Corneal infections are frequent and potentially vision-threatening diseases, and despite the significance of the immunological response in animal models of microbial keratitis (MK), it remains unclear in humans. The aim of this study was to describe the cytokine profile of tears in patients with MK. Characteristics of ocular lesions such as size of the epithelial defect, stromal infiltration, and hypopyon were analyzed. Immunological evaluation included determination of interleukine (IL)-1β, IL-6, IL-8, IL-10, IL-12 and tumor necrosis factor (TNF)-α in tear samples obtained from infected eyes of 28 patients with MK and compared with their contralateral non-infected eyes. Additionally, frequency of CD4+, CD8+, CD19+ and CD3−CD56+ cells was also determined in peripheral blood mononuclear cells in patients with MK, and compared with 48 healthy controls. Non-significant differences were observed in the size of the epithelial defect, stromal infiltration, and hypopyon. Nevertheless, we found an immunological profile apparently related to MK etiology. IL-8 > IL-6 in patients with bacterial keratitis; IL-8 > IL-6 > IL-1β and increased frequency of circulating CD3−CD56+ NK cells in patients with gram-negative keratitis; and IL-8 = IL-6 > IL-1β in patients with fungal keratitis. Characterization of tear cytokines from patients with MK could aid our understanding of the immune pathophysiological mechanisms underlying corneal damage in humans.

Aim: To evaluate the frequency, phenotype and the potential function of CD57+ T cell subsets in patients with pars planitis. Methods: CD4+CD57+ and CD8+CD57+ T cells were quantitated in peripheral blood from 15 patients with pars planitis and 15 healthy controls. To evaluate the phenotype and potential function of CD57+ T cell subsets CCR7, CD27, CD28, CD45RA, CD45RO, intracellular IFN-c, IL-4, perforin and granzyme-A expression were assessed by flow cytometry. Results: CD57+ T cells subsets were increased in patients with pars planitis (p = 0.002). The majority of CD4+CD57+ T cells were CCR72CD272CD282CD45RO+, while the most CD8+CD57+ T cells were CCR72CD272CD282CD45RA+. The number of cells positive for intracellular IFN-c and IL-4 was higher in the CD57+ T cell populations. A greater number of CD8+CD57+ T cells than CD8+CD572 T cells were positive to perforin (p = 0.006) and granzyme-A (p = 0.01). Conclusions: CD57+ T cells had a phenotype associated with peripheral memory (CCR72CD272CD282). Cytokine production by CD57+ T cells suggests that these cells may play a role in helper cell regulation. High expression of intracellular proteins involved in cytotoxicity suggests that CD8+CD57+ T cells may play an effector role. Taken together, this study proposes that CD57+ T cells function as memory-effector T cell subsets during pars planitis pathogenesis.

Summary In some chronic pathological conditions, antigen persistence activates and expands the CD4+ CD57+ T‐cell subset. The host immune response against tuberculosis infection is maintained through the continuous presence of antigen‐stimulated effector/memory helper T cells. To determine whether CD4+ CD57+ T cells were also expanded in human tuberculosis, we analysed (by flow cytometry) the phenotype of peripheral blood CD4+ T cells from 30 tuberculosis patients and 30 healthy controls. We observed a significant increase in the CD4+ CD57+ T‐cell subset in tuberculosis patients in comparison to healthy controls (P < 0·001). Most CD4+ CD57+ T cells exhibited a CD28− CD45RO+ CD62L− phenotype, which is associated with memory cells. In vitro, a higher number of antigen‐stimulated CD4+ CD57+ T cells produced intracellular interferon‐γ and interleukin‐4 compared with antigen‐stimulated CD4+ CD57− T cells (P < 0·001). These findings suggest that the majority of CD4+ CD57+ T cells correspond to a phenotype of activated memory T cells.

Taken together, these results could explain the anti-inflammatory in vivo effects observed when the amniotic membrane is used as a transplant.