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Dr Andrew Philip Sage Research Fellow

Dr Andrew Philip Sage, Research Fellow

Postdoctoral Research Associate

Immune regulation of Cardiovascular disease

Andrew Sage is accepting applications for PhD students.

Office Phone: 01223746724

Research Interests

I am investigating how different subsets of B cells regulate the development of atherosclerosis, in order to understand if immune therapies could slow or stabilise disease progression. Atherosclerosis is a complex disease with many contributing networks, including vessel wall inflammation, metabolism and the recruitment and activation of innate and adaptive immune systems.

Contrary to long-standing views, not all B cells play a protective, anti-atherogenic role. The identification of the diversity of B cell subsets and B cell functions means there may be multiple, potentially antagonistic, pathways by which B cells are involved in plaque development. Therefore, we are interrogating the mechanisms of B cell action and the subtypes of B cells that may be involved. We are also interested in how the BAFF family of ligands and receptors are involved in cardiovascular disease. We believe this research could lead to modification of current treatments used in other diseases to treat heart disease and stroke, may reveal novel pathways promoting atherosclerosis that could be targeted by new treatments and aid in understanding the links between autoimmune diseases and cardiovascular risk.

External Collaborators - Prof. Christopher Binder (Vienna, Austria) and Dr Pasquale Maffia (Glasgow, UK)


B cells ; immune tolerance ; MHC class II ; autoantibody ; IgG ; Fc gamma receptors ; adaptive immunity ; antigen presentation ; dendritic cells


  • atherosclerosis
  • immune response in cardiovascular disease

Key Publications

Sage AP, Nus M, Murphy D, Finigan A, Baker L, Masters L and Mallat Z. Regulatory B cell specific interleukin-10 does not regulate atherosclerosis in mice. ATVB. 35(8):1770-3. doi: 10.1161/ATVBAHA.115.305568

Sage A, Murphy D, Sabir S, Grazia G, Maffia P, Masters L, Baker L, Finigan A, Harrison J, Ludewig B, Reith W, Hansson G, Reizis B, Hugues S, Mallat Z. (2014) MHC class II-restricted antigen presentation by plasmacytoid dendritic cells drives pro-atherogenic immunity.  14;130(16):1363-73. doi: 10.1161/CIRCULATIONAHA.114.011090.

Sage AP & Mallat Z. (2014). Multiple potential roles for B cells in atherosclerosis. Ann Med. doi:10.3109/07853890.2014.900272

Ait-Oufella H, Sage AP, Mallat Z, Tedgui A. (2014). Adaptive (T and B cells) immunity and control by dendritic cells in atherosclerosis. Circ Res, 114(10), 1640-1660. doi:10.1161/CIRCRESAHA.114.302761

Zouggari Y, Ait-Oufella H, Bonnin P, Simon T, Sage A, Guérin C, Vilar J, Caligiuri G, Tsiantoulas D, Laurans L, Dumeau E, Kotti S, Bruneval P, Charo I, Binder C, Danchin N, Tedgui A, Tedder T, Silvestre J-S, Mallat Z. B lymphocytes trigger Ccl7-dependent mobilization of monocytes and promote adverse ventricular remodeling after acute myocardial infarction. Nat Med. 2013 Oct;19(10):1273-80. doi: 10.1038/nm.3284.

Sage AP, Tsiantoulas D, Baker L, Harrison J, Masters L, Murphy D, Mallat Z. (2012). BAFF receptor deficiency reduces the development of atherosclerosis in mice. Arterioscler Thromb Vasc Biol, 32(7), 1573-1576. doi: 10.1161/ATVBAHA.111.244731.

Sage AP, Lu J, Atti E, Tetradis S, Ascenzi MG, Adams DJ, Demer LL, Tintut Y. (2011). Hyperlipidemia induces resistance to PTH bone anabolism in mice via oxidized lipids. J Bone Miner Res, 26(6), 1197-1206. doi:10.1002/jbmr.312

Sage AP, Lu J, Tintut Y, Demer LL. (2011). Hyperphosphatemia-induced nanocrystals upregulate the expression of bone morphogenetic protein-2 and osteopontin genes in mouse smooth muscle cells in vitro. Kidney Int, 79(4), 414-422. doi:10.1038/ki.2010.390