Hypersensitivity reactions and cytotoxic effects.
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Antigens↗
Biomedical subjects
R H Swanborg
Publications and source records attributed to R H Swanborg.
Cell-mediated immunity to myelin basic protein in Lewis rats made unresponsive to experimental allergic encephalomyelitis.
Lewis rats with experimental allergic encephalomyelitis (EAE) exhibited cell-mediated immunity to myelin basic protein as determined both with in vivo and in vitro assays. Positive skin test reactions and production of migration inhibitory factor (MIF) were observed before onset and after recovery from EAE. Rats rendered unresponsive to EAE exhibited in vitro cell-mediated immunity to basic protein, although in vivo manifestations were depressed. However, tolerant rats failed to respond to the encephalitogenic determinant; rats with EAE exhibited cell-mediated immunity to this region of the molecule. The results indicate that EAE-unresponsive rats possess lymphocytes capable of responding to basic protein, but that reactivity to the encephalitogenic peptide is suppressed.
Animals↗
Regulation of self tolerance in experimental allergic encephalomyelitis. I. Differences between lymph node and spleen suppressor cells.
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Animals↗
A new rat lymphocyte surface marker: characterization and separation of cells with receptors for Helix pomatia hemagglutinin.
Thirty-two percent of neuraminidase-treated DA rat spleen lymphocytes and 48% of lymph node lymphocytes possess receptors for Helix pomatia hemagglutinin (HP). Moreover, these HP-receptor-bearing cells can be separated from B cells by affinity chromatography on HP-Sepharose columns. The virtual absence of immunoglobulin (Ig) receptors and the close correlation with reported T-cell content of these lymphoid tissues suggest that HP-receptor lymphocytes are probably T cells and that HP may provide a convenient marker, for both the identification and the purification of rat T lymphocytes.
Agglutinins↗
Antibody response to myelin basic protein: comparisons between Lewis rats with experimental allergic encephalomyelitis, and tolerant rats.
The hemagglutinating antibody responses of Lewis rats with experimental allergic encephalomyelitis (EAE) and of rats rendered unresponsive to this autoimmune disease by pretreatment with myelin basic protein (BP) were compared. Most tolerant animals produced low levels of hemagglutinating antibody. Similarly, most rats with EAE also produced anti-BP antibodies. We were unable to correlate hemagglutinin production or titer with protection against disease. Hemagglutination inhibition (HAI) studies reveal cross-reactivity between rat, guinea pig and bovine BP. HAI studies with BP-derived peptides suggest that at least three distinct antibody-binding determinants exist in the BP molecule, and that individual inbred Lewis rats respond differently with respect to antibody production to these sites.
Agglutinins↗
Immunoregulation of experimental allergic encephalomyelitis: conditions for induction of suppressor cells and analysis of mechanism.
We determined requirements for the induction of immunoregulatory suppressor cells in experimental allergic encephalomyelitis (EAE) in Lewis rats. Pretreatment of rats with myelin basic protein (BP) in incomplete Freund's adjuvant (IFA) stimulates the proliferation of suppressor cells that localize in lymph nodes and spleen (but not thymus) and exert control over the development of clinical EAE. Dosage studies revealed that 3 X 10(7) suppressor cells can adoptively transfer suppression to syngeneic recipients. Transferred unresponsiveness wanes within 3 weeks, indicating that the suppressor cells are short-lived lymphocytes, although actively induced unresponsiveness persists for at least 8 weeks, probably as a result of continual proliferation under the influence of antigen. No evidence was obtained to suggest that antigen carry-over or blocking antibody production accounts for adoptive transfer of unresponsiveness. Suppressor cells apparently act at the inductive phase of the immune response since they had no inhibitory effect on adoptive transfer of disease by effector lymph node cells. Other mechanisms also may play a role in unresponsiveness to EAE, since rats pretreated i.v. with high dosages of soluble BP were temporarily rendered unresponsive, although suppressor cells could not be detected in these animals.
Animals↗
Maintenance of immunologic self-tolerance by nonimmunogenic forms of antigen.
Immunologic tolerance to EAE in guinea-pigs appears to be a function of a determinant distinct from the encephalitogenic region of the myelin basic protein molecule. In Lewis rats (in which species the molecular sites for disease-induction and tolerance have not been completely characterized) the mechanism underlying this state of immunologic tolerance involves suppressor cell regulation of the autoimmune response. On the basis of these experimental findings we postulate that natural self-tolerance is maintained by suppressor T cells which are stimulated by nonimmunogenic fragments of self-antigen released during protein turnover.
Animals↗
Antigen-induced inhibition of experimental allergic encephalomyelitis. IV. Studies of the C-terminal end of the myelin basic protein molecule (1).
The C-terminal end of the myelin basic protein (BP) molecule (peptide 117.170) was obtained by cleavage with BNPS-skatole, and purified by gel filtration. Peptide 117-170 from guinea pig BP induced experimental allergic encephalomyelitis (EAE) in Lewis rats, whereas the corresponding peptide from bovine BP was inactive. Neither peptide showed more than trace activity when tested in guinea pigs. Guinea pigs and rats treated with peptide 117-170 in incomplete Freund adjuvant were not rendered unresponsive to EAE induced by subsequent challenge with an encephalitogenic emulsion of BP in complete Freund adjuvant. Indeed, peptide-pretreated rats tended to develop clinical EAE significantly earlier than untreated controls.
Amino Acids↗
Antigen-induced inhibition of experimental allergic encephalomyelitis. III. Localization of an inhibitory site distinct from the major encephalitogenic determinant of myelin basic protein.
Defined peptide fragments were isolated from the N-terminal half of the myelin basic protein (BP) molecule and employed for antigen-induced inhibition of experimental allergic encephalomyelitis (EAE). Guinea pigs pretreated with peptide 44-89, obtained by limited pepsin digestion and purified by column chromatography, were significantly protected against EAE subsequently induced by sensitization with BP in complete Fruend's adjuvant. Peptide 1-20, derived by cyanogen bromide cleavage, did not inhibit EAE, nor did the synthetic EAE peptide (residues 114-122), although this peptide was only weakly encephalitogenic for guinea pigs. These findings directly support our previous conclusion that different sites on the BP molecule are responsible for induction and inhibition of EAE, and suggest that disease inhibition can be attributed, at least in part, to a site within peptide 44-89.
Amino Acid Sequence↗
Suppressor cell control of unresponsiveness to experimental allergic encephalomyelitis.
Lymph node cells (LNC) from Lewis rats rendered unresponsive to experimental allergic encephalomyelitis (EAE) by pretreatment with myelin basic protein markedly suppressed clinical (but not histologic) EAE in normal recipients later challenged with an encephalitogenic emulsion. Unresponsiveness was immunologically specific, and required viable LNC; serum transfer was ineffective. These findings suggest that suppressor cells exert control over this autoimmune disease.
Animals↗