Background: The progression of systemic lupus erythematosus (SLE) leads to anemia in patients, adversely affecting prognosis. The diverse causes of anemia may include excessive eryptosis or premature suicidal erythrocyte death characterized by cell shrinkage and phosphatidylserine (PS) exposure on the cell surface. The present study explored if SLE enhances eryptosis and the underlying mechanisms. Materials and Methods: Eryptosis was assessed using flow cytometry in healthy volunteers (n = 20) and anemic patients hospitalized for SLE (n = 22), for parameters including PS exposure, cell volume, cytosolic calcium ion (Ca²⁺) levels and reactive oxygen species (ROS) and ceramide abundance. These indicators were measured in erythrocytes of experimental subjects and erythrocytes treated with plasma from healthy volunteers or SLE patients. Results: The hemoglobin and hematocrit levels were significantly lower in anemic SLE patients than in healthy volunteers (***p<0.001, p<0.001, respectively). The percentage of PS-exposing erythrocytes was significantly higher in SLE patients than in healthy volunteers (p<0.001), accompanied by an increase in cytosolic Ca²⁺ levels, oxidative stress. The measurements of PS and Ca²⁺ levels were significantly higher in the erythrocytes of healthy volunteers following incubation in plasma of SLE patients than in plasma of healthy volunteers for 24h (***p<0.001, *p<0.05 respectively). Conclusion: Eryptosis is enhanced in SLE and may contribute to anemia. The probable underlying mechanisms may be an excessive formation of ROS in erythrocytes. Also, some plasma components may trigger eryptosis by increasing the cytosolic Ca²⁺ concentration.

Long non-coding RNAs (lncRNAs) are increasingly recognized to play important roles in multiple autoimmune diseases. This study aimed to evaluate the association of four lncRNAs (ANRIL, lnc-DC, MALAT1, ZFAS1) genes single nucleotide polymorphisms (SNPs) with susceptibility to rheumatoid arthritis (RA) patients, as well as their expression levels. Seventeen SNPs of the four lncRNAs were genotyped in a cohort of 660 RA patients and 710 controls using improved multiple ligase detection reaction (iMLDR). The lncRNAs expressions in peripheral blood mononuclear cells (PBMCs) from 120 RA patients and 120 controls were detected by qRT-PCR. No significant differences were found for the allele and genotype frequencies distribution of ANRIL SNPs (rs1412830, rs944796, rs61271866, rs2518723, rs3217992), lnc-DC SNPs (rs7217280, rs10515177), MALAT1 SNPs (rs619586, rs4102217, rs591291, rs11227209, rs35138901), ZFAS1 SNPs (rs237742, rs73116127, rs6125607, rs6125608) between RA patients and normal controls (all P > 0.05). The genotype effects of dominant and recessive models were also evaluated, but no significant association was found. In addition, our results demonstrated that the rs944796 G allele, rs2518723 T allele, rs3217992 T allele frequencies were significantly associated with anti-CCP in RA patients (all P < 0.05). The haplotype CGTA frequency for ZFAS1 was significantly higher in RA patients (P = 0.036). Compared with normal controls, the expression levels of ANRIL, lnc-DC, MALAT1, ZFAS1 in PBMCs were significantly reduced in RA patients (all P < 0.001). Moreover, ZFAS1 expression was negatively associated with CRP in RA patients (P = 0.002). In summary, ANRIL, lnc-DC, MALAT1, and ZFAS1 genes SNPs were not associated with RA susceptibility, while altered ANRIL, lnc-DC, MALAT1, ZFAS1 levels in RA patients suggested that these lncRNAs might play a role in RA.

This study established the reference values for kaolin-activated TEG in the target Chinese population, which might provide a reference for both clinical and laboratory studies.

These data revealed that RF-PRT effectively inhibited proliferation and induced apoptosis of lymphocytes by promoting GADD45α expression, which subsequently activates p38 and JNK signaling pathways.

Background: Cold agglutinins are auto-antibodies that can be a nuisance in cross matching and in blood grouping. Here we report an unusual case of a high titer and wide amplitude cold agglutinin reduced by plasmapheresis. Methods and Materials: A 56-year-old man with severe anemia requested a transfusion of red blood cells. However, there was a problem in blood for blood grouping. The discrepancy of blood typing was subsequently resolved using group O absorbed plasma along with repetition of forward grouping with warm-washed red blood cells. The presence of high-thermal-amplitude and a high-titer anti-I cold agglutinin were detected in further serologic investigation. It revealed reactivity against autologous and adult O red blood cells at 37˚C by the thermal amplitude screening test, and demonstrated a very high titer of 65,536 against adult O cells by titration studies at 4˚C. The patient received two plasma exchange sessions of 1.5 plasma volumes each. There was a significant reduction of the titer of cold agglutinins and of the thermal amplitude by plasmapheresis as well (p < 0.01). Results: After successful cross-matching with post plasma exchanges, four units of red blood cells were infused to the patient without any hemolysis symptoms or signs. Conclusions: We now reported a patient with abnormally ascended titer of cold agglutinins and wide-thermal-amplitude, but we also successfully performed ABO typing and cross matching after 2 plasma exchange sessions of 1.5 plasma volumes each.