BACKGROUND: Dendritic cells (DCs) are the most potent antigen-presenting cells involved in initiating the immune response, presenting antigens to T cells and leading to T cell proliferation. In an immature state, DCs lack accessory signals required for T cell stimulation but are highly specialised to capture antigens. Full DC maturation changes the cell surface phenotype and facilitates stimulation of T cell proliferative responses. To examine the degree of DC maturity associated with vernal keratoconjunctivitis (VKC), the authors examined the phenotype and antigen-presentation capability of blood derived DCs from VKC patients and from normal controls. METHODS: Flow cytometry was used to identify the cell surface expression of markers of DC maturity (CD83, CD86, major histocompatibility complex class II) and mixed leucocyte reactions to assess DC induction of T cell proliferation. RESULTS: DCs derived from VKC patients were of a more mature phenotype than those from normal controls. However, these VKC DCs had reduced capability for induction of T cell proliferation compared with DCs from controls. CONCLUSION: The increased maturity of DCs in VKC patients correlates with the heightened immune responsiveness associated with this disorder. A number of mechanisms may underlie the impaired ability of DCs in atopy to stimulate T cell proliferation. This impairment of DC induction of T cell activation is likely to be one factor which contributes to the modified inflammatory response seen in VKC patients and the recognised susceptibility of these patients to viral infection.
BACKGROUND: Dendritic cells (DCs) are the most potent antigen-presenting cells involved in initiating the immune response, presenting antigens to T cells and leading to T cell proliferation. In an immature state, DCs lack accessory signals required for T cell stimulation but are highly specialised to capture antigens. Full DC maturation changes the cell surface phenotype and facilitates stimulation of T cell proliferative responses. To examine the degree of DC maturity associated with vernal keratoconjunctivitis (VKC), the authors examined the phenotype and antigen-presentation capability of blood derived DCs from VKC patients and from normal controls. METHODS: Flow cytometry was used to identify the cell surface expression of markers of DC maturity (CD83, CD86, major histocompatibility complex class II) and mixed leucocyte reactions to assess DC induction of T cell proliferation. RESULTS: DCs derived from VKC patients were of a more mature phenotype than those from normal controls. However, these VKC DCs had reduced capability for induction of T cell proliferation compared with DCs from controls. CONCLUSION: The increased maturity of DCs in VKC patients correlates with the heightened immune responsiveness associated with this disorder. A number of mechanisms may underlie the impaired ability of DCs in atopy to stimulate T cell proliferation. This impairment of DC induction of T cell activation is likely to be one factor which contributes to the modified inflammatory response seen in VKC patients and the recognised susceptibility of these patients to viral infection.