ABSTRACT
CD28 is a primary co-stimulatory receptor that is essential for successful T cell activation, proliferation, and survival. While ubiquitously expressed on naive T cells, the level of CD28 expression on memory T cells is largely dependent on the T-cell differentiation stage in humans. Expansion of circulating T cells lacking CD28 was originally considered a hallmark of age-associated immunological changes in humans, with a progressive loss of CD28 following replicative senescence with advancing age. However, an increasing body of evidence has revealed that there is a significant age-inappropriate expansion of CD4⁺CD28⁻ T cells in patients with a variety of chronic inflammatory diseases, suggesting that these cells play a role in their pathogenesis. In fact, expanded CD4⁺CD28⁻ T cells can produce large amounts of proinflammatory cytokines such as IFN-γ and TNF-α and also have cytotoxic potential, which may cause tissue damage and development of pathogenesis in many inflammatory disorders. Here we review the characteristics of CD4⁺CD28⁻ T cells as well as the recent advances highlighting the contribution of these cells to several disease conditions.
Subject(s)
Humans , Cellular Senescence , Cytokines , Memory , T-LymphocytesABSTRACT
Infliximab (Remicade(R)) has been used for treating many chronic inflammatory diseases, including rheumatoid arthritis, ankylosing spondylitis, Crohn's disease, and psoriasis. Complications such as infusion reaction and infection in infliximab therapy have been reported, but renal complications are rare. We present data on a patient with psoriasis for 15 years who developed new onset renal disorders (IgA nephropathy, acute tubulointerstitial nephritis, acute tubular necrosis) after treatment with infliximab (duration of therapy: 12 months, 8 times). Because the patient with psoriasis receiving infliximab may develop new onset renal disorders, we recommend the evaluation of renal function.