To the Editor: Whether or not persons who have already been infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) should be vaccinated is unclear. Only a few studies have shown that vaccinees who were previously infected with SARS-CoV-2 had a significantly higher antibody response than previously uninfected vaccinees. [1][2][3][4] In an observational cohort study, we enrolled 100 health care workers, including 38 (9 men and 29 women) with a documented history of SARS-CoV-2 infection (mean duration between infection and vaccination, 111 days). The mean age of these previously infected participants was 35.1 years (95% confidence interval [CI], 31.7 to 38.6). Our study also included 62 participants (25 men and 37 women) who had not been previously infected. The mean age of those participants was 44.7 years (95% CI, 41.0 to 47.6).Both groups of participants received the messenger RNA vaccine BNT162b2 (Pfizer-BioNTech). Serum samples were obtained from the previously infected participants 10 days after the administration of the first dose and from the previously uninfected participants 10 days after the administration of the second dose. Thereafter, all the participants were screened for the presence of specific anti-SARS-CoV-2 spike IgG by means of a chemiluminescence microparticle immunoassay.No significant difference in circulating antispike IgG antibody titers was observed between the samples from previously infected participants (mean level, 20,120 arbitrary units per milliliter; 95% CI, 16,400 to 23,800) and those from previously uninfected participants (mean level, 22,639 arbitrary units per milliliter; 95% CI, 19,400 to 25,900) (median levels are shown in Fig. 1A). Circulating anti-spike IgG antibodies were not detected in only one previously infected participant; that participant did not have an antibody response to natural infection with SARS-CoV-2.

The multiepitopic TS/PP vaccine induces a tumor-specific immune response in mice and is especially potent when used in combination with 5-FU-based chemotherapy.

Cetuximab is a human/mouse chimeric IgG1 monoclonal antibody (mAb) to epidermal growth factor receptor, approved for colorectal carcinoma treatment in combination with chemotherapy. The immune-mediated effects elicited by its human fraction of crystallization moiety might critically contribute to the overall anti-tumor effectiveness of the antibody. We therefore investigated cetuximab ability to promote colon cancer cell opsonization and phagocytosis by human dendritic cells (DCs) that are subsequently engaged in antigen-cross presentation to cytotoxic T-lymphocyte (CTL) precursors. Human colon cancer cell lines were evaluated for susceptibility to DC-mediated phagocytosis before and after treatment with chemotherapy 6 cetuximab in vitro. Human DCs loaded with control or drug-treated cetuximab-coated colon cancer cells were used to in vitro generate cytotoxic T cell clones from peripheral blood mononuclear cells of human leucocyte antigen-A(*)02.01 1 donors. T-cell cultures were characterized for immune-phenotype and tumor-antigen specific CTL activity. The results confirmed that treatment of tumor cells with irinotecan 1 L-folinate 1 5-flurouracil (ILF) or with gemcitabine 1 ILF increased tumor antigen expression. Moreover, malignant cells exposed to chemotherapy and cetuximab were highly susceptible to phagocytosis by human DCs and were able to promote their activation. The consequent DC-mediated cross-priming of antigens derived from mAb-covered/drug-treated cancer cells elicited a robust CTL anti-tumor response. On the basis of our data, we suggest a possible involvement of CTL-dependent immunity in cetuximab anti-cancer effects.The epidermal growth factor receptor (EGFR), also designated as HER1 or ERB-B1, is a member of the ERB-B family and is often overexpressed on epithelial cancer cells. 1-3 All ERB-B receptors are typical cell membrane receptor tyrosine kinases that are activated following ligand binding, and transmit activation signals to multiple downstream biochemical pathways. EGFR-dependent intracellular signals control proliferation, resistance to pro-apoptotic stimuli, production and release of pro-angiogenic factors, which are critical for the onset and maintenance of a malignant phenotype. 4,5