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M Aldo-Benson

Publications and source records attributed to M Aldo-Benson.

11 recordsLinked to original sources
PubMed1992

Alcohol can inhibit effect of IL-4 on activated murine B cells.

Ethanol addition to B lymphocytes in vitro inhibits antigen-induced antibody secretion and antigen-induced cell proliferation. We tested the hypothesis that ethanol can inhibit the effect of interleukins on B-cell proliferation by adding ethanol to in vitro functional assays for IL-2 and IL-4. Ethanol does not inhibit IL-2-induced B-cell differentiation, but it does inhibit IL-4-induced B-cell proliferation and IL-4-induced Ig class switching.

Animals↗
PubMed1992

Ethanol inhibits production of messenger ribonucleic acid for kappa-chain in stimulated B lymphocytes.

Alcohol consumption can adversely affect an individual's response to infection. We have shown that alcohol has a direct suppressive effect on numbers of antibody-secreting cells in antigen-activated B lymphocytes but does not suppress the early membrane and intracellular events that are associated with binding of antigens to specific receptors. The studies reported here were designed to determine whether alcohol inhibits immunoglobulin synthesis. When 150 mg/dl ethanol was added to anti-mu-stimulated purified B cells, proliferation was inhibited. Similar exposure to ethanol inhibited production of messenger RNA for kappa chain in anti-mu-stimulated B cells but did not affect total RNA production or messenger RNA for beta-actin. Thus alcohol inhibits both the proliferation of antigen-activated B lymphocytes and their synthesis of immunoglobulin.

Animals↗
PubMed1991

Direct tolerance induction in mature B lymphocytes may resemble clonal anergy phenomenon.

Several mechanisms have been postulated for direct induction of B-cell tolerance in mature B cells, such as the Bretscher and Cohn [5] hypothesis which states that an antigenic signal to B cells without the 'second signal' provided by T cells or lymphokines produces unresponsiveness. A second explanation is that tolerogens which cross-link immunoglobulin and Fc receptors abort the biochemical activation of the B cell via the phosphatidyl inositol pathway. Results of our studies are not consistent with either of these hypotheses. We speculated that DNP-MGG induces immunoglobulin receptor capping and internalization in mature B cells, but a suppressive signal is given to the B cell when DNP-MGG is present at the time of antigen receptor reexpression in a fashion similar to clonal anergy. The studies reported here test this hypothesis as a possible additional mechanism of direct B-cell tolerance. When pure DNP-specific B cells were incubated for 6 h with DNP-MGG in the presence of lymphokine-rich EL-4 supernatant, an immune response was induced; but 48 h preincubation with DNP-MGG in the presence of lymphokines induced tolerance. If B-cell cultures were preincubated with DNP-MGG for 6 h followed by a 24-hour incubation without conjugate and DNP-MGG was then added for the third preincubation period of 18 h (at a time when receptors are being reexpressed), tolerance was induced. Substitution of DNP-Ficoll antigen for DNP-MGG in either the first or third time period did not result in tolerance induction but substituting DNP-KLH during either of these two periods did result in tolerance.

Animals↗
PubMed1979

Arthritis associated with jejunoileal bypass: clinical and immunologic evaluation.

Arthritis is a common complication of small bowel bypass, occurring in 5-20% of the postsurgical patients. Thirteen patients with arthritis related to jejunoileal bypass were studied. These patients had a symmetrical polyarthritis, and 8 also had extraarticular connective tissue disease manifestations. Immunologic evaluations were done on these patients and on a control group of 12 age- and sex-matched postintestinal bypass patients without arthritis. The incidence of positive ANA, rheumatoid factors, immune complexes, and antibodies to intestinal flora was the same in both groups. Patients in both groups showed similar changes in numbers of circulating T and B lymphocytes. More patients in the group with arthritis than in the control group had elevated IgA levels (38% versus 8%), but the difference was not significant (P less than 0.05). This study demonstrates that immunologic abnormalities occur after jejeunoileal bypass irrespective of the onset of arthritis or related symptoms. No specific immunologic abnormalities could be associated with the arthritis occurring after small bowel bypass.

Adult↗
PubMed1976

Effect of anti-carrier antibody on carrier-determined tolerance.

These experiments were originally designed to determine whether an anti-carrier antibody, e.g., anti-allotype could break hapten-specific tolerance in vivo. Tolerance to 2,4-dinitrophenyl (DNP) was induced in C57BL/6J mice using DNP-BALB/c IgG2a conjugate. When anti-allotype serum was injected in C57BL/6J mice one day after a single injection of DNP-IgG2a the mice were not tolerant. In contrast, when tolerance was induced by four weekly injections of tolerogen, the anti-allotype serum had no effect on the tolerant state. This effect was specific for tolerance-inducing carrier. Anti-carrier antibody injected in C57BL/6J mice one day after DNP-IgG2a produced a small but significant anti-DNP response without administration of the immunogen, whereas the tolerogen (DNP-IgG2a) by itself was not immunogenic. Similarly, despite multiple injections of DNP-IgG2a bearing the foreign allotype, only one out of 7 C57BL/6J mice showed a weak anti-carrier response. In contrast, a marked anti-carrier (IgG2a) response was obtained when the anti-allotype antibody was passively administered in C57BL/6J mice. In conclusion, these experiments suggest that tolerance to an antigenic determinant may be broken by an antibody directed not to this determinant, but to another on the same molecule. The significance of this finding in relationship to the mechanism of the carrier-determined tolerance and the breakdown of self-tolerance is discussed.

Animals↗
PubMed1976

Loss of carrier-determined tolerance in vitro with loss of receptor blockade.

Experiments were done to determine whether carrier-determined tolerance is reversible and whether the loss of tolerance is accompanied by the loss of receptor blockade. Spleen cells from mice made tolerant with DNP-isologous IgG remained tolerant when transferred to irradiated syngeneic mice. If these same tolerant spleen cells were incubated for 24 hr or more before transfer the tolerance was lost. Autoradiology was done on the tolerant cells with either 125I anti-DNP or 125DNP-KLH, before and after incubation in vitro. When the cells were tolerant the number of DNP ABC was decreased whereas cells having DNP on their surface were increased. When the cells lost tolerance after in vitro incubation, the hapten-bearing cells were no longer present although the number of cells free DNP receptors increased to normal. These data suggest that in carrier determined tolerance the reactivation of tolerant lymphocytes may involve reversible receptor blockade.

Animals↗
PubMed1975

Carrier-determined tolerance in vitro.

A primary immune response to normal BDF1 spleen cells was obtained in vitro to the T-independent antigen TNP-T4 coliphage. This anti-TNP response was suppressed by exposing the spleen cells for 6 hr to TNP bound either to isologous or heterologous gamma-globulin. The suppression was hapten specific. In contrast, TNP-albumin conjugates did not induce tolerance in vitro.

Animals↗