Abstract
Cytokine cascades exist in many autoimmune disorders which amplify and sustain the autoimmune process and lead to chronic inflammatory injury to the host tissues. Increasing evidence indicates that chondrocytes can interact with T cells, which may be a crucial event in inflammatory arthritis. To address the reciprocal influences of cartilage-reactive T cells and chondrocytes, we constructed cartilage-reactive T cells by developing a type II collagen-specific chimeric antigen receptor (CII-CAR). An in vitro co-culture model of CII-CAR-T cells and fresh cartilage was developed, in which CII-CAR-T displayed specific proliferative capacity and cytokine release against fresh cartilage samples, and chondrocytes could respond to CII-CAR-T cells by secreting IL-6. The proposed model will help us to explore the possible cytokine cascades between cartilage-reactive T cells and cartilage.
Highlights
Cytokines are important mediators of immunity and major drivers of autoimmunity
Similar CD4-to-CD8 ratios were observed between collagen-specific chimeric antigen receptor (CII-chimeric antigen receptor (CAR))-transduced and control T cells (Figure 1D)
These results indicated that CII-CAR-T cells could release inflammatory cytokines against both fresh and FTcartilage and indirectly indicated that living chondrocytes might participate in the release of IL-6, which might enhance the inflammation response
Summary
Once the autoimmune process has been triggered, the cytokine cascades occur and play an important role in the pathogenesis [1]. Inflammatory arthritis, such as rheumatoid arthritis (RA) is one of the main diseases that cause the loss of labor and disability in the population [2, 3]. The cytokine network in RA is complex; pro-inflammatory cytokines, including tumor necrosis factor (TNF)-a, interleukin (IL)-6 and the mediators produced through downstream pathways constitute the milieu driving neoangiogenesis. T cell-mediated inflammation is closely related to the occurrence and development of RA [7,8,9,10]
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