Guido Biozzi

Lack of action of serum opsonins in phagocytosis of inert particles by cells of reticuloendothelial system.

Summary Incubation of carbon particles with normal sera originating from various animal species and with sera from R.E.S. stimulated mice does not affect the rate of carbon phagocytosis by R.E. cells. These findings show that serum opsonins do not act as a limiting factor in carbon phagocytosis. Depression of R.E.S. phagocytic function by “blockade”with colloidal carbon is due to a saturation of phagocytic cells rather than to a depletion of serum opsonins. These results confirm that the rate of carbon blood clearance is a reliable method for measuring phagocytic activity of R.E. cells.

The Genetic Control of Chemically and Radiation-Induced Skin Tumorigenesis: A Study with Carcinogenesis-Susceptible and Carcinogenesis-Resistant Mice

Abstract Pazzaglia, S., Mancuso, M., Rebessi, S., Di Majo, V., Tanori, M., Biozzi, G., Covelli, V. and Saran, A. The Genetic Control of Chemically and Radiation-Induced Skin Tumorigenesis: A Study with Carcinogenesis-Susceptible and Carcinogenesis-Resistant Mice. Radiat. Res. 158, 78–83 (2002). Outbred carcinogenesis-resistant (Car-R) and carcinogenesis-susceptible (Car-S) mouse lines were generated by phenotypic selection for resistance or susceptibility to two-stage skin carcinogenesis. These two Car mouse lines differ by >100-fold in susceptibility. In the present study, we tested the hypothesis that a subset of genetic loci responsible for susceptibility or resistance to chemical skin tumorigenesis may also be involved in radiation-induced skin tumorigenesis. Skin tumorigenesis was tested in groups of Car-S/R mice after X-ray initiation and 12-O-tetradecanoylphorbol-13-acetate (TPA) promotion. We found that ionizing radiation can initiate skin tumors in Car-S mice but not in Car-R mice. In Car-S mice, the most effective radiation doses (6 and 10 Gy given in four fractions) gave a threefold increase in tumor multiplicity and a twofold increase in tumor incidence compared to a TPA-only control group. We performed a molecular analysis of Hras gene mutations in skin tumors of Car-S mice induced by X-ray initiation/TPA promotion or by TPA promotion alone. The most notable difference emerging from the comparison of these mutation patterns is the high incidence (∼50%) of papillomas lacking Hras gene mutations in X-ray-initiated/TPA-promoted papillomas compared to 13% in papillomas induced by TPA alone, suggesting that lack of Hras gene mutations is a consistent feature of radiation-induced papillomas.

Immunocytochemical studies on B lymphocytes from the Biozzi high and low lines of mice selected for their responses to heterologous erythrocytes.

Summary The high and low antibody producing lines of mice developed by Biozzi were studied immunocytochemically in an attempt to determine several parameters of B lymphocyte function. At 8–9 weeks of age, both lines contain the same number of B cells in spleen, lymph node and thymus. The B cells of the high line contain about one-third more surface Ig; the distribution of surface Ig in cells of both lines as well as the redistribution of the surface Ig-anti Ig complexes were identical. At 13–14 weeks of age, the number of B cells was higher in the high antibody producing mice; at this age, however, the mean content of Ig per B lymphocyte was identical.

Regulatory function of Thy-1-negative cells: V. A lymphokine of B cell origin (BEF) induces in vitro high antibody response in genetically selected low responder mice.

Studies were conducted on two lines of mice genetically selected, respectively, for high (AB/H) and low (AB/L) antibody production, in order to identify the mechanism by which genes involved in the selection express their functions. It was found that B cell‐derived enhancing factor (BEF), a lymphokine of B cell origin which acts on T cells by preventing the activation of suppressor cells, is effective in inducing high responses in low responder mice, whereas it is ineffective in modulating antibody production in high responder mice. As a result, no difference was found between the responses of AB/H and AB/L mice when spleen cells were stimulated in vitro in the presence of BEF. AB/H and AB/L mice do not seem to differ in their B cell functions since no difference was found in the capacity of B cells of either line to synthesize antibodies in the presence of T cell‐replacing factor (TRF), or to produce endogeneous BEF. These data indicate that, at least in vitro, the character of general responsiveness of these two mouse lines mainly reflects differential reactivity of T suppressor cells. Since the two lines represent, respectively, the maximal and minimal responsiveness of an outbred population of animals, it is suggested that the individual difference in abtibody response is related to individual differences of T suppressor cells in responding to the immunogen.