Human Germinal Center CD4+ CD57+ T Cells Act Differently On B Cells Than Do Classical T-Helper Cells

We have isolated two subtypes of helper T cells from human tonsils: CD4+ CD57+ cells, mostly located in the germinal center (GC), and CD4+ CD57- cells, distributed through the interfollicular areas but also present in the GC. In a functional study, we have compared the capacities of these T-cell subtypes to stimulate B cells in cocultures. In order to block T-cell proliferation while maintaining their activation level, we pretreated isolated T cells with mitomycin C prior to culture in the presence of B cells and added polyclonal activators such as PHA and Con A, combined or not with IL-2. Contrary to CD4+ CD57- cells, CD4+ CD57+ cells did not markedly enhance B-cell proliferation. Even when sIgD-B cells typical of germinal center cells were tested, the CD4 CD57 cells had no significant effect. This is in accordance with the location of these cells: They mainly occupy the light zones of the GC where few B cells divide. Even when added to preactivated, actively proliferating cells, CD4+ CD57+ cells failed to modulate B-cell multiplication. On the supernatants of B-cell-T-cell cocultures, we examined by the ELISA technique the effect of T cells on Ig synthesis. Contrary to CD57- T cells, whose effect was strong, CD57+ T cells weakly stimulated Ig synthesis. More IgM than IgG was generally found. Because CD57 antigen is a typical marker of natural killer cells, we tested the cytolytic activity of tonsillar CD4+ CD57+ cells on K562 target cells. Unlike NK cells, neither CD4+CD57+ nor CD4+ CD57- cells exhibit any cytotoxicity. Thus, germinal center CD4+ CD57+ cells are not cytolytic and do not strongly stimulate either B-cell proliferation or Ig secretion. CD4+ CD57- cells, however, enhance B-cell proliferation and differentiation, thus acting like the classical helper cells of the T-dependent areas

Human FDC express PrPc in vivo and in vitro

Prion diseases are fatal neurodegenerative disorders caused by accumulation of abnormal prion protein (protease-resistant prion, PrPres). PrPres accumulation is also detected in lymphoid organs after peripheral infection. Several studies suggest that follicular dendritic cells (FDC) could be the site of PrPres retention and amplification

Lysozyme as a cotreatment during antibiotics use against vaginal infections: An in vitro study on Gardnerella vaginalis biofilm models

Bacterial vaginoses are frequent in women, most of them involving Gardnerella vaginalis. In more than 50% of the cases, usual antibiotic treatments are not capable of eliminating completely the infection, leading to recurrent vaginosis. In addition to the appearance of antibiotic resistance, recurrence can be due to the development of a biofilm by G. vaginalis. In vitro experiments on G. vaginalis biofilms showed that the biofilm protected bacteria from the antibiotic clindamycin. Also, recombinant human lysozyme (rhLys) was able to both degrade biofilms and prevent their formation. This degradation effect persisted whenever other vaginal commensal or pathogenic microorganisms were added to the culture and on each tested clinical biofilm-producing strain of G. vaginalis. The co-administration of rhLys and clindamycin or metronidazole improved both antibiotics’ efficiency and lysozyme-driven biofilm degradation. The comparison of both clindamycin and metronidazole antibacterial spectra showed that metronidazole was preferable to treat vaginosis. This suggests that human lysozyme could be added as an anti-biofilm cotreatment to vaginal antibiotherapy, preferably metronidazole, against Gardnerella vaginalis infection in vivo. [Int Microbiol 19(2): 101-107 (2016)]Keywords: Gardnerella vaginalis · recombinant human lysozyme · clindamycin · metronidazole · biofilms in pathogen

Do Bovine Lymphocytes Express a Peculiar Prion Protein?

The cellular prion protein (PrPc) is a glycolipid-anchored cell surface protein that usually exhibits three glycosylation states. Its post-translationally modified isoform, PrPsc, is involved in the pathogenesis of various transmissible spongiform encephalopathies (TSEs). In bovine species, BSE infectivity appears to be restricted to the central nervous system; few or no detectable infectivity is found in lymphoid tissues in contrast to scrapie or variant CJD. Since expression of PrPc is a prerequisite for prion replication, we have investigated PrPc expression by bovine immune cells. Lymphocytes from blood and five different lymph organs were isolated from the same animal to assess intra- and interindividual variability of PrPc expression, considering six individuals. As shown by flow cytometry, this expression is absent or weak on granulocytes but is measurable on monocytes, B and T cells from blood and lymph organs. The activation of the bovine cells produces an upregulation of PrPc. The results of our in vitro study of PrPc biosynthesis are consistent with previous studies in other species. Interestingly, western blotting experiments showed only one form of the protein, the diglycosylated band. We propose that the glycosylation state could explain the lack of infectivity of the bovine immune cells

Expression of Growth Hormone Receptors by Lymphocyte subpopulations in the Human tonsil

The ability of human tonsillar lymphoid cells to express growth hormone receptor (hGH-N-R) was analyzed by flow cytometry. FITC-coupled recombinant human growth hormone (hGH-N) was used to reveal the receptors, in combination with phenotype markers

Etude des plaques de Peyer de l'intestin du souriceau nouveau-né comme voie possible de pénétration du virus du cancer mammaire de la souris (MMTV)

Peer reviewe

Tolerance to the Foeto-Placental 'Graft': Ten Ways to Support a Child for Nine Months

Tolerance to the foetal 'allograft' has been extensively studied in the past few years, providing interesting new insights. In addition to a potential role for HLA-G, which has been widely discussed, there are hypotheses suggesting roles for several other molecules or cells: leukemia inhibitory factor and its receptor; indoleamine 2. 3-dioxygenase; the Th1/Th2 balance; suppressor macrophages; hormones such as progesterone or the placental growth hormone; CD95 and its ligand; and, as recently proposed, annexin II. Tolerance of the foetal allograft is probably the consequence of a wide panel of mechanisms that may or may not be pregnancy-specific, that are of major or secondary importance and that may be interconnected

DNA immunisation. New histochemical and morphometric data.

Splenic germinal center reactions were measured during primary response to a plasmidic DNA intramuscular injection. Cardiotoxin-pretreated Balb/c mice were immunized with DNA plasmids encodmg or not the SAG1 protein, a membrane antigen of Toxoplasma gondii. Specific anti-SAG1 antibodies were detected on days 16 and 36 after injection of coding plasmids. The results of ELISAs showed that the SAG1-specific antibodies are of the IgG2a class. Morphometric analyses were done on serial immunostained cryosections of spleen and draining or non-draining lymph nodes. This new approach made it possible to evaluate the chronological changes induced by DNA immunisation in the germinal centres (in number and in size). Significant increases in the number of germinal centres were measured in the spleen and only in draining lymph nodes after plasmid injection, the measured changes of the germinal centers appeared to result from the adjuvant stimulatory effect of the plasmidic DNA since both the coding and the noncoding plasmid DNA induced them. No measurable changes were recorded in the T-dependent zone of lymph organs

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