The microenvironment of lymphoma is an important factor affecting the development of lymphoma, which is involved in regulating the recognition and immune response of lymphoma cells by the immune system. In the era of immunotherapy of lymphoma, the state of microenvironment also affects the effect of monoclonal antibodies, small molecular compounds and other immune targeting drugs on lymphoma cells. Among them, microenvironment-related immune escape is one of the key factors leading to the failure of lymphoma treatment. This article reviews some microenvironment factors such as stromal immune cell subsets, vascular proliferation, hypoxia, immune checkpoint and the recent research progress of immune escape.

ObjectiveTo investigate the role of platelet in mouse pulmonary microvascular endothelial cell (PMVEC) injury caused by lipopolysaccharide( LPS)-activated neutrophil.MethodsPMVECs were obtained from pathogen-free C3H/HeN mice of both sexes aged 6-8 weeks weighing 18-25 g according to the method described by Lim YC et al.Platelets and neutrophils were isolated from mouse blood by twice centrifugation and denaity gradient centrifugation respectively.PMVECs were seeded into twelve- or six-well plates ( 1 or 2 ml/well) after 2-5 passages and were randomly divided into 4 groups (n =31 each): group LPS; group platelets (group P);group neutrophils (group N) and group platelets + neutrophils (group PN).Each well contained about 5 × 107/ml platelets and/or 5 × 105/ml neutrophils respectively.PMVECs were incubated with LPS1 μg/ml at 37 ℃ in a 5％ CO2 humidified atmosphere for 1,6,12,18 and 24 h respectively in all 4 groups.The cells were examined with phase contrast microscope for morphological changes and survival condition.Viability rate,apoptotic rate and activation rate of PMVECs were detected by flow cytometry at each time points.ResultsThere was no significant difference in morphology and number of endothelial cells (ECs) among the 4 groups,while the number of activated ECs was significantly increased but the number of living cells decreased in group PN compared with group LPS.The activation rate of ECs was significantly higher after being incubated with LPS for 6-12 h in groups P and N than in group LPS.The viability rate was significantly lower,while the apoptotic rate and activation rate were significantly higher after ECs were incubated with LPS in group PN than in groups LPS,P and N.ConclusionPlatelets play a decisive role in mouse PMVEC injury induced by LPS activated neutrophils.

Objective To investigate the related risk factors of cerebral microbleeds (CMBs) and their relations with leukoaraiosis and lacunar infarction in patients with cerebrovascular disease.Methods One hundred and sixty-four patients with cerebrovascular disease,admitted to our hospital from January 2015 and January 2017 were chosen;susceptibility weighted imaging (SWI) was performed,and the distribution and number of CMBs were recorded by Microbleed Anatomical Rating Scale (MARS).The demographic data,personal history,previous medical history,biochemical indices and imageological examination results of the patients were collected and multivariate Logistic regression analysis was carried out on the basis of these data.Spearman dependence analysis was used to analyze the relations of CMBs with leukoaraiosis and lacunar infarction.Results Age (OR=1.071,P=0.024,95％ CI:1.009-1.137),hypertension (OR=3.875,P=0.012,95％CI:1.347-11.148),leukoaraiosis(OR=2.080,P=0.005,95％ CI:1.245-3.475),lacunar infarction (OR=2.326,P=0.003,95％ CI:1.336-4.050) were independently associated with CMBs.And number of CMBs had positive correlation with severity of leukoaraiosis and number of lacunar cerebral infarcts (r=0.564,P=0.000;r=0.762,P=0.000).Conclusion Age,hypertension,leukoaraiosis,and lacunar infarction are the independent risk factors of CMBs;the severity of CMBs is positively correlated with severity of leukoaraiosis and lacunar infarction.