Poly(2-dimethylamino ethylmethacrylate)-Based Polymers To Camouflage Red Blood Cell Antigens

peer reviewedPoly(2-dimethylamino-ethylmethacrylate) (PDMAEMA) is a cationic polymer when dissolved in a 7.4 pH fluid. Owing to its ionic nature, this polycation interacts with the negatively charged cell membrane surface of red blood cells (RBCs). The electrostatic self-assembly of PDMAEMA on RBCs membrane can be employed for inducing the formation of a polymeric shield camouflaging blood group antigens on RBCs as a valuable strategy for developing “universal RBCs” for blood transfusion. The purpose of this research was to evaluate the camouflaging ability of PDMAEMA homopolymers and PDMAEMA-copoly(nethylene glycol) copolymers differing in molecular weight and architecture. Surprisingly, the PDMAEMAs caused a partially masking, no masking, and sensitization of the same RBCs population. The MW and architecture of the polymers as well as temperature of PDMAEMA-RBCs treatment influenced the results observed. Herein, the very particular reactivity of PDMAEMAs and RBCs is analyzed and discussed

Hepatitis C of genotype 2: the role of medical invasive exams.

BACKGROUND AND AIM: Hepatitis C virus genotype 2 is the third in order of frequency in Belgium. The aim of this study was to better define the genotype 2 carriers' epidemiology characteristics. METHODS: In a database comprising 1726 viremic hepatitis C virus patient from the south part of Belgium, the files of 98 genotype 2 carriers were reviewed. RESULTS: There was a strong association between genotype 2 and the mode of transmission. The rate of contamination by invasive medical exams was very high (23%), and statistically different from the one of the others genotypes. Eligibility for antiviral therapies and the rate of sustained viral response were high. CONCLUSION: HCV genotype 2 was highly associated with transmission by invasive medical exams.Peer reviewe

Determination of anti-tetanus antibodies using protein A labeled with iodine 125

We present a quantitative measurement of specific antitetanic IgG immunoglobulins with protein "A" labeled with I125. The Laurell's immunoelectrophoresis was the reference method. After having fixed optimum conditions of duration and temperature of de reaction, we studied the different concentrations of the coated antigen and also the different dilution of serum. We can so eliminate the most aspecific effects of the antigen-antibody reaction. The correlation between the two methods of measurement is more than 98%

Is 'ABO-D' really a ready-made package? Why these parameters should be analysed separately in correlation studies?

peer reviewe

Lymphocytes subsets before and after neoadjuvant polychemotherapy for head and neck cancers

peer reviewedSubpopulations of blood lymphocytes were quantified among head and neck cancer patients receiving a neoadjuvant chemotherapy. Significant changes took place : increase of T lymphocytes opposed to marked depletion of B cells and null cells. An effect against cancer is possible either by amplification of cytotoxicity as well as by decrease of suppressor function

Changes of lymphocytes subsets after neoadjuvant chemotherapy for head and neck cancers

Significant variations in lymphocytes subsets are observed in a population of 61 head and neck cancer patients receiving a neoadjuvant chemotherapy. Tumour regression seems to go along with amplification of T lymphocytes functions, increase of H/S ratio and fall in percentage of null cells

DO MESENCHYMAL STROMAL CELLS PROMOTE HLA SPECIFIC ANTIBODIES FORMATION AFTER INFUSION IN LIVER TRANSPLANT RECIPIENTS?

Background: Mesenchymal stromal cells (MSC) immunogenicity is debated. We recently published a prospective, controlled, phase I study evaluating a single administration of third-party MSC in 10 liver transplant recipients (LTR). Here, we focus on the development of antibodies (Ab) against MSC-donor HLA (MSCDSA) in LTR following MSC infusion. Methods: Ten LTR under standard immunosuppression received 3rd-party unrelated MSC on postoperative day 3, and were prospectively compared to 10 control LTR. Recipients and donor of either liver or MSC were genotyped for HLA A/B/C/DR/DQ. Recipients were tested for HLA Ab before and 1, 3 and 6 months after transplant by Luminex". Ab were considered as positive in case of MFI >1500 and in accordance with the manufacturer’s recommendations. Results: In MSC-treated group, 2 patients showed pre-transplant MSCDSA. During follow-up, MSCDSA were detected in 6 additional patients who had received multiple red blood cell allo-transfusions before and/or rapidly after transplant. These patients also developed Ab against various MSC-unrelatedHLA. Two patients did not develop any MSCDSA throughout the follow-up, and one of them did not receive any allo-transfusion. MFI of detected MSCDSA were not significantly different from MFI of other detected HLA Ab. In control group, 3 patients were sensitized pre-transplant, and 6 patients developed de novo multiple HLA Ab. Four of these had received multiple allo-transfusions. Conclusion: In the large pool of HLA Ab identified in LTR post transplant, the detection of MSCDSA is most likely caused by allo-transfusions rather than related to MSC infusion. Further studies are required to confirm that MSC are “immune privileged”

A KEL*02mod allele responsible for an apparent maternity exclusion

peer reviewedThe patient’s rare KEL:1,-2 phenotype was highlighted in course of a routine preoperative erythrocyte typing. Unexpectedly, her two daughters presented a KEL:-1,2 phenotype what appeared first as an apparent maternity exclusion. Flow cytometry, genotyping and adsorption-elution analyses were then performed for those 3 patients. KEL genotyping showed that the patient’s genotype was KEL*01/KEL*02 whereas that of her daughters was KEL*02/KEL*02. By using polyclonal anti-KEL2 reagent, weak amount of KEL2 was identified on the patient’s erythrocytes, a result which was confirmed by both flow cytometry and adsorption-elution assays, suggesting that patient’s phenotype was in fact KEL:1,2w. These results are in favour of a weak expressed KEL*02 allele (KEL*2mod) transmission coding for a KEL2 antigen detected in some technical conditions only. Those results allowed to explain the apparent maternity exclusion based on initial KEL phenotype. This study also seems to confirm the presence of a compensatory mechanism of the KELmod allele deficient expression in heterozygote patients. A KEL phenotype retrospective study of 80.000 subjects showed a local KEL:1,-2 frequency four times lower than that described in literature. Moreover, a significant number of those individuals would in reality be KEL:1,2w, what still would decrease the real frequency of the KEL:1,2 subjects