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Abstract
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 (CD28 null). 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 CD28 null CD4 T cells.
Highlights
Immunosenescence is thought to contribute to the increase of autoimmune diseases in older people
Following the introduction of highly active anti-retroviral therapy (HAART), a dramatic increase of conditions linked to an increase in CD4 T-cell counts was observed, which underscores the important role of CD4 T cells as effectors in such autoimmune diseases[4,5]
One explanation for such associations is that major histocompatibility complex (MHC) molecules allow specific, disease-associated peptides to be presented to CD4 T cells
Summary
CD28null CD4 T cells are an unusual population of chronically stimulated cells In humans, they appear to accumulate in the presence of CMV infection. They appear to accumulate in the presence of CMV infection They are cytotoxic, produce large quantities of cytokines (a secretory phenotype associated with senescence) and display increased levels of adhesion markers, which suggests that they have access to diverse tissues. Their mere presence in autoimmune disease does not prove that they are involved in it or even cause it. Grant information The author(s) declared that no grants were involved in supporting this work
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