Ilene Nowicki Montgomery

A messenger RNA for capsid protein isolated from tobacco mosaic virus-infected tissue.

Abstract A low molecular weight virus-related RNA component (LMC) was isolated from extracts of TMV-infected leaf tissue by employing a combination of the techniques of sucrose density gradient sedimentation and polyacrylamide gel electrophoresis. It was found that LMC has an estimated molecular weight of 2.5 × 10 5 and acts as a template for the synthesis of TMV capsid protein in a wheat germ-derived cell-free protein synthesizing system. Evidence is presented for the possible existence of other unique virus-related RNA species in extracts of infected tissue.

Expression of mosaicism in females heterozygous for Jimpy

The Jimpy mouse is a sex-linked neurological mutant characterized by a paucity of myelin in the central nervous system (CNS). The distribution of myelin in the optic nerves of female carriers of the Jimpy gene exhibits a mosaic pattern such that patches of tissue along the nerve are identical in appearance to the hemizygote male, while other areas appear normal.

Production and characterization of high titer antibodies to galactocerebroside

High titer antibodies primarily of the IgG class were produced against galactocerebroside (GalC) by including keyhole limpet hemocyanin (KLH) and supplemental M. tuberculosis in the adjuvant mixture used for immunization of rabbits. Antibody titers were determined by an ELISA in which microtiter wells were coated with liposomes containing lecithin, cholesterol and GalC. The antibodies showed reactivity with GalC and psychosine, but not glucocerebroside, sulfatide, mixed gangliosides or asialo GM1. Specificity was further demonstrated by absorption of antibodies with GalC. Binding was inhibited by galactose, but only at high concentrations. Further, the antibodies did not bind to any brain proteins on immunoblots, indicating lack of reactivity with glycoproteins which might contain a terminal galactose. Antibodies to GalC are directed against different determinants than those reacting with peanut agglutinin since the lectin will not react with GalC, and the antibodies will not react with asialo GM1. The antibodies raised to GalC by this method show specific staining for oligodendroglia in culture. Peanut agglutinin binds intensely to process-bearing GalC+ oligodendroglia, but very poorly to the membrane sheets elaborated by oligodendroglia after longer times in culture. Other process-bearing GalC-, GFAP- cells were also stained with peanut agglutinin; these cells may represent glial precursors.

Chronic Theiler's virus infection in mice: appearance of myelin basic protein in the cerebrospinal fluid and serum antibody directed against MBP

Abstract Myelin basic protein (MBP) appears frequently in the cerebrospinal fluid (CSF) of mice with chronic demyelination following intracerebral infection with Theilers murine encephalomyelitis virus (TMEV); antibody to MBP can frequently be found in the sera. The peaks of the immune responses to both MBP and TMEV coincide with the time course of the clinical signs of disease. Adsorption of mouse sera with TMEV or MBP indicate the non-identity of the antigens and the specificity of the antisera as measured by ELISA. Immunoblot analysis of sera confirmed the ELISA findings. The mechanism of induction of antibody directed against MBP and its role in TMEV-associated demyelination remain to be determined.

Effects of cardiotoxin d from naja naja siamensis snake venom upon murine splenic lymphocytes

Cardiotoxin D from Naja naja siamensis is cytotoxic to T-lymphocytes above 150 femtomoles/10(6) cells. Equivalent lysis of macrophages or B-lymphocytes requires at least 1000 times more toxin. Reduction and carboxamidomethylation of cardiotoxin D does not effect T cell lysis. At higher toxin concentrations, 50% T-cell lysis occurs within 10 min. Splenocytes cultured with mitogens are up to five times more susceptible to toxin than unstimulated cells. Cardiotoxin D may directly disrupt the plasma membrane, since lysis is unaltered at 4 degrees C.

Experimental allergic encephalomyelitis: Prevention with a nontoxic derivative of a cobra neurotoxin

Abstract Treatment with a cobra neurotoxin derivative protects guinea pigs from experimental allergic encephalomyelitis induced by myelin basic protein. The neurotoxin derivative and myelin basic protein cross react immunologically at both the cellular and humoral levels. We propose that the molecular basis for the immunologie relationship between these proteins is centered in their respective tryptophan-containing regions.

Experimental allergic encephalomyelitis in mice: presence of myelin basic protein in cerebrospinal fluid

The concentration of myelin basic protein (MBP) in cerebrospinal fluid (CSF) correlates with the development of experimental allergic encephalomyelitis following intradermal injection with encephalitogen in adjuvant; MBP is absent in controls inoculated with adjuvants only. The presence of MBP is a sensitive indicator of disease inasmuch as CNS-inoculated mice with neurologic signs had an average of 0.29 ng/microliter of MBP in their CSF and controls, including normal or adjuvants only, had an average of 0.03 ng/microliter. The amount present per microliter of CSF, as well as the absolute amount, obtained from an individual mouse do not always reflect the severity of disease as indicated by clinical signs and the pathology observed in a sampling of the neuraxis. The presence of MBP does correlate with demyelination, although the extent of pathology observed by light microscopy in the mouse model is minimal, associated only with the inflammatory response, and does not extend beyond the zone of the perivascular cuff.

Clinical correlates of enzyme-immunoassay versus radioimmunoassay measurements of antibody against acetylcholine receptor in patients with myasthenia gravis

Antibody against human nicotinic acetylcholine receptor [Ab(AcChR)] was measured in the sera obtained from 55 patients with myasthenia gravis (MG) using both radioimmunoassay (RIA) and enzyme-linked immunosorbent assay (ELISA). By at least one assay, 91% of the patients had elevated Ab(AcChR). We found no correlation between the amount of Ab(AcChR) measured by RIA and that measured by ELISA. Patient subpopulations defined by ELISA- or RIA-measured Ab(AcChR) were associated with different disease durations. All of those who had high Ab(AcChR) levels by both assays had experienced symptoms for less than 2 years. 87% of those with high Ab(AcChR) levels by ELISA had had MG for less than 4 years. Those patients with high Ab(AcChR) only by RIA had a mean disease duration of over 8 years. With regard to correlations of Ab(AcChR) with patient age and sex, females under 50 years of age had high levels of Ab(AcChR) by RIA, but had lower levels by ELISA, whereas men over 50 had high Ab(AcChR) levels by ELISA. Using either assay, no relationship was established between concentrations of Ab(AcChR) and the patients functional status, previous thymectomy, or current therapy. In this study, 16% of the MG patients with elevated Ab(AcChR) would have been considered within the non-disease range of Ab(AcChR) had only the RIA been performed, thus recommending the routine use of both assays for diagnostic purposes.

Experimental allergic encephalomyelitis in mice: Adoptive transfer of disease is modulated by the presence of natural suppressor cells

Normal, untreated syngeneic recipients of lymphocytes from mice with experimental allergic encephalomyelitis (EAE) do not generally express adoptively transferred disease. Cell transfer of EAE is more successful when syngeneic recipients are treated with cyclophosphamide (CY) prior to the injection of donor cells. Normal, untreated recipients that do not develop EAE after receiving EAE donor lymphocytes are also unresponsive to subsequent encephalitogenic challenge. Those CY-treated recipients that fail to develop EAE after cell transfer do develop EAE after subsequent challenge. After reconstitution with normal splenic lymphocytes, CY-treated recipients do not develop EAE after subsequent challenge. These findings suggest the presence of an intrinsic natural suppressor cell subpopulation in naive mice which modulate the expression of adoptively transferred T lymphocytes.