CD22 is a critical inhibitory coreceptor predominantly expressed on the surface of B cells, playing a pivotal role in modulating B cell receptor (BCR) signaling and maintaining immune homeostasis. Its high B cell lineage specificity, rapid internalization capacity, and signal attenuation mediated by immunoreceptor tyrosine-based inhibitory motifs (ITIMs) render it an ideal therapeutic target for B cell-related pathologies. In recent years, CD22-targeted therapeutic strategies have demonstrated significant clinical breakthroughs in the treatment of hematological malignancies and autoimmune diseases. These strategies encompass immunotoxins, radioimmunoconjugates, antibody–drug conjugates (ADCs), bispecific antibodies, and chimeric antigen receptor (CAR) T cell therapy. Notably, while monotherapies have achieved high response rates, dual-targeting approaches (e.g., CD19/CD22 CAR-T) have further mitigated the risk of antigen escape and profoundly enhanced long-term durable efficacy. This review systematically summarizes the molecular mechanisms of CD22 and the latest clinical advancements in its targeted therapies. Furthermore, we highlight the promising translational potential of CD22-targeted strategies—particularly CAR-T cell therapy—from oncology to the management of autoimmune disorders, outlining future research priorities within this rapidly evolving field.

Non-long terminal repeat (Non-LTR) retrotransposons are mobile genetic elements that replicate through a “copy-and-paste” mechanism, enabling their expansion within the genome. Aberrant activation of these elements can induce genomic instability, elicit cellular stress responses, and activate inflammasome signaling, leading to tissue injury and disease. The central process of sterile inflammation involves the release and recognition of damage-associated molecular patterns (DAMPs), endogenous molecules that initiate inflammatory responses and form a common basis for many sterile inflammatory disorders. Recent studies have identified non-LTR retrotransposons as key endogenous triggers of DAMP-like signaling that drive sterile inflammation in both neuronal and non-neuronal tissues, contributing to the development of neurodegenerative and other chronic inflammatory diseases. In this review, we summarize recent advances in understanding how non-LTR retrotransposons, particularly LINE and SINE elements, influence sterile inflammation and disease pathogenesis. We highlight how their mobilization reshapes genomic architecture and gene regulation, and how the resulting signaling cascades promote chronic inflammation, immune dysregulation, and tissue injury. We also discuss emerging therapeutic strategies aimed at suppressing retrotransposon activity or interrupting downstream inflammatory signaling for treating sterile inflammation-related diseases.