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The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) epidemic continues to spread globally. The rapid dispersion of coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 drives an urgent need for effective treatments, especially for patients who develop severe pneumonia. The excessive and uncontrolled release of pro-inflammatory cytokines has proved to be an essential factor in the rapidity of disease progression, and some cytokines are significantly associated with adverse outcomes. Most of the upregulated cytokines signal through the Janus kinase-signal transducer and activator of transcription (JAK/STAT) pathway. Therefore, blocking the exaggerated release of cytokines, including IL-2, IL-6, TNF-α, and IFNα/β/γ, by inhibiting JAK/STAT signaling will, presumably, offer favorable pharmacodynamics and present an attractive prospect. JAK inhibitors (JAKi) can also inhibit members of the numb-associated kinase (NAK) family, including AP2-associated kinase 1 (AAK1) and cyclin G-associated kinase (GAK), which regulate the angiotensin-converting enzyme 2 (ACE-2) transmembrane protein and are involved in host viral endocytosis. According to the data released from current clinical trials, JAKi treatment can effectively control the dysregulated cytokine storm and improve clinical outcomes regarding mortality, ICU admission, and discharge. There are still some concerns surrounding thromboembolic events, opportunistic infection such as herpes zoster virus reactivation, and repression of the host's type-I IFN-dependent immune repair for both viral and bacterial infection. However, the current JAKi clinical trials of COVID-19 raised no new safety concerns except a slightly increased risk of herpes virus infection. In the updated WHO guideline, Baricitinb is strongly recommended as an alternative to IL-6 receptor blockers, particularly in combination with corticosteroids, in patients with severe or critical COVID-19. Future studies will explore the application of JAKi to COVID-19 treatment in greater detail, such as the optimal timing and course of JAKi treatment, individualized medication strategies based on pharmacogenomics, and the effect of combined medications.

Current cancer treatment strategies have been advanced by chimeric antigen receptor (CAR) cell therapy, a rapidly emerging cellular immunotherapy. The numerous revolutionary achievements of CAR T cells against hematological malignancies initiated an upsurge in research on translating this therapy into a treatment for solid tumors. Unfortunately, no equivalent success has yet been achieved in treating solid tumors. The main challenges posed by solid tumors have gradually been recognized and include a lack of unique antigen targets, antigen heterogeneity, limited infiltration into the tumor, and an immunosuppressive tumor microenvironment. Surmounting the limitations of solid tumors remains critical in popularizing CAR T cell applications. Various approaches to augmenting the efficiency of CAR T cells through directly optimizing CAR constructs or through innovative combination strategies such as vaccines, biomaterials, and oncolytic virus have arisen. In addition to describing the main obstacles that restrict the promotion of CAR T cells, this paper focuses on reviewing new ongoing strategies to circumvent these limitations.

Rationale Thrombotic thrombocytopenic purpura (TTP) is a critical thrombotic microangiopathy involving multiple organs. To the best of our knowledge, there are no reports of TTP complicated by acute aortic dissection. Patient concerns We herein described a 53-year-old male with TTP who did not have a significant medical history. After immediate plasma exchange and glucocorticoid therapy, the patient's clinical condition improved. However, the patient suddenly experienced chest pain with elevated blood pressure. Diagnoses Computed tomography angiography suggested acute type B aortic dissection. Interventions The patient was immediately transferred to the cardiac aortic surgery department for thoracic aortic endovascular repair. Outcomes The patient was discharged after successful thoracic aortic endovascular repair. Unfortunately, 3 months later, the patient experienced chest and back pain at home and died suddenly, possibly due to the recurrence of aortic dissection. Lessons Even if patients have no identifiable risk factors, physicians should be aware of this rare and life-threatening acute complication of TTP, which may have multiple causes, including preexisting connective tissue disease, abnormal blood pressure fluctuations, and increased risk of hemorrhage. Early identification and timely treatment of acute aortic dissection are critical for improving prognosis.