Chimeric antigen receptor (CAR) T-cell therapy is highly effective in the treatment of B-cell acute lymphoblastic leukemia (ALL) or B-cell lymphoma, providing alternative therapeutic options for patients who failed to respond to conventional treatment or relapse. Moreover, it can bridge other therapeutic strategies and greatly improve patient prognosis, with broad applicable prospects. Even so, 30–60% patients relapse after treatment, probably due to persistence of CAR T-cells and escape or downregulation of CD19 antigen, which is a great challenge for disease control. Therefore, understanding the mechanisms that underlie post-CAR relapse and establishing corresponding prevention and treatment strategies is important. Herein, we discuss post-CAR relapse from the aspects of CD19-positive and CD19-negative and provide some reasonable prevention and treatment strategies.

Chimeric antigen receptor (CAR) T-cell therapy exhibits desirable and robust efficacy in patients with acute lymphoblastic leukemia (ALL). Stimulated by the revolutionized progress in the use of FDA-approved CD19 CAR T cells, novel agents with CAR designs and targets are being produced in pursuit of superior performance. However, on the path from bench to bedside, new challenges emerge. Accessibility is considered the initial barrier to the transformation of this patient-specific product into a commercially available product. To ensure infusion safety, profound comprehension of adverse events and proactive intervention are required. Additionally, resistance and relapse are the most critical and intractable issues in CAR T-cell therapy for ALL, thus precluding its further development. Understanding the limitations through up-to-date insights and characterizing multiple strategies will be critical to leverage CAR T-cell therapy flexibly for use in clinical situations. Herein, we provide an overview of the application of CAR T-cell therapy in ALL, emphasizing the main challenges and potential clinical strategies in an effort to promote a standardized set of treatment paradigms for ALL.

Psoriasis is a multifactorial immune-mediated disease. The highly effective and eligible treatment for psoriasis is limited, for its specific pathogenesis is incompletely elucidated. Skin microbiota is a research hotspot in the pathogenesis of immune-mediated inflammatory skin diseases nowadays, and it may have significant involvement in the provocation or exacerbation of psoriasis with broadly applicable prospects. It is postulated that skin microbiota alternation may interplay with innate immunity such as antimicrobial peptides and Toll-like receptors to stimulate T-cell populations, resulting in immune cascade responses and ultimately psoriasis. Achieving a thorough understanding of its underlying pathogenesis is crucial. Herein, we discuss the potential immunopathogenesis of psoriasis from the aspect of skin microbiota in an attempt to yield insights for novel therapeutic and preventive modalities for psoriasis.