, SARS-CoV-2 and self proteins. Given the non-polymorphic nature of HLA-E we are now aiming to develop immunotherapies and vaccines for both chronic infections and cancers.


In addition to my research programme over the last 45 years, I have founded and led the MRC Human Immunology Unit in Oxford, directed the Weatherall Instiute of Molecular Medicine and have served on a number of Boards including the CHAVI/CHAVID/CHAVD Scientific Leadership Group. I am currently an Emeritus Professor and Group Leader in the Oxford Centre for Immuno-Oncology.

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