Improving glycemic control in patients with type 2 diabetes mellitus through a peer support instant messaging service intervention (DiabPeerS): study protocol for a randomized controlled trial.

BACKGROUND: Diabetes mellitus is one of the four priority non-communicable diseases worldwide. It can lead to serious long-term complications and produces significant costs. Due to the chronicle character of the disease, it requires continuous medical treatment and good therapy adherence of those suffering. Therefore, diabetes self-management education (DSME) (and support DSMES) plays a significant role to increase patient's self-management capacity and improve diabetes therapy. Research indicates that these outcomes might be difficult to maintain. Consequently, effective strategies to preserve the positive effects of DSMES are needed. Preliminary results show that peer support, which means support from a person who has experiential knowledge of a specific behavior or stressor and similar characteristics as the target population, is associated with better outcomes in terms of HbA1c, cardiovascular disease risk factors or self-efficacy at a lower cost compared to standard therapy. Peer-supported instant messaging services (IMS) approaches have significant potential for diabetes management because support can be provided easily and prompt, is inexpensive, and needs less effort to attend compared to standard therapy. The major objective of the study is to analyze the impact of a peer-supported IMS intervention in addition to a standard diabetes therapy on the glycemic control of type 2 diabetic patients. METHODS: A total of 205 participants with type 2 diabetes mellitus will be included and randomly assigned to an intervention or control group. Both groups will receive standard therapy, but the intervention group will participate in the peer-supported IMS intervention, additionally. The duration of the intervention will last for 7 months, followed by a follow-up of 7 months. Biochemical, behavioral, and psychosocial parameters will be measured before, in the middle, and after the intervention as well as after the follow-up. DISCUSSION: Type 2 diabetes mellitus and other non-communicable diseases put healthcare systems worldwide to the test. Peer-supported IMS interventions in addition to standard therapy might be part of new and cost-effective approaches to support patients independent from time and place. TRIAL REGISTRATION: ClinicalTrials.gov NCT04797429 . Registered on 15 March 2021.

Costimulatory signals potently modulate the T cell inhibitory capacity of the therapeutic CD11a antibody Efalizumab.

The therapeutic CD11a antibody Efalizumab interferes with psoriasis pathogenesis by blocking T cell activation and migration. We have performed a detailed analysis on its effects during the activation of human T cells and found that the capability of Efalizumab to inhibit proliferation and cytokine production of T cells critically depends on the quality and quantity of costimulatory signals. Efalizumab potently inhibited the proliferation and cytokine production of human T cells costimulated via ICOS, OX40, CD27 or 4-1BB, but did not significantly inhibit T cells that received stimuli via CD2 or CD28. The capacity of CD2 and CD28 signals to interfere with the T cell inhibitory effects of Efalizumab was also observed upon stimulation of T cells with allogeneic DC. Furthermore, studies with T cells from psoriasis patients indicated that Efalizumab therapy induces inhibition of T cell responses that can be reverted by CD2 or CD28 signals.

T cell stimulator cells, an efficient and versatile cellular system to assess the role of costimulatory ligands in the activation of human T cells.

It is well established that full activation of T cells requires the interaction of the TCR complex with the peptide-MHC complex (Signal 1) and additional signals (Signal 2). These second signals are generated by the interaction of costimulatory ligands expressed on antigen presenting cells with activating receptors on T cells. In addition, T cell responses are negatively regulated by inhibitory costimulatory pathways. Since professional antigen presenting cells (APC) harbour a plethora of stimulating and inhibitory surface molecules, the contribution of individual costimulatory molecules is difficult to assess on these cells. We have developed a system of stimulator cells that can give signal 1 to human T cells via a membrane bound anti-CD3 antibody fragment. By expressing human costimulatory ligands on these cells, their role in T cell activation processes can readily be analyzed. We demonstrate that T cell stimulator cells are excellent tools to study various aspects of human T cell costimulation, including the effects of immunomodulatory drugs or how costimulatory signals contribute to the in vitro expansion of T cells. T cell stimulator cells are especially suited for the functional evaluation of ligands that are implicated in costimulatory processes. In this study we have evaluated the role of the CD2 family member CD150 (SLAM) and the TNF family member TL1A (TNFSF15) in the activation of human T cells. Whereas our results do not point to a significant role of CD150 in T cell activation we found TL1A to potently costimulate human T cells. Taken together our results demonstrate that T cell stimulator cells are excellent tools to study various aspects of costimulatory processes.