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S Specter

Publications and source records attributed to S Specter.

98 records · Page 6Linked to original sources
PubMed1977

Immunocycte stimulation in vitro by nontoxic bacterial lipopolysaccharide derivatives.

Intact lipopolysaccharides (LPS), considered nonspecific enhancers of B cell responses, as well as nontoxic derivatives from Serratia marcescens LPS, were studied with regard to their ability to stimulate in vitro immune responses to a T-dependent antigen, sheep erythrocytes. Intact LPS, at a dose of 10 to 50 microgram, consistently enhanced the in vitro anti-SRBC immune response by normal splenocytes. The LPS also increased the background PFC response to SRBC in nonimmunized cultures. A chemically detoxified preparation derived from LPS (Mex B) had no stimulatory activity in vitro. A completely nontoxic, relatively small m.w., polysaccharide-rich preparation (PS), free of detectable lipid and protein, was stimulatory in vitro and at a dose of 10 microgram resulted in a 40 to 70% enhancement of the anti-SRBC response. The PS also stimulated an enhanced background response to SRBC as well as several other RBC species in nonimmunized cultures. PS had no mitogenic effect in vitro since addition of this bacterial derivative failed to stimulate thymidine incorporation into mouse splenocytes, as occurred with the intact LPS. The use of nontoxic preparations from gram-negative bacterial LPS for dissecting the stimulatory vs antigenic properties of bacterial products provides a model system for determining the role of a mitogenic stimulus in B cell activation.

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PubMed1976

Immunosuppression induced in vitro by cell-free extracts of Friend leukemia virusinfected splenocytes.

The immunologic responsiveness by normal BALB/c spleen lymphocytes immunized in vitro with sheep erythrocytes was markedly suppressed by calrified cell-free homogenates of Friend leukemia virus (FLV)-infected mouse spleens. Suppression was achieved with a 3,000Xg supernatant of FLV-containing homogenates freed of cellular debris but not with crude unclarified homogenates or pelleted material after centrifugation. The immunosuppressive effects of the virus were dose dependent, whether the virus was added directly to the target spleen cells or separated from them by a 0.4mu Nuclepore filter. Suppression was prevented by heating of the virus at 100 degrees C for 10 minutes or by neutralization with antiserum to FLV. Addition of the virus as late as 48 hours after in vitro immunization of splenocytes affected the immune response. However, suppression was maximum when the clarified virus was added to the splenocytes 1 or 2 days before immunization. The agent in the FLV-infected spleen homogenates responsible for immunosuppression appeared to be the virus per se; however, virus-associated soluble factor(s) might have been involved.

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PubMed1976

Restoration of leukemia virus-suppressed immunocytes in vitro by peritoneal exudate cells.

Depressed antibody responsiveness to sheep erythrocytes in mice infected with Friend leukemia virus continued in vitro when spleen cell cultures from infected animals were cultured in the presence of antigen. Addition of PE cells from normal donor mice to the immunologically depressed splenocyte cultures resulted in a marked restoration of antibody responsiveness. Restoration of the immune response was PE cell dose-dependent; a ratio of 1 PE cell per 10 splenocytes resulted in the largest numbers of PFC's. These results suggest that impaired antibody responsiveness by spleen cell cultures from FLV-infected mice may be due, in part, to effects on antigen-processing macrophages, since restoration of immune responsiveness occurs by PE cell supplements.

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PubMed1975

Leukemia virus-induced immunosuppression: scanning electron microscopy of infected spleen cells.

Spleen cells from mice infected with Friend leukemia virus were examined by scanning electron microscopy. Whereas splenocytes from normal noninfected animals showed the expected morphologic classes of lymphocytes, including those with smooth surfaces and with numerous villous projections, an alteration of cell type was evident within a few days after infection. Friend leukemia virus caused a rapid decrease in the number of villous cells, with a concomitant increase in the number of cells with smoother surfaces. By the end of the first 1 to 12 weeks after infection the majority of cells were smooth, many showing distinct morphologic changes, including "holes" and a spongy appearance. Nearly all of the splenocytes were abnormal in appearance by days 17 to 30 after infection, with most showing a spongy topography. These changes paralleled the marked immunosuppression induced by Friend leukemia virus infection, as well as the appearance of virus-associated surface antigen on individual splenocytes. Topographic changes evident by examination with scanning electron microscopy were not readily apparent by either standard histology or transmission electron microscopy.

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PubMedDate not supplied

Enhancement of plasma levels of tumor necrosis factor alpha but not interleukin-6 following endotoxin injection of Friend leukemia virus infected mice.

Friend leukemia virus complex (FLC) infection of BALB/c mice causes a rapid, progressive suppression of most immune functions. In the present study, FLC infection resulted in increased induction by bacterial lipopolysaccharide (LPS) of tumor necrosis factor alpha (TNF alpha) but not IL-6. TNF alpha levels were significantly elevated beginning 11 days post infection and increasing levels were measured through day 21. The highest TNF alpha levels in FCL-infected mice were as much as 100-fold higher than in LPS treated non-infected mice. Peak plasma levels of TNF alpha were seen between 1 and 2 hr after LPS induction, as compared to a peak at 1 hr in controls. The ability of LPS to stimulate TNF alpha was concentration dependent over a range of 0.005 to 50 micrograms per mouse. Using anti-TNF alpha antiserum, cytotoxic activity of plasma was shown to be due specifically to TNF alpha. These data suggest that induction of TNF alpha and IL-6 is regulated by different mechanisms in FLC-infected mice.

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