EFFECTS OF LOW-DOSE-GAMMA RAYS ON THE IMMUNE SYSTEM OF DIFFERENT ANIMAL MODELS OF DISEASE

We reviewed the beneficial or harmful effects of low-dose ionizing radiation on several diseases based on a search of the literature. The attenuation of autoimmune manifestations in animal disease models irradiated with low-dose γ-rays was previously reported by several research groups, whereas the exacerbation of allergic manifestations was described by others. Based on a detailed examination of the literature, we divided animal disease models into two groups: one group consisting of collagen-induced arthritis (CIA), experimental encephalomyelitis (EAE), and systemic lupus erythematosus, the pathologies of which were attenuated by low-dose irradiation, and another group consisting of atopic dermatitis, asthma, and Hashimoto’s thyroiditis, the pathologies of which were exacerbated by low-dose irradiation. The same biological indicators, such as cytokine levels and Tcell subpopulations, were examined in these studies. Low-dose irradiation reduced interferon (IFN)-gamma (γ) and interleukin (IL)-6 levels and increased IL-5 levels and the percentage of CD4+CD25+Foxp3+Treg cells in almost all immunological disease cases examined. Variations in these biological indicators were attributed to the attenuation or exacerbation of the disease’s manifestation. We concluded that autoimmune diseases caused by autoantibodies were attenuated by low-dose irradiation, whereas diseases caused by antibodies against external antigens, such as atopic dermatitis, were exacerbated

Evolutionarily Conserved Protein Sequences of Influenza A Viruses, Avian and Human, as Vaccine Targets

10.1371/journal.pone.0001190PLoS ONE21

Primary stimulation by dendritic cells induces antiviral proliferative and cytotoxic T cell responses in vitro.

We used well-gassed hanging drop (20 microliters) cultures with high concentrations of purified T cells from normal BALB/c mice to examine whether dendritic cells (DC) can induce primary antiviral proliferative T cell responses and generate virus-specific CTL. We found that DC exposed to infectious influenza virus in vitro or in vivo in small numbers (0.1-1%) resulted in strong proliferation of responder T cells within 3 d, and this was strongly inhibited by antibodies to class II MHC molecules. In addition, in 5-d cultures, the influenza-treated DC generated CTL specifically able to lyse influenza-infected syngeneic target cells bearing MHC class I antigens. The most potent nucleoprotein (NP) epitope recognized by BALB/c CTL is peptide 147-158 (Arg156-) and influenza-infected DC in vitro stimulated CTL recognizing this peptide, thus mimicking the response in mice primed by intranasal influenza infection. We also induced T cell proliferation and virus-specific CTL in cultures of normal T cells by stimulating with DC pulsed with the natural NP sequence 147-158 or the potent peptide 147-158 (Arg156-). Small numbers of peritoneal exudate cells, after activation with Con A to produce class II MHC expression and after removal of DC with a specific mAb (33DI), did not lead to primary CTL generation but initiated secondary stimulation in vitro. Our results using the hanging drop culture method and DC as APC have implications for studying the T cell repertoire for viral components in humans without the necessity of previous immunization

Influenza virus-specific cytotoxic T cells in man; induction and properties of the cytotoxic cell.

Human peripheral blood lymphocytes have been sensitized in vitro to influenza virus antigen. After an induction period of 4--14 days, cytotoxic cells which lyse autologous influenza virus-infected lymphoid cells could be demonstrated. The cytotoxic cell is a T lymphocyte which shows specificity for sensitizing influenza virus type A or B. It cannot distinguish between major subtypes of influenza A virus. The use of virus-infected normal lymphoid cells as target cells overcame the difficulties of nonspecific killing encountered with some transformed cells

B-cell or T-cell immunity?

The influenza virus behaves unpredictably and can cause devastating pandemics. Nearly 50 years after its first isolation it is probably the most infectious agent known that we cannot yet control. Why? The answer lies in the virus's unique capacity to alter antigenically and in the inability of the host's immune system to respond satisfactorily to the vaccines currently available. What follows is a record, prepared exclusively for Immunology Today, of a conference held in Oxford on March 21-24 this year, to discuss problems relating to protection against influenza

HLA restriction of cell-mediated lysis of influenza virus-infected human cells.

MURINE T lymphocytes that mediate the lysis of virus-infected cells show specificity both for the viral cell surface antigens and for the H-2K or D antigens of the major histo-compatibility complex1-8. The cytotoxic T lymphocytes and the target cell must share H-2K or D products. The experiments reported here demonstrate that there is a similar requirement for partial HLA identity between human cytotoxic lymphocytes and influenza virus-infected target cells. © 1977 Nature Publishing Group