Animal models of rheumatoid arthritis (RA) are essential for studying the pathogenesis of RA in vivo and determining the efficacy of anti‑RA drugs. During the past decades, numerous rodent models of arthritis have been evaluated as potential models and the modeling methods are relatively well‑developed. Among these models, the collagen‑induced arthritis (CIA) mouse model is the first choice and the most widely used because it may be generated rapidly and inexpensively and is relatively similar in pathogenesis to human RA. To date, there have been numerous classic studies and reviews discussing related pathogeneses and modeling methods. Based on this knowledge, combined with the latest convenient and effective methods for CIA model construction, the present review aims to introduce the model to beginners and clarify important details regarding its use. Information on the origin and pathogenesis of the CIA model, the protocol for establishing it, the rate of successful arthritis induction and the methods used to evaluate the severity of arthritis are briefly summarized. With this information, it is expected that researchers who have recently entered the field or are not familiar with this information will be able to start quickly, avoid unnecessary errors and obtain reliable results.

Leukocyte immunoglobulin‑like receptor B2 (LILRB2) functions as an immunosuppressive receptor that has a prominent role in immune regulation. The expression of LILRB2 is higher in a variety of solid malignant tumors compared with that in corresponding normal tissues. LILRB2 can be expressed in tumor cells and tumor stromal cells within the tumor microenvironment. Upregulation of LILRB2 in tumors is significantly associated with a poorer tumor phenotype, increased tolerance to certain therapeutic drugs, tumor immune escape and shorter patient overall survival time. Therefore, LILRB2 can be utilized as a novel biomarker to predict the prognosis of patients with solid malignant tumors, and targeting LILRB2 may be an effective strategy for targeted cancer therapy. The present review provides a general overview of the role and mechanisms of LILRB2 in the microenvironment of solid tumors, and emphasizes the significance of targeting LILRB2 as a promising approach for tumor‑specific therapy.

CD147 is a T cell activation-associated molecule which is closely involved in the formation of the immune synapse (IS). However, the precise role of CD147 in T cell activation and IS formation remains unclear. In the present study, we demonstrated that CD147 translocated to the IS upon T cell activation and was primarily distributed in the peripheral super molecular cluster (p-SMAC). The knock down of CD147 expression in T cells, but not in B cells, impaired IS formation. CD147 participated in IS formation between T cells and different types of antigen-presenting cells (APCs), including macrophages and dendritic cells. Ligation of CD147 with its monoclonal antibody (mAb) HAb18 effectively inhibited T cell activation and IL-2 secretion. CD98, a critical molecule interacting with CD147, was distributed in IS in a CD147-dependent way. Phosphorylation levels of T cell receptor (TCR) related molecules, like ZAP-70, ERK, and cJun, were down-regulated by CD147 ligation, which is crucial for the interaction of CD147 and TCR signaling transduction. CD147 is indispensable for the formation of immune synapses and plays an important role in the regulation of its function.