Disease relevance of Rosette Formation

• As indicated by rosette formation of the sensitized platelets around protein A-Sepharose beads, two quinine- and two quinidine-dependent antibodies reacted with both normal and Bernard-Soulier syndrome platelets at a high (300 microM) concentration of drug [1].
• Sera of children with kwashiorkor containing the E rosette inhibitory substance did not inhibit in vitro rosette formations by autologous lymphocytes whereas rosette formations by homologous lymphocytes were inhibited [2].
• In both species, regardless of gender, with > or = 3 mg/kg cisplatin treatment (lethal dose) at day 0, retinal damage characterized by the appearance of aggregations of TUNEL-positive cells scattered in the undifferentiated neuroblastic layer was seen at 24 hrs, and led to rosette formation at day 3 and 7 (retinal dysplasia) [3].
• The ability of acute sera to inhibit rosette formation was not significantly different between 18 cerebral malaria cases and 20 controls tested [mean reduction in rosetting rate 6.1% (SD 11.5) versus 8.4% (SD 12.3), P = 0.57] [4].
• The sera from 51 patients with schistosomiasis were studied for the presence of circulating immune complexes (IC) using two methods, inhibition of EAC rosette formation and precipitation of radio-labelled Clq [5].

High impact information on Rosette Formation

• Addition of simple sugars to the assay mixture has little effect, but rosette formation is inhibited by a series of mannose-rich glycoproteins (yeast invertase, yeast mannans and horseradish peroxidase) [6].
• The other downregulated both CR1 and CR2, although not as efficiently as 7G6, and was unable to inhibit EC3d rosette formation [7].
• IgG preparations from the serum of some P. falciparum-immune donors and heparin inhibited rosette formation [8].
• In the present study using mouse serum-induced thioglycollate-elicited peritoneal M phi (TPM) as a model system for SER expression, mAb SER-4 IgG2a completely blocked rosette formation at 1 microgram/ml [9].
• Pretreatment of RBMM with trypsin prevented rosette formation, but neuraminidase enhanced it [10].

Chemical compound and disease context of Rosette Formation

• In the present study, we investigated whether RBCs of species besides mice have the structure recognized by anti-A. niger glucose oxidase mAb by using rosette-formation and complement-mediated hemolysis [11].
• Study of spontaneous rosette formation and changes of sialic acid content in the surface glycoproteins of macrophages induced by hamster transplantable melanomas [12].
• Subnormal inhibition of active E rosette formation by isoproterenol in bronchial asthma [13].
• In order to establish the possible relationship between serum changes occurring during hemolysis and reduction of SRC-rosetting lymphocytes, the effect in vitro of varying concentrations of bilirubin and hemoglobin on the rosette formation capacity of lymphocytes was studied [14].

Biological context of Rosette Formation

• The antibody specificity was confirmed by immunoprecipitation of CR1 from extracts of surface-labeled cells, by inhibition of rosette formation between B lymphocytes and the erythrocytes intermediate EAC14oxy23b, and by the characteristic distribution of the antigen among cells of human peripheral blood [15].
• Detection of nerve growth factor binding sites on neuroblastoma cells by rosette formation [16].
• During the first 24 hr in culture, IgG-mediated phagocytosis and C3-mediated rosette formation declined [17].
• IgG-BF were affinity purified on Sepharose beads coated with rabbit or mouse IgG and identified by their biologic activities, i.e., inhibition of in vitro secondary IgG antibody production to SRBC and inhibition of rosette formation between Fc gamma receptor-positive spleen cells and rabbit IgG-sensitized erythrocytes [18].
• Concomitant with the inhibition of macrophage spreading and rosette formation, MacMARCKS mutant also inhibits integrin-dependent tyrosine phosphorylation of paxillin [19].

Anatomical context of Rosette Formation

• The occurrence and distribution of distinct receptors for three C3 fragments on purified human blood lymphocytes were studied by rosette formation [20].
• This was shown by immunofluorescence studies using specific monoclonal antibodies, rosette formation with C3bi-coated erythrocytes, and immunoprecipitation for the LFA-1 complex [21].
• Expression of the human class II MHC molecule HLA-DP on Dd-positive murine fibroblasts resulted in a greatly enhanced response of the CD4-positive T cell hybridoma, measured either by lymphokine production or by rosette formation [22].
• Pretreatment of transfected COS cells with anti-CD2 antibody, or pretreatment of human erythrocytes with anti-LFA-3 antibody, abolished rosette formation [23].
• No surface Ig or spontaneous erythrocyte rosette formation was observed with eosinophils [24].

Associations of Rosette Formation with chemical compounds

• This glycoprotein was partially affinity purified and found to block E rosette formation and to compete with anti-T11 mAb for the E receptor [25].
• Neither sialic acid, galactose, manose, nor N-acetyl-glucosamine alone inhibits rosette formation [26].
• The data suggest that fetuin glycopeptide inhibits rosette formation by binding to the thymus-dependent cell where competition occurs with sheep erythrocytes for specific lymphocyte surface receptors [26].
• Seventeen of 24 (71%) of the ITP patients had platelets which demonstrated increased monocyte-platelet rosette formation [rosette index (RI) greater than 2], whereas only four (11%) of the non-ITP patients had such platelets [27].
• The rosette formation accompanied a strikingly polarized and overlapped deposition of ECM components including tenascin-carrying HNK-1 epitopes, laminin, type IV collagen, heparan, and chondroitin sulfate proteoglycans [28].

Gene context of Rosette Formation

• CD2(+) HMC-1 cells were found to form spontaneous aggregates and rosettes with sheep erythrocytes in excess over CD2(-) cells, and a T11-1 antibody inhibited both the aggregation and rosette formation [29].
• Interestingly, inhibition of the p38 pathway also resulted in a complete blockade of IgA rosette formation [30].
• Analysis of the effects of the inhibitors on rosette formation between human eosinophils and IgA- or IgG-coated beads revealed that activation of MEK was not required for IgA binding after priming with IL-4 or IL-5 [30].
• This fact indicates that the new rosette-forming receptor is different from CR1 in accordance with the lack of rosette formation of Raji cells with EAC43 [31].
• C3 receptors isolated from human erythrocytes inhibited the new rosette formation, while they did not inhibit the rosette formation of Daudi cells via CR2, indicating that the new rosette-forming receptor is different from CR2 [31].

Analytical, diagnostic and therapeutic context of Rosette Formation

• Immunoblotting analyses showed that laminin B1 and B2 chains were constitutively expressed, whereas a fully assembled form of laminin and type IV collagen appeared only after spheroid development, suggesting that these ECM components play a morphogenetically important role in rosette formation [28].
• The compositions of both the original and the modified lymphocyte populations were determined by (a) viability counting following treatment with antisera and complement, (b) direct and indirect immunofluorescence, (c) antibody-coated erythrocyte rosette formation, and (d) response to thymus- and bone marrow-derived cell mitogens [32].
• To avoid rosette formation (aggregation), which would preclude crystallization, this hydrophobic tail was removed from a membrane-free form of HN by proteolytic digestion [33].
• The presence of Fc receptors, but not C3 receptors, on human and bovine spermatozoa was shown by sperm-induced rosette formation of antibody-treated ox erythrocytes and by immunofluorescence of aggregated human gammaglobulin (AHG) treated spermatozoa [34].
• Enhancement in FCS and 10% BSA occurred after 1 day, but not 2 or more days, of storage at 4 degrees C, but was not seen when cells were stored at 37 degrees C. Rosette formation was about doubled by centrifugation of lymphocytes through BSA gradients prior to rosette tests; centrifugation through NaM gradients had no such effect [35].

References