Search PubMed⌕ Search

Biomedical subjects

R H Swanborg

Publications and source records attributed to R H Swanborg.

At least 55 records · Page 3Linked to original sources
PubMed1986

Autoimmune effector cells. VII. Cells isolated from thymus and spinal cord of rats with experimental allergic encephalomyelitis transfer disease.

Effector cells mediating experimental allergic encephalomyelitis (EAE) were recovered from the thymus glands and spinal cords of Lewis rats immunized with myelin basic protein (BP) and complete Freund's adjuvant (CFA), as demonstrated by adoptive transfer to syngeneic recipients following in vitro activation with BP. The thymic effector cells (TCs) were lymphoblasts. Sequential transfer studies suggested that the effector TCs probably recirculated back to the thymus from the periphery. The transfer of EAE with cells derived from the spinal cords of paralyzed donors indicates that disease-inducing effector cells are present in the target organ.

Animals↗
PubMed1984

Regulation of experimental allergic encephalomyelitis. Part 5. Role of the recipient in suppressor cell induction.

Suppressor cells that regulate experimental allergic encephalomyelitis (EAE) are present in spleens of Lewis rats that have recovered from the disease, as demonstrated by adoptive transfer of suppression to normal recipients. However, lethally irradiated recipients (850 rad) of spleen cells from recovered donors are not protected against EAE. Indeed, onset of EAE is accelerated in these irradiated recipients. These findings suggest that the host participates in the suppression of EAE.

Animals↗
PubMed1984

Autoimmune effector cells. VI. Transfer of experimental allergic encephalomyelitis with spleen cells activated in mixed lymphocyte cultures.

Although spleen cells (SpC) from Lewis rats that have been immunized with guinea pig myelin basic protein in complete Freund's adjuvant do not transfer experimental autoimmune encephalomyelitis (EAE) to syngeneic recipients, we report that effector cells of EAE can be activated in SpC suspensions during mixed lymphocyte reactions (MLR) to allogeneic SpC. Effector cell activation correlates with interleukin 2 (IL 2) production. The results are consistent with the hypothesis that autoreactive cells may be generated as a result of an immune response to exogenous antigens.

Animals↗
PubMed1983

Autoimmune effector cells. IV. Induction of experimental allergic encephalomyelitis in Lewis rats without adjuvant.

Experimental autoimmune encephalomyelitis (EAE) was induced in Lewis rats without the aid of adjuvant. Radioresistant cells were activated from spleens of nonimmune donor rats by in vitro culture with myelin basic protein (BP). After adoptive transfer, these cells recruited EAE effector cells in normal syngeneic recipients, as demonstrated after transfer to secondary hosts. The induction of EAE without adjuvant may lead to a better understanding of the mechanisms of autoimmune disease induction.

Animals↗
PubMed1983

Autoimmune effector cells. V.A monoclonal antibody specific for rat helper T lymphocytes inhibits adoptive transfer of autoimmune encephalomyelitis.

The in vitro activation of spleen cells from donor rats immunized with myelin basic protein results in enhanced adoptive transfer of experimental allergic encephalomyelitis to syngeneic recipients. In this study, adoptive transfer was inhibited when monoclonal antibody W3/25, which defines an antigen on rat helper T lymphocytes, was included in the in vitro cultures. Partial inhibition was achieved with monoclonal antibody OX-3, which recognizes la antigen, whereas other anti-T cell monoclonal reagents were ineffective. These results support the conclusion that W3/25+T cells play an essential role in the induction of this autoimmune response.

Animals↗
PubMed1982

Autoimmune effector cells. II. Transfer of experimental allergic encephalomyelitis with a subset of T lymphocytes.

This study was conducted to further characterize the effector cells of experimental allergic encephalomyelitis (EAE) which are activated in vitro when spleen cells from Lewis rats previously immunized with myelin basic protein and adjuvant are cultured with antigen prior to transfer to syngeneic recipients. The effector cells were isolated on discontinuous Percoll gradients in the cell fraction that floated on Percoll with a buoyant density of 1.067 kg/l. These cells (designated fraction 1) transferred EAE and incorporated [3H]dThd in culture. Fraction 1 was enriched for T cells when evaluated with monoclonal anti-rat T cell serum W3/13 and deficient in Ig+ cells; approximately 33% were positive with monoclonal anti-rat T cell serum W3/25. In contrast, the small, nonproliferating cells found in higher density Percoll fractions did not transfer EAE. When fraction 1 was recultured in the presence of basic protein and interleukin 2 for 72 h, these cells retained the ability to transfer EAE. Moreover, these recultured cells exhibited an increase in the W3/25 antigen and a decrease in the W3/13 marker. It was concluded that a subset of T cells which bear the W3/25 marker is involved in the transfer of EAE.

Animals↗
PubMed1982

Regulation of experimental allergic encephalomyelitis. Part 4. Further characterization of postrecovery suppressor cells.

Suppressor cells that regulate experimental allergic encephalomyelitis (EAE) are present in lymph nodes of Lewis rats that have recovered from the disease, as demonstrated by adoptive transfer of suppression for at least 108 days following challenge of donor rats with myelin basic protein (BP) in complete Freund's adjuvant (CFA). These suppressor lymph node cells (LNC) inhibit the occurrence of active, but not passive EAE in recipients, suggesting that they function early in the inductive phase of the response to BP. The suppressor cells are nylon-adherent, and suppression can be partially abrogated by depletion of B cells with anti-immunoglobulin (ig) and complement (C). Serum from recovered donors has, at best, only a modest suppressive effect when transfused into syngeneic recipients. These findings suggest that the B cells do not mediate suppression on EAE via production of blocking antibody, but may function directly, perhaps by triggering T cells to become suppressor cells.

Animals↗
PubMed1982

Helix pomatia receptors on rat T lymphocytes and bone marrow cells.

Helix pomatia (HP) receptors are present on approximately 60 percent of neuraminidase (NANAase)-treated rat T lymphocytes. The HP+ spleen cells (SpC) can be separated from HP-, immunoglobulin-bearing (Ig+) cells by affinity chromatography. The HP+ SpC mediate the local graft-versus-host reaction (GVHR). Less than 1% of rat lymphocytes bear both HP and Ig markers. Approximately 25% of Lewis rat bone marrow cells are HP+ (only 1% are HP+ Ig+), suggesting that the HP receptor may be a differentiation marker.

Animals↗
PubMed1982

Autoimmune effector cells. III. Role of adjuvant and accessory cells in the in vitro induction of autoimmune encephalomyelitis.

The present investigation shows that autoreactive effector cells that transfer experimental allergic encephalomyelitis (EAE) can be activated from spleens and lymph nodes of Lewis rats given a single injection of 25 micrograms myelin basic protein (BP) in incomplete Freund's adjuvant (IFA), despite the fact that the cell donors do not develop EAE. Rather, these donor rats are unresponsive to EAE when given an encephalitogenic emulsion of BP in complete Freund's adjuvant (CFA). Lymphoid cells from rats given a single injection of BP-IFA were almost as effective as cells from BP-CFA-treated rats with respect to transferring EAE after in vitro activation with BP or concanavalin A (Con A). Irrespective of whether donors received BP in IFA or CFA, BP-cultured spleen and lymph node cells (SpC and LNC, respectively) transferred EAE, whereas Con A-cultured SpC but not LNC exhibited effector cell activity. Con A-cultured LNC were able to transfer EAE if the cultures were reconstituted with irradiated adherent phagocytic cells (which could be obtained from normal Lewis rat spleens) or with conditioned medium from these adherent SpC. These findings indicate that accessory cells are required for in vitro induction of this T cell-mediated autoimmune response.

Adjuvants, Immunologic↗
PubMed1981

Inhibition of experimental allergic encephalomyelitis by carrier administered prior to challenge with encephalitogenic peptide-carrier conjugate.

Guinea pigs can be rendered unresponsive to experimental allergic encephalomyelitis (EAE) challenge by prior injections of myelin basic protein (BP) or peptides derived from BP. The synthesized tryptophan-containing peptide (TrpP, corresponding to residues 114-122) which is the primary encephalitogenic sequence in BP (for guinea pigs) had been conjugated to the non-central nervous system protein bovine serum albumin (BSA) and used for EAE challenge. It has been shown in this study that prechallenge treatment with the BSA carrier alone can significantly inhibit the induction of EAE by TrpP-BSA conjugate. That carrier treatment is immunologically specific was determined when prior treatment with cytochrome c did not protect animals from EAE challenge with TrpP conjugated to BSA. In addition, in disease induced with BP or TrpP, and while TrpP did protect guinea pigs challenged with TrpP, it did not protect those challenged with BP. This last finding raises the possibility of a second encephalitogenic sequence in BP or an important role for the carrier in the TrpP conjugate.

Animals↗
PubMed1981

Regulation of experimental allergic encephalomyelitis. III. Demonstration of effector cells in tolerant rats.

Effector cells, which transfer experimental allergic encephalomyelitis (EAE), can be demonstrated in the spleens of Lewis rats which have been rendered tolerant to myelin basic protein (BP). Transfer of EAE was achieved following in vitro culture of tolerant donor spleen cells with antigen. The donor animals were, themselves, protected against EAE induced by active challenge with BP in complete Freund's adjuvant, although BP-activated effector spleen cells could partially override this protection. The finding that effector cells are present in unresponsive animals supports the hypothesis that immunologic self tolerance is actively regulated by suppressor mechanisms.

Animals↗
PubMed1980

Autoimmune effector cells. I. Transfer of experimental encephalomyelitis with lymphoid cells cultured with antigen.

Relatively low numbers of spleen and lymph node cells from Lewis rats previously challenged with myelin basic protein efficiently transfer experimental allergic encephalomyelitis (EAE) to normal syngeneic recipients after in vitro culture with antigen. Moreover, cells obtained from rats that have recovered and are resistant to EAE can also transfer disease. Cell separation studies show that a nylon wool-adherent cell is responsible for transfer of EAE. Density gradient ultracentrifugation revealed that these effector cells are probably lymphoblasts.

Allergens↗
PubMed1980

Suppression of experimental allergic encephalomyelitis with thoracic duct lymphocytes.

Thoracic duct lymphocytes (TDL) from Lewis rats immunized 9-10 days previously with basic protein in complete Freund's adjuvant (BP-CFA) failed to induce experimental allergic encephalomyelitis (EAE) in syngeneic recipients. This contrasts with the successful transfer of EAE by lymph node cell suspensions from donors immunized 9 days previously with BP-CFA. Only minor EAE was induced passively by TDL from rats immunized 11-12 days before with BP-CFA. TDL collected 9-20 days after BP-CFA immunization, however, were successful in transferring specific suppression of EAE tested by the lack of disease in the recipients immunized actively with BP-CFA 1 week after the TDL transfer. The data indicate that the thoracic duct contains specific suppressor cells shortly before, during and after the development of clinical EAE.

Animals↗
PubMed1980

Susceptibility of Lewis rats to experimental autoimmune encephalomyelitis after recovery from passively induced disease.

Experimental autoimmune encephalomyelitis (EAE) was induced in Lewis rats by adoptive transfer of 5 x 10(7) sensitized syngeneic lymphoid cells from donors challenged 12 to 43 days earlier with myelin basic protein and complete Freund's adjuvant. The donor cells were cultured for 72 hours with antigen prior to transfer. Following recovery, the recipients remained susceptible to EAE induced by challenge with antigen and adjuvant. The relevance of this finding to host recovery mechanisms is discussed.

Animals↗
PubMed1980

Regulation of experimental allergic encephalomyelitis. II. Appearance of suppressor cells during the remission phase of the disease.

Lewis rats are susceptible to experimental autoimmune encephalomyelitis (EAE). Most rats recover from paralysis and are subsequently resistant to the disease. In an adoptive transfer system, we found that lymph node cells (LNC) from rats that had recovered from EAE protect syngeneic recipients from the disease when the latter are challenged with encephalitogenic myelin basic protein and adjuvant after receiving donor cells. Suppression is antigen-specific and requires viable LNC. In contrast to the suppressor cells we previously studied in tolerized rats, which were nonadherent T lymphocytes, the suppressor cells found in rats that have recovered from EAE adhere to glass wool. However, they are not retained on Sephadex G-10 columns to which macrophages adhere. Suppressor activity is enriched in the nylon wool-adherent LNC population (which consists of approximately 80% Ig+ cells). Our findings suggest that activation of adherent suppressor cells may be implicated in recovery from EAE. These may be adherent T cells, or B cells that produce anti-BP blocking antibodies.

Animals↗
PubMed1978

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↗