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Biomedical subjects

J Leu

Publications and source records attributed to J Leu.

6 recordsLinked to original sources
PubMed1999

Modulation by cytokines of induction of oral tolerance to type II collagen.

OBJECTIVE: To determine whether the simultaneous administration of drugs and/or cytokines such as transforming growth factor beta (TGFbeta) can render oral tolerance to type II collagen (CII) more effective in causing resistance to collagen-induced arthritis (CIA) in mice, and to investigate whether oral tolerance can still be induced when high levels of anti-CII are present. METHODS: Tolerance was induced by intragastric feeding of low-dose CII to DBA/1 mice during a 2-week period, either before immunization with CII in Freund's complete adjuvant or after initiation of arthritis. Some mice were simultaneously injected with TGFbeta1 or with the H2 receptor agonist dimaprit. RESULTS: Both TGFbeta1 and dimaprit increased the degree of oral tolerance obtained. TGFbeta1 augmented the induction of immunoregulatory CD8 T cells, which transferred the resistance to CIA induction to normal recipients. Feeding of CII for 2 weeks, starting after the onset of arthritis, still significantly ameliorated the course of CIA. CONCLUSION: Administration of TGFbeta1 or dimaprit, both of which are believed to promote the development of immunoregulatory T cells, may reinforce induction of oral tolerance, even after the onset of arthritis.

Adjuvants, Immunologic↗
PubMed1996

Inter- and intraclade neutralization of human immunodeficiency virus type 1: genetic clades do not correspond to neutralization serotypes but partially correspond to gp120 antigenic serotypes.

We have studied genetic variation among clades A through E of human immunodeficiency virus type 1 (HIV-1) at the levels of antibody binding to gp120 molecules and virus neutralization. We are unable to identify neutralization serotypes that correspond to the genetic clades. Instead, we observe that inter- and intraclade neutralization of primary isolates by HIV-1-positive sera is generally weak and sporadic; some sera show a reasonable degree of neutralization breadth and potency whereas others are relatively sensitive to neutralization, but no consistent pattern was found. However, a few sera were able to neutralize across clades with significant potency, an observation which may have implications for the feasibility of a broadly effective HIV-1 vaccine involving humoral immunity. Serological assays measuring anti-gp120 antibody binding also failed to identify serotypes that correspond precisely to the genetic clades, but some indications of clade-specific binding were observed, notably with sera from clades B and E. A representative protein for each clade (A through E) was selected on the basis of its specificity, defined as high seroreactivity with sera from individuals infected with virus of that clade and lower reactivity with sera from individuals infected with viruses from other clades. The seroreactivity patterns against these five proteins could be used to predict the genotype of the infecting virus with moderate success.

Amino Acid Sequence↗
PubMed1995

Tolerogenic forms of auto-antigens and cytokines in the induction of resistance to experimental allergic encephalomyelitis.

Resistance to experimental allergic encephalomyelitis (EAE) induction by homogenized myelin (MSCH) in complete Freund's adjuvant (CFA) and pertussigen (P) in SJL mice was seen 1 week after intravenous injection of PLP 139-151 coupled to spleen cells (PLP-ECDI-SP). Although this resistance could be transferred by spleen cells enriched for CD8+ T cells and thus had a component of immunoregulatory T cells, it was primarily due to anergy, as it was reversible by four daily injections of interleukin (II)-2 starting 3 days after the PLP-ECDI-SP. Earlier treatment with IL-2 did not reverse the tolerance. In view of the known higher sensitivity to anergy induction of Th1 than of Th2 cells, a change in the cytokine balance in the response to MSCH+CFA after anergy induction might be responsible for the resistance to EAE induction. The effect of treatment with cytokines alone on induction of EAE was therefore also determined. Short-term (1-2 weeks) daily pretreatment with IL-2 (4000 U) or TGF-beta 2 (1 micrograms) somewhat decreased the susceptibility to subsequent EAE induction, but IL-4 (5 ng), IL-10 (5 micrograms) or IL-12 (50-200 ng) had no effect under those conditions, even if low doses of PLP were injected simultaneously. Daily injections of IL-4 over an 8-week period prior to immunization, however, significantly lowered the incidence of EAE. Simultaneous injections of IFN-gamma (2000 U/day) completely abolished this effect of IL-4. The effect of these cytokines administered immediately after the immunization with MSCH + CFA + P was also examined. As shown earlier, TGF-beta 2 (100-1000 ng/day) caused a marked protection when it was given intraperitoneally on days 5-9 after injection of MSCH + CFA. IL-4 (5 ng/day), in contrast, was very protective when administered on days 0-4 and less so when given on days 5-9 or even on days 0-12. IL-10 (1 microgram/day) was not protective under these conditions and IL-12 (50 ng/day) significantly increased the severity and mortality of EAE when given on days 0-4 after MSCH + CFA.

Animals↗
PubMed1991

Primary anti-trinitrophenyl memory cells investigated by plaque-forming cells and ELISA.

Primary anti-trinitrophenyl antibody production was investigated from spleen cells of mice immunized with trinitrophenylated-keyhole limpet hemocyanin, using the plaque-forming cell method and ELISA. Cells taken 5 days after antigen injection do not produce IgE, but do produce IgM and IgG1 anti-trinitrophenyl antibodies as demonstrated by plaque-forming cells. Substantial increase of IgM, IgG1, and IgE antibody production was seen from cells taken 7 days after immunization, followed by a rapid decline. By ELISA it was seen that cells taken 3 days after immunization already produce small amounts of anti-trinitrophenyl antibodies. Presence of antigen from the start of the cultures did not increase antibody production from cells taken 3 days after immunization, but potentiated antibody secretions from cells taken 5 days or later after immunization. This potentiation was interpreted as recruitment of antibody-forming cells from early memory B cells. The presence of IL-4 from the start of the cultures had no appreciable effect. Cell sorting with specific antibody-coated magnetic beads showed that plaque-forming cells from nonsorted cells, membrane IgE+ or membrane IgE- cells secreted similar amounts of anti-trinitrophenyl IgG1 and IgE antibodies. No difference in anti-trinitrophenyl IgM, IgG1, or IgE production was found in controls; cells sorted negatively or positively for CD23. The data show that memory B cells can be demonstrated already on Day 5 after immunization, and their antigen-induced antibody secretion is IL-4 dependent.

Animals↗
PubMed1988

Effects of aging on neuronal electrical membrane properties.

The electric membrane properties (EMP) of dorsal root ganglion (DRG) neurons in cell cultures prepared from control mice (8-14 weeks) and old mice (90-92 weeks) were compared. The old neurons had a number of significant alterations in EMP compared to controls including decreased electrical excitability, increased action potential duration and more pronounced biphasicity of the repolarization phase. The old neurons also had larger action potential overshoot and afterhyperpolarization. The pattern of altered electric membrane properties was consistent with an age-induced shift from voltage-sensitive sodium channels to less excitable voltage-sensitive calcium channels and also a decrease in potassium permeability during the repolarizing phase of the action potential.

Aging↗