After infection and a prolonged incubation period, the scrapie agent causes a degenerative disease of the central nervous system in sheep and goats. Six lines of evidence including sensitivity to proteases demonstrate that this agent contains a protein that is required for infectivity. Although the scrapie agent is irreversibly inactivated by alkali, five procedures with more specificity for modifying nucleic acids failed to cause inactivation. The agent shows heterogeneity with respect to size, apparently a result of its hydrophobicity; the smallest form may have a molecular weight of 50,000 or less. Because the novel properties of the scrapie agent distinguish it from viruses, plasmids, and viroids, a new term "prion" is proposed to denote a small proteinaceous infectious particle which is resistant to inactivation by most procedures that modify nucleic acids. Knowledge of the scrapie agent structure may have significance for understanding the causes of several degenerative diseases.

http://science.sciencemag.org/content/sci/216/4542/136.full.pdf

Novel proteinaceous infectious particles cause scrapie

The biology of interleukin-6.

When stimulated with antigen, B cells are influenced by T cells to proliferate and differentiate into antibody-forming cells. Since it was reported that soluble factors could replace certain functions of helper T cells in the antibody response, several different kinds of lymphokines and monokines have been reported in B-cell growth and differentiation. Among these, human B-cell differentiation factor (BCDF or BSF-2) has been shown to induce the final maturation of B cells into immunoglobulin-secreting cells. BSF-2 was purified to homogeneity and its partial NH2-terminal amino-acid sequence was determined. These studies indicated that BSF-2 is functionally and structurally unlike other known proteins. Here, we report the molecular cloning, structural analysis and functional expression of the cDNA encoding human BSF-2. The primary sequence of BSF-2 deduced from the cDNA reveals that BSF-2 is a novel interleukin consisting of 184 amino acids.

Complementary DNA for a novel human interleukin (BSF-2) that induces B lymphocytes to produce immunoglobulin

Publisher Summary This chapter focuses on structure and expression of interleukin-6 (IL-6), which is a cytokine with pleiotropic activities that plays a central role in host defense. IL-6 can exert growth-inducing, growth-inhibitory, and differentiation-inducing activities, depending on the target cells. These activities include (1) terminal differentiation (secretion of immunoglobulins) in B cells and (2) growth promotion on various B cells. IL-6 has been implicated in the pathology of many diseases including multiple myeloma, mesangial proliferative glomerulonephritis, rheumatoid arthritis, and acquired immunodeficiency syndrome (AIDS). Selective inhibition of the synthesis or of the action of IL-6 may have therapeutic benefit against the IL-6-associated diseases. On the other hand, IL-6 has potent antitumor activity against certain types of tumors. Application of IL-6 is promising in cancer treatment as well as in treatment of radiation- or chemotherapy-induced myelosuppression. The cell biology of the intracellular events that link transduction to gene regulation is an important area, and work on these topics helps to understand such phenomena as multifunction of IL-6 and bidirectional effects of cell growth depending on the cell type.

Interleukin-6 in biology and medicine

A fractionating column for analysis of nucleic acids

WE have recently shown that the immune response to sheep red blood cells (SRBC) in vitro is T-cell dependent, that is, it can be abrogated by pretreatment of the spleen cells with anti-θ serum and complement1. We further reported that reconstitution of the system can be achieved by, among other things, the addition of allogeneic thymocytes2, while syngeneic thymocytes failed to function as helper cells. Positive allogeneic effects were only obtained if the added thymocytes could recognize the remaining B-cells as foreign. One of the explanations evoked for this allogeneic effect was the participation of a potentiating factor2,3. It seemed possible that on the heavy antigenic stimulation provided by the histocompatibility antigens carried by the B-cells, added T-cells produce a soluble factor which stimulates the immune response of B-cells to unrelated antigens. We now want to report the existence of two distinct factors, one of which can completely replace T-cells.

Replacement of t-cell function by a t-cell product.

The extraction of infectious virus nucleic acid with hot phenol

There is a wealth of experimental evidence supporting the idea that T cells have to intervene in the immune response to many antigens to ensure an optimal antibody response (Reviewed in Greaves et al. 1973). We have addressed our work to the question at whicli step of B cell activation this intervention is necessary. An in vitro culture system (Mishell & Dutton 1967) was applied using spleen cells of thie functionally athymic nu/nu mice and heterologous blood cells as antigens. SRBC can operationally be defined as T cell dependent antigens since the IgM immune response in T cell deprived cultures is far from the optimal response obtained in the presence of T cells (Schimpl & Wecker 1970). In an attempt to restore the immune response in T cell deprived cultures with thymocytes we found that allogeneic thymocytes were greatly superior to syngeneic ones (Schimpl & Wecker 1971). Subsequent experiments showed that the effect could be ascribed to a soluble factor produced by allogeneically or Concanavalin A (Con A) stimulated T cells (Schimpl & Wecker 1972, Wecker et al. 1974). Soluble mediators with similar T cell replacing activities have now been described by many different groups (Dutton et al. 1971, Doria et al. 1972, Gorczynski et al. 1972, Feldmann & Basten 1972, Britton 1972, Sjoberg et al. 1972, Gisler et al. 1973, Rubin et al. 1973, Waldmann & Munro 1973, Watson 1973, Kishimoto & Ishizaka 1973, Amerding & Katz 1974), some factors being obtained from T cells, activated by antigen in vivo and incubated with the same antigen in vitro. The assumption imderlying all further considerations is that such mediators are regularly produced upon stimulation of T cells and that they

A third signal in B cell activation given by TRF.

A simple test for serodifferentiation of poliovirus strains within the same type.

By means of indirect immunofluorescence analysis we investigated the effect of HIV-1 infection on HLA class I surface antigens. We report here that in CD4+ HeLa cells, in H9 cells, and in peripheral T lymphocytes HLA class I antigens are downregulated following infection with HIV-1. The downregulation is effected at a posttranscriptional level since the amounts of HLA class I specific mRNA are similar in infected and uninfected cells. This phenomenon is not only correlated with the state of infection, that is, the presence of P24 of HIV-1 in the cells, but also depends on the time of infection. Upon HLA class I downregulation by HIV infection, the specific lysis of peripheral blood cells by allogeneic CTL is reduced.

/pdf/downregulation-of-hla-class-i-antigens-in-hiv-1-infected-1vdoqd6f4e.pdf

Downregulation of HLA class I antigens in HIV-1-infected cells.

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