γδ T cells have been shown to stimulate the recruitment and activation of neutrophils through the release of a range of cytokines and chemokines. Here, we investigated the reverse relationship, showing that human neutrophils suppress the function of human blood γδ T cells. We show that the upregulation of CD25 and CD69 expression, the production of IFN‐γ, and the proliferation of γδ T cells induced by (E)‐1‐hydroxy‐2‐methylbut‐2‐enyl 4‐diphosphate are inhibited by neutrophils. Spontaneous activation of γδ T cells in culture is also suppressed by neutrophils. We show that inhibitors of prostaglandin E2 and arginase I do not exert any effect, although, in contrast, catalase prevents the suppression of γδ T cells induced by neutrophils, suggesting the participation of neutrophil‐derived ROS. We also show that the ROS‐generating system xanthine/xanthine oxidase suppresses γδ T cells in a similar fashion to neutrophils, while neutrophils from chronic granulomatous disease patients only weakly inhibit γδ T cells. Our results reveal a bi‐directional cross‐talk between γδ T cells and neutrophils: while γδ T cells promote the recruitment and the activation of neutrophils to fight invading pathogens, neutrophils in turn suppress the activation of γδ T cells to contribute to the resolution of inflammation.

Interaction between hyaluronic acid (HA) and CD44 has been considered a key event in tumor invasion and metastasis. HA is a linear, high molecular weight glycosaminoglycan in its native state, but fragmented low molecular forms are found at sites of neoplastic or inflammatory infiltrates. Both high and low molecular weights HA are involved in diverse biological functions. In this study, we used two clonal variants of a T cell murine lymphoma designated LBLa and LBLc. These cell lines were found to differ in their in vivo and in vitro growth rates. LBLa grew faster and exhibited an enhanced invasive capacity as compared to LBLc. In contrast, cell lines did not differ in the expression of surface markers (CD8, CD24, CD25, CD44, and CD18), or in their capacity to bind HA. However, LBLa cells exhibited higher capacity to migrate to low molecular weight HA than did LBLc. Migration was mediated by CD44 since it was abrogated by anti-CD44 monoclonal antibody as well as by hyaluronidase. We suggest that interaction between CD44 and low molecular weight HA may trigger migration mechanisms in LBLa cells, thus contributing to enhanced invasive cell capacity.

BACKGROUND The prevalence of obstructive sleep apnea (OSA) increases with age. However, older adults have limited perception of the symptoms related with poor sleep quality. Objectives To know the frequency and characteristics of age-related OSA in a large population with clinical suspicion of sleep apnea. Methods We conducted a retrospective study. OSA was studied by respiratory polygraphy (RP). Patients were grouped by age (G): GI was between 18-45; GII: 46-65 and GIII > 65 years old. Other demographic characteristics, symptoms and RP indicators were compared. Epworth Sleep Scale (ESS) was used to analyze symptoms. Results We included 2491 patients with sleep apnea symptoms. OSA frequency (AHI > 15) in each group was 33.2 % in GI; 45.8 in GII and 50.3 in GIII (p < 0.001). Despite the significant increase in OSA severity, GIII group reported fewer symptoms (ESS: 6.0; p < 0.001). Multivariate adjusted analysis showed that the odds ratio of having OSA is three times as high at age > 65 (OR: 3.32 (2.29 - 4.88) p < 0.001). Conclusions As in previous reports, OSA prevalence in our population was higher among the elderly. The early identification of this syndrome in a population with poor perception of symptoms would aid to improve patient management.