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Cambridge Immunology Network



I work on understanding how T cells recognise and control cytomegalovirus infection in the research group of Dr Mark Wills (Division of Infectious Disease, Department of Medicine).  Human cytomegalovirus (HCMV) is a persistent virus which undergoes intermittent reactivation in tissues with shedding of infectious virus in body fluids.  Despite the exposure of the virus to the immune response during initial infection and subsequent reactivation events the virus is not cleared from infected people.  Lifelong infection with HCMV does not usually cause overt disease, however it causes significant problems for people with compromised or immature immune systems, such as HIV/AIDS patients, transplant patients or unborn babies.  

We have shown that there are T cell responses to viral proteins encoded during cytomegalovirus latency and part of my current research is discovering whether these T cell populations are able to target a specific immune response against latently infected cells to help to clear the virus from infected people.  We are also interested in investigating whether there are changes to the immune response against HCMV antigens with increasing donor age.  So far we have shown that the breadth and quality of the T cell response against HCMV is not affected by donor age in a small cohort of healthy donors.  We are now expanding these observations and also asking whether the response to latent associated viral proteins are altered in older donors by examining a larger number of donors in association with the Cambridge BioResource.


Key publications: 

Mason GM, Jackson SE, Okecha G, Poole E, Sissons JGP, Sinclair J and Wills MR. (2013) Human cytomegalovirus latency-associated proteins elicit immune-suppressive IL-10 producing CD4+ T cells.  PLOS Pathogens. 9(10):e1003635

Libri V*, Jackson SE*, Azevedo RI*, Di Mitri D, Lachmann R, Fuhrmann S, Vukmanovic-Stejic M, Yong K,  Battistini L, Kern F, Soares MVD and Akbar AN. (2011)  Cytomegalovirus infection induces the accumulation of short-lived, multifunctional CD4+CD45RA+CD27+ T cells: the potential involvement of interleukin-7 in this process.  Immunology 132 (3): 326 – 39.

[* contributed equally to this work]

van de Berg PJ, Griffiths SJ, Yong S, Macaulay R, Bemelman FJ, Jackson S, Henson SM, ten Berge IJM, Akbar AN, van Lier RAW. (2010)  Cytomegalovirus infection reduces telomere length of the circulating T cell pool.  J. Immunol 184(7):3417 – 3423 

Henson SM, Franzese O, Macaulay R, Libri V, Azevedo RI, Kiani-Alikhan S, Plunkett FJ, Masters JE, Jackson S, Griffiths SJ, Pircher HP, Soares MV, Akbar AN. (2009)  KLRG1 signalling induces defective Akt(ser473) phosphorylation and proliferative dysfunction of highly differentiated CD8+ T cells.  Blood 113(26):6619 – 6628

Fletcher JM, Vukmanovic-Stejic M, Dunne PJ, Birch KE, Cook JE, Jackson SE, Salmon M, Rustin MH, Akbar AN.  (2005) Cytomegalovirus-specific CD4+ T cells in healthy carriers are continuously driven to replicative exhaustion.  J. Immunol 175:8218-25

Dr Sarah  Jackson
Not available for consultancy