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Biomedical subjects

M I Luster

Publications and source records attributed to M I Luster.

195 records · Page 11Linked to original sources

Measles virus-specific IgD antibodies in patients with subacute sclerosing panencephalitis.

Indirect immunofluorescent analysis revealed that sera from five patients with subacute sclerosing panencephalitis possessed IgD antibodies directed against measles virus components in persistently infected HeLa cells. IgD levels in these sera were within the normal range. Control studies indicated that the reaction was specific for measles virus. The detection of IgD measles antibodies in these patients suggested that IgD may be involved in the pathogenesis of this viral disease.

Antibodies, Viral↗

Alloantigens defined by cytotoxic isoantisera prepared against peripheral rabbit lymphocytes.

Seven lymphocytotoxic antisera were produced in rabbits by means of isoimmunization with purified peripheral lymphocytes. The phenotypic profile of the defined lymphocyte antigens was determined in a panel of 97 rabbits. The results indicated the existence of at least two major antigenic determinants. Further typing and cross-absorptions were performed with several of the lymphocytotoxic antisera in order to demonstrate monospecificity. The anti-3 antiserum was used to determine the distribution of the respective antigens in various rabbit organs. The highest concentration of the alloantigen was contained in the spleen, followed in descending order by the lymph nodes, lung, skin, kidney, heart and liver. Fat and red blood cells (rbc) contained no detectable antigen. A two-stage physical adherence column method was used to separate T-derived from B-derived lymphocytes and each fraction was tested for the alloantigen. Alloantigen was detected on both cell types. The fact that the anti-3 antiserum never killed more than 30% of the cells suggests that it could define a subpopulation of lymphocytes.

Absorption↗

Erythrocyte antinuclear antibodies in sera of chickens hyperimmunized with group A streptococcal vaccine.

Chickens hyperimmunized with group A streptococcal vaccine often synthesize high levels of antibody to group A streptococcal carbohydrate (SACHO). Indirect immunofluorescent analysis revealed that sera of these chickens also contain antinuclear antibodies capable of reacting with chicken erythrocyte nuclei (EANA) at titers up to 2,560. Removal of the anti-SACHO antibodies from hyperimmune serum did not significantly reduce EANA titers, indicating that anti-SACHO antibodies are not responsible for the EANA reactions. The time course for antibody development as well as the immunoglobulin class distribution of EANA and anti-SACHO antibodies were very similar. Localization of EANA activity to Fab fragments indicated that the immunfluorescent reaction represents an antigen-antibody reaction. Findings point out an important consequence of using chicken immunoglobulin Y in immunofluorescent assays. The purified Fc fragment of immunoglobulin Y is cytophilic for the substrate when tested at high concentrations, which suggests that some cytophilic immunoglobulins are involved in the reaction.

Animals↗

Structure and biological functions of human IgD. VI. Serum IgD in patients with allergic bronchopulmonary aspergillosis.

Serum IgD levels were quantified in a large population of individuals with a variety of atopic and/or pulmonary disorders. As a group, patients with allergic bronchopulmonary aspergillosis (ABPA) have markedly elevated (5.03 mg%) serum IgD when compared with serum IgD levels from either normal individuals (2.17 mg%) or patients with a variety of pulmonary and/or atopic disorders. Evidence is presented suggesting that the increased serum IgD levels in ABPA patients are not necessarily related to a hyper-IgE or panhyperimmunoglobulinemia common to most of all these patients, but is rather associated with an additional quantitative difference in the immunological responsiveness of some of these individuals. An understanding of why these patients produce supranormal levels of IgD may reveal the basis for inducing an IgD antibody response and subsequently help in elucidating the biological function(s) of IgD.

Aspergillosis↗

Structure and biological functions of human IgD. VII. IgD antinuclear antibodies in sera of patients with autoimmune disorders.

Indirect immunofluorescent tests were employed to study antinuclear antibodies (ANA) of the IgD class in sera from patients with autoimmune disease. In sera containing IgG-ANA, IgD-ANA was detected in 48% of patients with systemic lupus erythematosus, 37% with rheumatoid arthritis, 30% with Raynaud's disease, 23% with systemic scleroderma and 20% with discoid lupus erythematosus. Quantitative comparison of serum IgG, IgA, IgM and IgD between IgG-ANA-positive sera with and without IgD-ANA revealed that patients with IgD-ANA also had elevated serum IgA levels. The detection of IgD-ANA in over 36% of the patient population suggests that IgD may play a role in autoimmune disorders.

Antibodies, Antinuclear↗

Histopathology of acetaminophen-induced liver changes: role of interleukin 1 alpha and tumor necrosis factor alpha.

Administration of 500 mg/kg acetaminophen (APAP) to female B6C3F1 mice resulted in well-documented pathophysiological changes in the liver manifested as increased serum concentration of liver enzymes (aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, and serum sorbitol dehydrogenase), centrilobular congestion, and hepatocellular degeneration and necrosis. The role of proinflammatory cytokines, including tumor necrosis factor alpha (TNF-alpha) and interleukin 1 alpha (IL-1 alpha), on the hepatotoxicity of APAP was examined at 4, 8, 12, and 24 hr following APAP administration. Neutralization of TNF-alpha or IL-1 alpha with specific antibodies partially prevented the hepatotoxic effects of APAP at the 4- and 8-hr time points. In addition, prior administration of anti-TNF-alpha antibodies shortened the recovery time following APAP treatment. While IL-1 receptor antagonist (IL-1ra) had only a modest protective effect against APAP-induced liver damage, as determined by serum enzyme release, IL-1ra had no effect on the degree of hepatic congestion or necrosis at any of the time points examined. On the other hand, administration of antibodies against IL-1ra exacerbated APAP-induced liver toxicity. These results suggest that TNF-alpha and IL-1 alpha play an important role in the degree of damage and recovery that the liver undergoes following APAP intoxication.

Acetaminophen↗

Role of endotoxin in tumor necrosis factor alpha expression from alveolar macrophages treated with urban air particles.

The effects of urban air and diesel particles on inflammatory cytokine gene expression, tumor necrosis factor alpha (TNF-alpha) in particular, were studied in rat alveolar macrophages. TNF-alpha, interleukin (IL)-1, IL-6, cytokine-induced neutrophil chemoattractant (CINC), and macrophage inflammatory protein (MIP)-2 gene expression and TNF-alpha secretion were increased in cells treated with 50 to 200 micrograms/mL of urban air particles in a concentration-related manner. There was no cytokine induction by diesel particles at any of the concentrations tested. Cytokine expression was not related to reactive oxygen species since antioxidants, such as catalase, TMTU, or DMSO, had no effect on TNF-alpha secretion. However, cytokine induction by urban air particles was completely prevented by polymyxin B, an antibiotic capable of neutralizing bacterial lipopolysaccharide (LPS) activities. Furthermore, LPS was detected on the urban air particles, but not on diesel particle. These results suggest that activation of cytokine gene expression and secretion in rat alveolar macrophages by urban air particles is due to the presence of endotoxin on the particles.

Air Pollutants↗

Depression of humoral immunity in rats following chronic developmental lead exposure.

Chronic pre- and postnatal exposure of CD rats to low levels of lead resulted in a marked depression in the antibody response to SRBC as well as decreased serum IgG levels. Serum IgM and IgA levels were normal. The fact that the antibody response to LPS, a thymus independent antigen, was not altered, suggested that the T-lymphocyte rather than the B-lymphocyte is affected by lead exposure. Additional significance is lent to these results when blood lead levels in treated rats were found to be similar to levels found in many children in urban areas.

Animals↗

Acetaminophen-induced hepatotoxicity is associated with early changes in NF-kB and NF-IL6 DNA binding activity.

Nuclear transcription factors, such as NF-kB and NF-IL6, are believed to play an important role in regulating the expression of genes that encode for products involved in tissue damage and inflammation and, thus, may represent early biomarkers for chemical toxicities. In the present study changes in DNA binding activity of these factors were examined in livers of mice administered hepatotoxic doses of acetaminophen (APAP). NF-kB and NF-IL6 DNA binding occurred constitutively in control mouse liver. However, within 4 hr following administration of hepatotoxic doses of APAP, their binding activities were transiently lost and is in contrast to AP-1 transcription factor where activation occurs under similar conditions. These changes corresponded with increased release of inflammatory mediators (IL-6, serum amyloid A) and increased levels of enzymatic markers of hepatocyte damage. Similarly, treatment of mice with gadolinium chloride, an inhibitor of Kupffer cell activation and known to protect against APAP-induced hepatotoxicity, reduced the observed pathophysiological response in the liver while altering the APAP-associated changes in NF-kB DNA binding activity. NF-kB was found predominantly in parenchymal and endothelial cells and was composed primarily of relatively inactive p50 homodimer subunits in control liver. Taken together, these studies suggest that hepatotoxicity is associated with early and complex changes in DNA binding activities of specific transcription factors. In particular, NF-kB and NF-IL6 may serve as negative regulators of hepatocyte-derived inflammatory mediators and is analogous to that previously observed in certain other cell systems such as B lymphocytes.

Acetaminophen↗