[Presence of a non-HLA antigen in B-lymphocytes from patients with rheumatic fever and their relatives defined using monoclonal antibodies]. / Presencia de un antígeno no-HLA en los linfocitos B de pacientes con fiebre reumática y sus familiares definido mediante anticuerpos monoclonales.

Numerous investigators have suspected that there is a genetic predisposition to rheumatic fever (RF). In this context a group of investigators at Rockefeller University have produced a monoclonal antibody that identifies an antigen present in 100% of all RF studied at that center. Using this antibody, labeled D8/17, we studied 47 patients with acute rheumatic fever and rheumatic heart disease. Of these, 39 were not receiving steroids at the of the test and 35 were positive for the marker (89.7%). The highest percentage of positive cells was seen in the probands with 34.6 +/- 13.16%, while unaffected mothers, fathers and siblings gave 24.9, 5.2 and 7.3% respectively. The control group had an average of 7.5% of positive cells. This study and previous ones, performed by the Rockefeller University group in which HLA typing was included, suggest an autosomal recessive mode of inheritance, not associated with the MHC system, for the D8/17 antigen. Rheumatic fever; non-HLA antigen in; genetic predisposition in.

Presence of a non-HLA B cell antigen in rheumatic fever patients and their families as defined by a monoclonal antibody.

Numerous investigators have suspected that there is a genetic predisposition to rheumatic fever (RF). In this context we have recently produced a series of monoclonal antibodies directed against B cells obtained from RF patients one of which, labeled D8/17, identifies a B cell antigen present in 100% of all RF patients studied. While the highest percentage of positive cells were exhibited by RF probands (33.5% +/- SE), the percentage of cells in unaffected siblings and parents was 14.6 and 13%, respectively. The percentage of positive cells in APSGN probands, unaffected siblings, and parents was 2.96, 3.86, and 2.8%, respectively. A low level of B cells (5-7%) bearing the D8/17 marker was seen in control patients. The segregation pattern of the phenotypes defined by the percentage of D8/17 positive cells within HLA-typed RF families are consistent with an autosomal recessive mode of inheritance not associated with the human MHC system. We postulate that these phenotypes indicate the presence of at least one necessary genetic factor for susceptibility to RF.

Monoclonal antibody reveals radial glia in adult avian brain.

An antibody prepared against adult canary brain, 40E-C, stains ventricular zone cells that send long, unbranched processes into the forebrain parenchyma. We identify these cells as radial glia. The same antibody also stains a subset of brain astroglia and reacts with nonbrain material such as mesenchyme, Sertoli cells, and the Z-line of muscle. A weaker reaction is given by erythrocytes and some endothelial cells. 40E-C also reacts with the radial glia of the developing rat brain but fails to show any such glia in adult rodent brain. Western blot analysis shows that this antibody recognizes vimentin, a molecule shared by all 40E-C-positive cell types. We believe that the presence of radial glia in the adult avian forebrain and their apparent absence in mammals is related to neurogenesis in adulthood, which occurs in birds and much less or not at all in mammals. In addition, the presence of radial glia in adult birds may also relate to other, still-hypothetical, differences in the physiology of adult avian and mammalian brains.

A virally induced obesity syndrome in mice.

An obesity syndrome was found in a number of mice infected as young adults with canine distemper virus, a morbillivirus antigenically related to measles. Body weights of obese animals 16 to 20 weeks after infection were comparable to those reported for genetically obese mice and for mice rendered obese by hypothalamic lesions. The total number of adipocytes in specific fat deposits was greater in obese animals than in their lean littermates. This hyperplasia was accompanied by moderate cell enlargement. Pancreatic islet tissue was also hypercellular in the obese mice. Brain tissue from the obese mice showed no overt pathology, and immunofluorescence staining for viral antigens was negative. There may be a selective, virus-induced disruption of critical brain catecholamine pathways.

Antibodies to a neural cell adhesion molecule disrupt histogenesis in cultured chick retinae.

Cell-surface proteins are believed to have important roles in cell-cell interactions during brain development, particularly in such processes as cellular adhesion, neurite outgrowth and synapse formation. The chick neural cell adhesion molecule, CAM, is a cell-surface protein specific to the nervous system and has been implicated in cell adhesion among cells and neurites of the developing retina and brain. Previous studies have shown that F(ab') fragments of antibodies directed against CAM inhibit the in vitro aggregation of cells obtained from 9-day embryonic chick retina. The specific antibody fragments also reduce the diameter of neurite fascicles that grow out from cultured dorsal root ganglia, apparently by blocking side-to-side adhesion between the neurites. In addition, anti-CAM antibodies alter the appearance of histotypic patterns in retinal cell aggregates maintained in culture for several days. We now demonstrate that the antibodies can disrupt histogenesis of the developing retina in organ culture, strengthening the notion that the cell-cell adhesion properties mediated by CAM are involved in the normal development of histological layers in the chick retina.