Oct-2, a POU homeo domain transcription factor, is believed to stimulate B-cell-restricted expression of immunoglobulin genes through binding sites in immunoglobulin gene promoters and enhancers. To determine whether Oct-2 is required for B-cell development or function, or has other developmental roles, the gene was disrupted by homologous recombination. Oct-2 -/-mice develop normally but die within hours of birth for undetermined reasons. Mutants contain normal numbers of B-cell precursors but are somewhat deficient in IgM + B cells. These B cells have a marked defect in their capacity to secrete immunoglobulin upon mitogenic stimulation in vitro. Thus, Oct-2 is not required for the generation of immunoglobulin-bearing B cells but is crucial for their maturation to immunoglobulin-secreting cells and for another undetermined organismal function.

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The splenic B-cell repertoire of unimmunized C57BL/6 mice can be examined for anti-(4-hydroxy-3-nitrophenyl)acetyl (NP) B cells of relatively high affinity by using a dual strategy. (14,15) and showed that it could prevent the generation of anti-HSA memory B cells in a dose-dependent manner. Adoptive transfer studies showed that the toleragen affected donor T and B cells, the former effect being more profound. Another way of studying the relative contributions of Tand B-lymphocyte populations to an antibody response is to make use of various hapten-carrier combinations (16-18). T-dependent anti-hapten antibody formation requires that anti-hapten B cells be "helped" by carrier-specific T cells. The anti-(4-hydroxy-3-nitrophenyl)acetyl (NP) response of C57BL/6 mice has been extensively investigated (19-21) because of the preferential appearance of B-cell clones utilizing the VH 186.2 V gene and the Al light chain gene, facilitating the study of V gene hypermutation. It is also a system in which clones making relatively high-versus relatively low-affinity antibody can be discriminated by the use of, respectively, relatively lowly versus relatively highly haptenated protein conjugates in an ELISA (22,23). In the present study, we immunized mice with highly haptenated NP-HSA, and attempted tolerance induction with lowly haptenated, freshly deaggregated, NP-HSA, with HSA carrier alone, or with NP attached to irrelevant carriers. The key findings were that NP-HSA .Jways worked better than carrier alone or NP attached i other carriers in preventing memory cell appearance and that tolerance could still be induced after immunogenic challenge, up to the time of the first appearance of V gene mutations. Apparently, the functional silencing of T and B cells is necessary for the full tolerance effect, and T-ceil help is still required for continued B-memory cell generation after the germinal center reaction is well under way.

The objective of this study was to determine the effectiveness of a statewide campaign aimed at increasing chlamydia awareness and testing among younger people. In November 2002, a narrowcast media campaign targeting men and women aged 16-29 years was launched in Victoria, Australia. This was expanded in June 2003. Data on chlamydia testing via Medicare and chlamydia notifications, before and after the campaign, were compared to determine possible effects of the campaign on population rates of chlamydia testing and detection. During the campaign, chlamydia testing rates increased significantly for both women (P=0.04) and men (P=0.04), while testing rates before and after the campaign remained relatively stable. Although testing rates increased, only 4.3% of Victorian women and 1.9% of men aged 16-30 were tested through Medicare in 2003. The increase in chlamydia testing over the study period was closely paralleled by an increase in notification rates for chlamydia, with strong correlations between the two (r=0.97, P<0.001). In conclusion, an estimated minimum of A$70 was spent on the campaign for each additional chlamydia test performed. Testing within the framework of a national chlamydia screening programme may be a more cost-effective way of increasing chlamydia testing.

The anti-human serum albumin (HSA) B-cell repertoire of C57BL/6 mice was examined by culturing splenocytes at limiting dilution following polyclonal stimulation with Escherichia coli lipopolysaccharide and a lymphokine mixture. The frequency of anti-HSA precursors was determined before and after immunization with alum-precipitated HSA and 109 killed Bordetella pertussis organisms, by submitting clonal supernatants to an ELISA. Anti-HSA IgGl-forming precursors were rare in unimmunized spleens, representing 1 in 500,000 splenocytes or only -100 cells per spleen. Between day 5 and day 7 after immunization, this figpre increased to -20,000 cells per spleen. Over the following 3 weeks, there was a progressive increase in the mean optical density generated in the clonal ELISA, presumably due to affmity maturation of the B-cell population. When freshly deaggregated HSA was injected before or even up to 4 days after challenge immunization, the appearance of anti-HSA IgGl-forming cell precursors was largely prevented. The effect was most marked with 5 mg or 1 mg of soluble HSA, but impressive partial effects could be seen with as little as 10 ,ug of HSA if administered before challenge immunization. Most of the few clones seen after the higher doses of the toleragen appeared to make antibody of low affinity. The capacity to influence the B-cell pool by soluble antigen administered just 1-2 days before the sudden appearance of IgG1 precursors argues against the totality of the effect being due to T-cell-mediated suppression and in favor of a direct effect on B cells.Previous work from this laboratory (1-3) has shown that the preimmune B-cell repertoire of murine spleen contains surprisingly few cells with sufficient affinity for protein antigens (1, 2) or syngeneic intracellular structures (3) to bind in an ELISA when IgG1 antibody is the clonal product. Five days after challenge immunization with protein antigens and adjuvants, there is a sudden burst of appearance of IgG1 antibody-forming cell precursors (AFCP), most of which had already undergone an isotype switch in vivo (2) and were surface IgM-negative IgG1-positive cells. The relationship between these newly appearing B cells and the anti-protein IgM AFCP noted in unimmunized mice is not clear, but the former are unlikely, on kinetic grounds, to be the direct, unmutated progeny of the latter. Linton et al. (4) (Sigma). Some groups of mice were serially bled from the orbital venous plexus, and serum samples were prepared for antibody assay.Cell Preparation and Culture. Five thousand 3T3 BALB/c fibroblasts (Commonwealth Serum Laboratories, Melbourne, Australia) were aliquoted into flat bottomed 96-well microtiter trays in 100 A.l. Culture medium (CM) was RPMI 1640 containing 100 AsM 2-mercaptoethanol and 5% (vol/vol) fetal calf serum (Flow Laboratories). Spleen cell suspensions were prepared as described (6, 7) including 0.83% NH4CI for erythrocyte lysis followed by damaged and dead cell removal. Splenocytes were dispensed in 100 Al of CM containing Escheri...

This paper describes the evaluation findings of a hepatitis B immunisation pilot project, which aimed to increase the uptake and compliance of hepatitis B vaccinations among female prisoners in Victoria. The evaluation used a mixed methods approach including in‐depth interviews, focus group discussions and an analysis of quantitative data. Fifty‐five per cent of potential participants (391/712) were offered hepatitis B immunisation. Of those offered immunisation, 204 were eligible for immunisation and 169 (83%) received the first dose. Ninety‐three per cent of eligible women received two doses and 84% completed the three‐dose series. Lessons learnt from the pilot led to the revision of key prison hepatitis B immunisation policies and practices to ensure uniformity across Victorian prisons.

Adult C57BL/6 mice were injected with 100 ,ug of soluble, freshly deaggregated human serum albumin (HSA) to produce partial immunologic tolerance. UnhEjected normal control (N) mice contain only 100 B cells in their spleens with the capacity to (i) be activated in vitro into clonal proliferation by Escherichia coli lipopolysaccharide plus interleukins 2, 4, and 5, (ii) form IgG1 as well as IgM antibody, and (iii) display specificity for HSA when only IgG1 is allowed to score in an enzyme-linked immunosorbent assay (ELISA). Such N mice generate ==50,000 clonable anti-HSA IgG1 antibody-forming cell precursors in their spleens after T-dependent immunization with HSA adsorbed onto alum and given with BordeteUa pertussis adjuvant. Mice prei'jected with soluble HSA (TOL)-generate far fewer anti-HSA IgG1 antibodyforming cell precursors, termed anti-HSA memory cells. Splenocytes were transferred from N or TOL mice into lethally irradiated syngeneic recipients together with syngeneic bone marrow. Whereas N splenocytes generated plentiful memory cells within 2 weeks in antigenically challenged recipients, TOL splenocytes did not. Work with Ly-5 congenic mice ruled out memory cell generation from either the host or the bone marrow inoculum within this limited time. N T cells plus TOL B cells showed consistently lowered memory cell generation. TOL T cells plus N B cells showed an even greater lowering of adoptive memory cell generation. Thus the lowered response capacity of TOL mice resided in the T-and B-cell compartments. Attempts to show a suppressor component within the T-cell population were inconclusive, but a profound defect in capacity to respond to HSA in vitro was exhibited by the CD4' T cells of TOL mice. B lymphocytes were harvested from T-dependently immunized mice 5 days after challenge, incubated with soluble HSA for 18 hr, and then adoptively transferred together with N T cells. The recently activated B cells were not rendered tolerant by this manipulation. The results argue for a major T-cell component in the process whereby soluble protein antigens ablate affinity maturation and memory cell generation.