Imatinib mesylate (STI571, imatinib) inhibited DNA synthesis in primary human T cells stimulated with allogeneic mature dendritic cells or phytohemagglutinin (PHA) but did not induce apoptosis. The values for the concentration that inhibits 50% (IC₅₀) of T-cell proliferation stimulated by dendritic cells and PHA were 3.9 μM and 2.9 μM, respectively, that is, within the concentration range found in patients treated with imatinib mesylate. Interestingly, imatinib mesylate did not inhibit expression of T-cell activation markers CD25 and CD69, although it reduced the levels of activated nuclear factor-κB (NF-κB) and changed phosphorylation or protein levels of Lck, ERK1/2, retinoblastoma protein, and cyclin D3. When T cells were washed free of imatinib mesylate, they proliferated in response to PHA, demonstrating that inhibition is reversible. Treatment with imatinib mesylate led to accumulation of the cells in G₀/G₁ phase of the cell cycle. The in vitro observations were confirmed in vivo in a murine model of delayed-type hypersensitivity (DTH). In mice treated with imatinib mesylate, DTH was reduced in comparison to sham-injected controls. However, the number of splenic T cells was not reduced showing that, similarly to in vitro observations, imatinib mesylate inhibited T-cell response, but did not cause apoptosis. These findings indicate that long-term administration of high-dose imatinib mesylate might affect immunity.

The amount of the 64-kDa subunit of polyadenylation/cleavage stimulatory factor (CstF-64) increases 5-fold during the G₀ to S phase transition and concomitant proliferation induced by serum in 3T6 fibroblasts. Higher levels of CstF-64 result in an increase in CstF trimer. The rise in CstF-64 occurs at a time when the amount of poly(A)-containing RNA rose at least 5–8 fold in the cytoplasm. Primary human splenic B cells, resting in G₀, show a similar 5-fold increase in CstF-64 when cultured under conditions inducing proliferation (CD40 ligand exposure). Therefore, the increase in CstF-64 is associated with the G₀ to S phase transition. As B cell development progresses, RNA processing changes occur at the Ig heavy chain locus resulting in a switch from the membrane- to the upstream secretory-specific poly(A) site. Treating resting B cells with agents triggering this switch in Ig mRNA production along with proliferation (CD40 ligand plus lymphokines or Stapylococcus aureus protein A) induces no further increase in CstF-64 above that seen for proliferation alone. The rise in CstF-64 is therefore insufficient to induce secretion. After stimulation of a continuously growing B cell line with lymphokines, a switch to Ig μ secretory mRNA and protein occurs but without a change in the CstF-64 level. Therefore, an increase in CstF-64 levels is not necessary to mediate the differentiation-induced switch to secreted forms of Ig-μ heavy chain. Because augmentation of CstF-64 levels is neither necessary nor sufficient for Ig secretory mRNA production, we conclude that other lymphokine-induced factors play a role.

Prion diseases are caused by conformational alterations in the prion protein (PrP). The immune system has been assumed to be non‐responsive to the self‐prion protein, therefore, PrP autoimmunity has not been investigated. Here, we immunized various strains of mice with PrP peptides, some selected to fit the MHC class II‐peptide binding motif. We found that specific PrP peptides elicited strong immune responses in NOD, C57BL/6 and A/J mice. To test the functional effect of this immunization, we examined the expression of proteinase‐K‐resistant PrP by a scrapie‐infected tumor transplanted to immunized syngeneic A/J mice. PrP peptide vaccination did not affect the growth of the infected tumor transplant, but significantly reduced the level of protease‐resistant PrP. Our results demonstrate that self‐PrP peptides are immunogenic in mice and suggest that this immune response might affect PrP‐scrapie levels in certain conditions.

Seroprevalence studies of SARS-CoV-2 antibodies are useful in assessing the epidemiological status in the community, and the degree of spread. To study the seroprevalence rates of SARS-CoV-2 antibodies among healthy blood donors in Jordan, at various points of time and as the pandemic evolves in the community. In total, 1374 blood donor samples, from three groups, were tested for SARS-CoV-2 total immunoglobulin antibodies. In the first group, samples from 734 individuals (from donations made between January and June 2020) were tested in June. In the second group, 348 individuals were tested in September 2020. The third group of 292 individuals was tested in February 2021. A qualitative assay was used for testing (specificity 99.8%, sensitivity 100%). The first two groups, from January–June and September 2020, when confirmed Covid-19 cases numbered between several hundred and 3000, showed a seroprevalence rate of 0% (95% CI 0.00–0.51%). The third group (early February 2021), when the number of confirmed cases had reached 100 times that of September 2020, revealed a seroprevalence of 27.4% (95% CI 22.5–32.9%). A dramatic rise in seroprevalence of SARS-CoV-2 antibodies was seen among healthy blood donors in Jordan, in parallel with widespread intracommunity transmission of the disease. This information is useful for assessing the degree of herd immunity, and provides for better understanding of the pandemic.