CD28null CD4 T-cell expansions in autoimmune disease suggest a link with cytomegalovirus infection [version 1; peer review: 2 approved]
Aalia Bano,
Alejandra Pera,
Ahmad Almoukayed,
Thomas H.S. Clarke,
Sukaina Kirmani,
Kevin A. Davies,
Florian Kern
Affiliations
Aalia Bano
Department of Clinical and Experimental medicine, Brighton and Sussex Medical School, Brighton, Sussex, BN1 9PX, UK
Alejandra Pera
Department of Immunology, Maimonides Institute for Biomedical Research (IMIBIC), Reina Sofia Hospital, University of Cordoba, Av. Menendez Pidal, 14004, Cordoba, Spain
Ahmad Almoukayed
Department of Clinical and Experimental medicine, Brighton and Sussex Medical School, Brighton, Sussex, BN1 9PX, UK
Thomas H.S. Clarke
Department of Clinical and Experimental medicine, Brighton and Sussex Medical School, Brighton, Sussex, BN1 9PX, UK
Sukaina Kirmani
Department of Clinical and Experimental medicine, Brighton and Sussex Medical School, Brighton, Sussex, BN1 9PX, UK
Kevin A. Davies
Department of Clinical and Experimental medicine, Brighton and Sussex Medical School, Brighton, Sussex, BN1 9PX, UK
Florian Kern
Department of Clinical and Experimental medicine, Brighton and Sussex Medical School, Brighton, Sussex, BN1 9PX, UK
Immunosenescence is thought to contribute to the increase of autoimmune diseases in older people. Immunosenescence is often associated with the presence of an expanded population of CD4 T cells lacking expression of CD28 (CD28null). These highly cytotoxic CD4 T cells were isolated from disease-affected tissues in patients with rheumatoid arthritis, systemic lupus erythematosus, multiple sclerosis, or other chronic inflammatory diseases and their numbers appeared to be linked to disease severity. However, we recently demonstrated that the common herpes virus, cytomegalovirus (CMV), not ageing, is the major driver of this subset of cytotoxic T cells. In this review, we discuss how CMV might potentiate and exacerbate autoimmune disease through the expansion of CD28null CD4 T cells.
