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Biomedical subjects

M A Leon

Publications and source records attributed to M A Leon.

At least 37 records · Page 2Linked to original sources
PubMed1987

Roles of IL-2 and antigen in the later stages of the primary antibody response.

Spleen cells, obtained 2-5 days after in vivo priming with sheep erythrocytes (SRBC), were cultured to determine the presence of plaque-forming cell (PFC) precursors capable of developing into mature PFC under the influence of various stimulants. Lipopolysaccharide (LPS), added together with SRBC at the initiation of a 48-hr in vitro culture, enhanced the PFC response of primed spleen cells. In vivo priming for a minimum of 3 days was required, and maximal numbers of PFC were obtained from spleen cells primed for 4 days. Depletion of T lymphocytes from Day 3-primed spleen cells abrogated LPS-mediated enhancement, and addition of concanavalin A supernatants to the T-cell depleted system restored the enhancement, suggesting that LPS action required co-operation with a product(s) of activated T cells. Addition of various interleukin-2 preparations including recombinant human IL-2 to the system restored the LPS-mediated enhancement. The response of Day 3 cells from which T cells were eliminated as vigorously as possible was similarly restored by the addition of IL-2, LPS and antigen, suggesting that IL-2 reacts directly with PFC precursors that have developed IL-2 receptors. LPS-mediated enhancement, in the presence or absence of T cells, was also markedly dependent on the presence of SRBC during in vitro culture. These data suggest that, in co-operation with IL-2 and other co-factors, antigen plays a significant role in driving the later stages of differentiation and/or division of PFC precursors to mature PFC.

Animals↗
PubMed1983

Role of complement in murine corneal infection caused by Pseudomonas aeruginosa.

The role of complement components C3 and C5 was examined in murine corneal infection induced by Pseudomonas aeruginosa. DBA/2 and Swiss-Webster mice are naturally resistant to experimental P. aeruginosa corneal infection. Mice of these two strains are able to restore a clear cornea within 4-6 weeks following Pseudomonas corneal challenge and are genetically deficient in the fifth component of complement. In contrast, ocular infection of congenic C5-deficient B10.D2o/Sn or normocomplementemic B10.D2n/Sn mice results in an identical pattern of susceptibility in which corneal perforation and phthisis bulbi occur. Taken together, these results indicate that C5 plays little or no role in susceptibility or resistance to Pseudomonas eye infection. In contrast, depletion of C3 in normally resistant DBA/2 mice using cobra venom factor (CoVF) diminishes the ability of these mice to restore a clear cornea following Pseudomonas infection. A single inoculation of CoVF, 24 hours prior to ocular challenge, is as effective in altering the response of DBA/2 mice as is continuous depletion of C3 during the course of infection using multiple inoculations of CoVF. Mice that are unable to clear Pseudomonas ocular infection following CoVF treatment regain this ability when the contralateral eye is infected after recovery of normal levels of C3. Depletion of C3 by CoVF treatment of DBA/2 mice, which had previously restored a clear cornea following Pseudomonas eye infection, again renders these mice susceptible.

Animals↗
PubMed1982

The use of hybridoma antibodies to probe the antigenic determinants of thyroglobulin.

Using monoclonal antibodies we have begun to define the epitopes of the murine thyroglobulin molecule that elicit autoimmune responses. Based on the principle of complementation, 18 monoclonal antibodies were classified into 8 groups, defined by their reactions with the same or neighboring determinants. Further distinctions between the monoclonals were drawn from comparisons of their cross-reactions with thyroglobulins of other species and their patterns in isoelectric focusing. One low molecular weight fragment of bovine thyroglobulin, which cross-reacts extensively with thyroglobulins of other species, has been isolated and partially characterized.

Animals↗
PubMed1982

Peripheral T lymphocytes from rheumatoid arthritis patients recognize determinants on light chains and/or Fab fragments of immunoglobulin G.

Peripheral blood T lymphocytes from 29 of 31 patients with rheumatoid arthritis incorporated significant quantities of thymidine when cultured with pooled human immunoglobulin G (IgG). In contrast to the observation of general reactivity to pooled Igg, responses to pooled IgM were rare (3 of 26 patients). None of 11 controls responded to either IgG or IgM. Response to IgG is maximal on day 6 of culture and is dependent on concentration of IgG. The responding cells recognize determinants on monoclonal light chains and/or Fab fragments. Response to light chains follows one of three patterns: preferential response to lambda chains, preferential response to kappa chains, and essentially equal response to either kappa of lambda chains.

Arthritis, Rheumatoid↗
PubMed1979

Genetic control of the murine corneal response to Pseudomonas aeruginosa.

Inbred mouse strains differ in susceptibility to intracorneal challenge with Pseudomonas aeruginosa. Genetic studies indicate that resistance to corneal infection is dominant over susceptibility and is controlled by autosomal genes, at least one of which is located outside of the H-2 locus. On the basis of genetic complementation studies, the susceptible strains BALB/c and C57BL/6 each bear one resistance gene, since the F1 hybrid (BALB/c X C57BL/6) was uniformly resistant to infection.

Animals↗
PubMed1979

Reversal by insulin of concanavalin A inhibition of myotube formation and evidence for common binding sites.

Concanavalin A (Con A) inhibits fusion of trypsin-treated myoblasts. This inhibition is reversed by the addition of supraphysiological concentrations (4 micrograms/ml) of insulin either during continuous presence in culture or by pulse additions at 36 and 48 h of culture, just before the time that cultures not treated with Con A undergo myoblast fusion. This reversal is not due to the mitogenic effects of insulin. Under reversal conditions, no specific displacement of bound [125I]iodo-Con A was detected nor did insulin stimulate metabolite uptake. Cell surface replicas of hemocyanin-tagged Con A showed that insulin reversal of the inhibition of myotube formation correlated with the alteration of Con A-binding sites from a clustered configuration present in the inhibited cells to a dispersed state correlated with normal myotube formation. Although a causal relationship has yet to be shown, the data suggest that insulin-mediated reversal of Con A inhibition of myoblast fusion may be related to the ability of insulin at supraphysiological levels to alter the translational mobility of cell surface components containing glucose and/or mannose residues capable of binding Con A. Evidence is presented which suggests that insulin and Con A share common binding sites, since in the physiological range of insulin concentrations (1 ng/ml), Con A pretreatments results in an inhibition of specific [125I]iodo-insulin binding, and antagonistic interactions of insulin and Con A on metabolite uptake and cell proliferation occur. Thus, it appears that the insulin receptors of developing skeletal muscle are glycoproteins containing glycopyranosides.

Animals↗
PubMed1977

Suppression of myoblast fusion by concanavalin A: possible involvement of membrane fluidity.

Experimental evidence is presented which is consistent with the involvement of membrane fluidity during myoblast fusion. Treatment of pretrypsinized myoblasts with tetrameric Con A, but not with the dimeric succinyl derivate, inhibits fusion. Inhibition is reversed by treatment with alpha-methyl-D-mannoside or subsequent trypsinization. No inhibition is observed when the lectin is incubated with cells at 4 degrees C unless the incubation is followed by treatment with glycogen, a multivalent Con A cross-linking agent. This effect of glycogen is reversed by subsequent treatment with alpha-amylase. Direct observation of Con A-binding site topography by transmission electron microscopy of membrane replicas of cells labelled with Con A and haemocyanin reveals that inhibition of fusion correlates with a clustered distribution of Con A-binding sites, whereas normal fusion correlates with a dispersed distribution.

Animals↗
PubMed1976

Isolation of a human lymphocyte mitogen from wheat germ with N-acetyl-D-glucosamine specificity.

A lectin, isolated from wheat germ by affinity chromatography on chitin, was mitogenic for purified human peripheral blood lymphocytes. Peak incorporation of 3H-thymidine was observed after incubation of lymphocyte cultures with wheat germ mitogen for 7 to 10 days. When lymphocytes were separated into two fractions based on their ability to form rosettes with unsensitized sheep erythrocytes, the mitogen induced a negligible proliferative response in either fraction. Mixing experiments demonstrated a strong response in the T lymphocyte fraction which required the collaboration, but not proliferation, of cells present in the nonrosetting fraction. Stimulation was specifically abolished by addition of N-acetyl-D-glucosamine at initiation of culture.

Acetylglucosamine↗
PubMed1976

The immune response to dextran in BALB/c mice. I. Modification of "thymus-independent" response by the T cell mitogen concanavalin A.

Normal and congenitally athymic mice respond to immunization with dextran, thus indicating that the response is thymus independent. Athymic mice have lower plaque-forming cell (PFC) response than normal mice 3 days after immunization, but similar PFC response as normal mice by 5 days. Seven to 10 days after immunization, athymic mice maintain a high level of PFC response whereas the PFC response declines sharply in normal mice. Concanavalin A (Con A), added at initiation of in vitro culture, enhances the response of spleen cells from primed normal mice. Treatment with methyl-alpha-D-mannoside (MAM), a competitive inhibitor of binding of Con A, immediately after addition of Con A, abolishes the enhancement. Treatment with MAM, 3 to 6 hr after Con A addition, partially blocks the enhancement. The enhancing effect is dependent on the dose of Con A and the duration of in vivo priming before in vitro culture. Con A does not enhance the in vitro PFC response of cells from primed athymic mice. Supernatants from Con A-treated non-primed normal spleen cell cultures enhance the PFC response of "nude" cells, thereby indicating that enhancement by Con A is mediated through a soluble T cell product(s) with no apparent antigen specificity. Hydroxyurea, an inhibitor of DNA synthesis, blocks the enhancement by Con A of cells primed for 1 to 3 days. Release of hydroxyurea block after 19 hr incubation does not restore the PFC response, thereby indicating the responding anti-dextran PFC precursor cells are engaging actively in DNA synthesis. PFC response of primed cells taken at the peak of anti-dextran response (day 5) shows that they are less susceptible to the hydroxyurea block. Con A enhances the PFC response of cells primed for 5 days even in the absence of DNA synthesis.

Animals↗
PubMed1975

Modification of the biological activities of concanavalin A by anti-concanavalin A.

Concanavalin A (Con A) bound to cell membrane glycoproteins, may be dissociated from the membrane receptors by competitive ligands such as alpha-methyl-D-mannoside. Addition of antibody to Con A to the system forms complexes of antibody and Con A which are still bound to the membrane receptors. Such complexes are not dissociable from the membrane by alpha-methyl-D-mannoside. Presence of the complexes on the membrane is monitored by radioactive label or by passive lysis of the cells with guinea pig complement. Antibody to Con A can completely suppress Con A mediated stimulation of lymphocytes as measured by incorporation of tritiated thymidine. However production of lymphokines involved in migration inhibition, enhancement of plaque forming cells or blastogenesis are differentially suppressed by antibody to Con A.

Animals↗