Primary blast lung injury is an acute lung injury caused by the direct impact of explosive shock wave acting on the lung;the serious case can develop acute respiratory distress syndrome,which is one of the leading causes of mortality in blast injury personnel.The pathophysiological characteristics of primary lung blast injury are relatively clear:rupture of the alveolar capillaries and subsequent intrapulmonary haemorrhage and edema,accompanied by oxidative stress,apoptosis,inflammatory reaction and other physiological processes.However,the molecular mechanism needs to be further studied.This paper focuses on the research progress of phosphatidylinositol 3-kinase/protein kinase,nuclear factor κB,mitogen-activated protein kinase and other signaling pathways in the research of primary blast lung injury.

T-cell inhibitory receptors(IR)are involved in the composing of co-inhibitory signaling pathways between T cells and immune cells,and transmit immunosuppressive signals to limit immune effects of T cells such as activation and proliferation.Ab-normal co-inhibitory signals may destroy the peripheral immune tolerance of the body,leading to hyperresponsiveness of various organ-specific autoimmunity.Rheumatoid arthritis(RA)is a complex systemic disease in which there is an immune disorder centered on T cells.In this process,the abnormal expression and distribution of T-cell IR are fully involved in the imbalance of T-cell subsets and pathological immune responses,affecting the development and progression of the disease.Targeting T-cell IR and its ligands and thus strengthening the co-inhibitory signaling pathway mediated by them has been studied for suppressing immune responses and maintain-ing immune tolerance,but their potential for clinical application in RA remains to be explored.In the present,we review the advances of T-cell IR involved in the immunopathology of RA,and discusses the therapeutic prospects of targeting these receptors.

T-cell inhibitory receptors(IR)are involved in the composing of co-inhibitory signaling pathways between T cells and immune cells,and transmit immunosuppressive signals to limit immune effects of T cells such as activation and proliferation.Ab-normal co-inhibitory signals may destroy the peripheral immune tolerance of the body,leading to hyperresponsiveness of various organ-specific autoimmunity.Rheumatoid arthritis(RA)is a complex systemic disease in which there is an immune disorder centered on T cells.In this process,the abnormal expression and distribution of T-cell IR are fully involved in the imbalance of T-cell subsets and pathological immune responses,affecting the development and progression of the disease.Targeting T-cell IR and its ligands and thus strengthening the co-inhibitory signaling pathway mediated by them has been studied for suppressing immune responses and maintain-ing immune tolerance,but their potential for clinical application in RA remains to be explored.In the present,we review the advances of T-cell IR involved in the immunopathology of RA,and discusses the therapeutic prospects of targeting these receptors.

Objective:To explore the impact of clinical features, serological indicators, and pulmonary function test (PFT) on the prognosis of rheumatoid arthritis-associated interstitial lung disease (RA-ILD).Methods:Clinical data of RA-ILD patients who were diagnosed by HRCT and were followed up in Changhai Hospital or Yancheng First People's Hospital from 2011 to 2021 were collected Respiratory functional impairment of the patients was evaluated according to the changes of HRCT score and PFT, and the patients were divided into progressive group and stable group. COX survival analysis and ROC curve were used to determine the factors related to the progression of RA-ILD.Results:Finally 98 RA-ILD patients were included. The mean age of ILD onset was (62.9±12.1) years old, the median course of RA was 7.0 (1.0, 15.3)years, and the median follow-up time was 36.5 months (14.0, 79.5). There were 49 cases in the progressive group, and the clinical characteristics and laboratory tests of the two groups were compared. The results showed that: progressive time [(23(8.5,43.0)months vs 63(32.5,90.9) months, Z=-4.55, P=0.001)], HRCT score [(115(109,135) vs 111(105,116), Z=-2.70, P=0.007)], forced vital capacity(FVC) predicted [(70.1±15.7)% vs (80.8±19.7)%, t=2.12, P=0.039)], diffusing capacity of the lungs for CO(DLCO) predicted [(57.5±16.3)% vs (83.4±18.8)%, t=4.87, P=0.001)], male [(44.9% vs 18.4%, χ2=7.97, P=0.005)], UIP pattern [(36(73.5%) vs 9(18.4%), χ2=29.96, P<0.001)], RF>200 U/ml[(21(65.6%) vs 18(41.9%), χ2=4.15, P=0.042)], anti-CCP>75 U/ml [(42(91.3%) vs 35(71.4%), χ2=6.10, P=0.013], all had significantly different between the two groups. In multivariate analyses, UIP[ HR(95% CI)=3.25(1.62,6.50), P<0.001], anti-CCP antibody >75 U/ ml[ HR(95% CI)=3.85 (1.20,12.33), P=0.023] and smoking [ HR (95% CI): 5.74(1.10, 30.13), P=0.039] were significantly correlated with the progression of pulmonary fibrosis in RA-ILD patients. PFT was performed in only 44 patients with RA-ILD. The univariate analyses and ROC curve suggested that DLCO predicted [ HR (95% CI)=1.04 (1.02,1.06), P<0.001] was a significant risk factor for the progression of RA-ILD, and the area under curve (AUC) of DLCO was 0.845 [95% CI=(0.729,0.961)]. Conclusion:UIP pattern, high titer of anti-CCP antibody, smoking, and reduced DLCO predicted % may be potential predictors for poor prognosis of RA-ILD patients.