Purpose Workplace bullying is a common negative event suffered by employees in the workplace. The harm it brings to the organization has become the focus of the field of organizational behavior. The purpose of this study was to explore whether workplace bullying has an impact on employee knowledge hiding and to discover the underlying mechanism between the two. Design/methodology/approach Based on the conservation of resource theory and the cognitive-affective personality system theory, this paper surveys 327R&D employees of Chinese technological corporations at two time points and explores the relationship between workplace bullying and knowledge hiding as well as the underlying mechanism. This study used confirmatory factor analysis, bootstrapping method and structural equation model to validate the research hypothesis. Findings The results show that workplace bullying positively correlates with knowledge hiding; emotional exhaustion and organizational identification play a mediation role between workplace bullying and knowledge hiding, and both variables play a chain mediation role in that relationship; and forgiveness climate moderates the positive impact of workplace bullying on emotional exhaustion, further moderating the chain mediation role of emotional exhaustion and organizational identification. Originality/value The findings of this study can not only complement the existing researches on the influence of negative workplace events on employees’ knowledge hiding behaviors but also strengthen scholars’ attention and understanding of the internal mechanism between workplace bullying and knowledge hiding.

The goal of cancer immunotherapy is to stimulate the host immune system to attack malignant cells. Antibody-dependent cellular cytotoxicity (ADCC) is a pivotal mechanism of antitumor action of clinically employed antitumor antibodies. IL-15 administered to patients with metastatic malignancy by continuous i.v. infusion at 2 μg/kg/d for 10 days was associated with a 38-fold increase in the number and activation status of circulating natural killer (NK) cells and activation of macrophages which together are ADCC effectors. We investigated combination therapy of IL-15 with rituximab in a syngeneic mouse model of lymphoma transfected with human CD20 and with alemtuzumab (Campath-1H) in a xenograft model of human adult T cell leukemia (ATL). IL-15 greatly enhanced the therapeutic efficacy of both rituximab and alemtuzumab in tumor models. The additivity/synergy was shown to be associated with augmented ADCC. Both NK cells and macrophages were critical elements in the chain of interacting effectors involved in optimal therapeutic responses mediated by rituximab with IL-15. We provide evidence supporting the hypothesis that NK cells interact with macrophages to augment the NK-cell activation and expression of FcγRIV and the capacity of these cells to become effectors of ADCC. The present study supports clinical trials of IL-15 combined with tumor-directed monoclonal antibodies.

IL-15 has potential as an immunotherapeutic agent for cancer treatment because it is a critical factor for the proliferation and activation of natural killer (NK) and CD8 ؉ T cells. Administration of anti-CD40 antibodies has shown anti-tumor effects in vivo through a variety of mechanisms. Furthermore, activation of CD40 led to increased expression of IL-15 receptor-␣ by dendritic cells, an action that is critical for trans-presentation of IL-15 to NK and CD8 ؉ T cells. In this study, we investigated the therapeutic efficacy of the combination regimen of murine IL-15 (mIL-15) with an agonistic anti-CD40 antibody (FGK4.5) in murine lung metastasis models involving CT26 and MC38, which are murine colon cancer cell lines syngeneic to BALB/c and C57BL/6 mice, respectively. Treatment with mIL-15 or the anti-CD40 antibody alone significantly prolonged survival of both CT26 and MC38 tumor-bearing mice compared with the mice in the PBS solution control group (P < 0.01). Furthermore, combination therapy with both mIL-15 and the anti-CD40 antibody provided greater therapeutic efficacy as demonstrated by prolonged survival of the mice compared with either mIL-15 or the anti-CD40 antibody-alone groups (P < 0.001). We found that NK cells isolated from the mice that received the combination regimen expressed increased levels of intracellular granzyme B and showed stronger cytotoxic activity on the target cells. The findings from this study provide the scientific basis for clinical trials using the combination regimen of IL-15 with an anti-CD40 antibody for the treatment of patients with cancer.animal model ͉ cancer immunotherapy ͉ IL-15 receptor-␣