Pro-inflammatory signaling pathways and associated cytokine responses in dendritic cells and CD4+ T cells

The pro-inflammatory signaling pathways and associated cytokine responses in dendritic cells (DCs) and CD4+ T cells represent a complex biological axis central to the adaptive immune response. Dendritic cells serve as primary antigen-presenting cells that detect pathogens through pattern recognition receptors, initiating intracellular signaling via the NF-κB and MAPK pathways [1]. This activation prompts DCs to secrete polarizing cytokines such as IL-12 and IL-23, which are essential for the differentiation of naive CD4+ T cells into pro-inflammatory Th1 and Th17 effector subsets [2]. These T cells subsequently produce cytokines like IFN-γ and IL-17, creating a self-reinforcing loop of inflammation [3]. While vital for host defense, chronic dysregulation of this axis is a primary driver of autoimmune diseases such as rheumatoid arthritis, psoriasis, and Crohn's disease [4]. Modern pharmacotherapy targets this system by utilizing monoclonal antibodies to neutralize specific cytokines or small molecules to inhibit signaling transducers like Janus kinases (JAKs) [5].

Other names

DC-T cell inflammatory axisDendritic cell-T cell signaling crosstalkPro-inflammatory cytokine cascade

Therapeutic strategies involve the neutralization of specific pro-inflammatory cytokines, blockade of their respective receptors, or the inhibition of downstream intracellular signaling enzymes such as Janus kinases (JAKs) and MAP kinases to suppress the overactive immune response.