CD4+CD25+ regulatory T lymphocytes in allergy and asthma

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Abstract
Allergic asthma is characterized by airway hyper-responsiveness and chronic mucosal inflammation mediated by CD4(+) Th2 lymphocytes. Regulatory CD4(+)CD25(+) T cells are important components of the homeostasis of the immune system, as impaired CD4(+)CD25(+) T cell activity can cause autoimmune diseases and allergy. The mechanism of suppression by CD4(+)CD25(+) T cells remains controversial; different in vivo and in vitro studies raise possible roles for the immunosuppressive cytokines interleukin-10 and transforming growth factor-beta, forkhead transcription factor Foxp3, glucocorticoid-induced tumor necrosis factor receptor, cytotoxic lymphocyte associated antigen-4, 4-1BB costimulator receptor, a CD4-related molecule LAG-3, and neuropilin-1. Current data suggest that Th2 responses to allergens are normally suppressed by CD4(+)CD25(+) T cells. Suppression by CD4(+)CD25(+) T cells is decreased in allergic individuals. Furthermore, CD4(+)CD25(+) T cells play a key role in regulating airway eosinophilic inflammation. The immunomodulatory properties of CD4(+)CD25(+) T cells do extend to Th2 responses, most notably by limiting the development of a proinflammatory CD4(+) Th2 phenotype characterized by reduced cytokine production. An understanding of the roles of CD4(+)CD25(+) T cells in vivo could provide better insight into the design of novel approaches to modulate the chronic airway inflammatory reaction evident in bronchial asthma.

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