Dilemmas of Polish-Jewish identity. Miriam Akavia's "My Own Vineyard"

Praca dotyczy dylematów tożsamość polsko-żydowskiej. Problem ten ukazuję na przykładzie sagi Miriam Akavii pt: "Moja winnica". Pierwszy rozdział dotyczy zależności między autorką, narratorką a bohaterką. Wskazuje na różnice między "pisaniem sobą" a "pisaniem siebie". Z kolei drugi rozdział skupia się wokół tożsamości bohaterów. Ukazuje jak stereotypy kulturowe oraz wyznaczone przez tradycję żydowską i judaizm role kobiety i mężczyzny wpływają na proces kształtowania "ja". Pracę zamyka rozdział poświęcony problemowi zakorzenienia w przestrzeni oraz języku. Podkreśla on istotną zależność między pamięcią, tożsamością a przestrzenią.The following work concerns the Polish - Jewish identity. This particular subject is presented in Miriam Akavi's novel 'My Own Vineyard'. The first chapter introduces the relation between the author, narrator and the main protagonist. Also, the chapter describes the main difference between 'writing - oneself' and 'self - writing'. The second chapter focuses on the main characters' identity. It reveals the cultural stereotypes and specific for women and men roles determined by the Jewish tradition and Judaism. Furthermore, the thesis describes the problem of estabilishment in the surrounding world and language as well. It puts an emphasis on the strong dependance on the relationship between remembrance, identity and the whole world

Differential Regulation of DAP12 and Molecules Associated with DAP12 during Host Responses to Mycobacterial Infection

DAP12 and its associating molecules MDL-1, TREM-1, and TREM-2 are the recently identified immune regulatory molecules, expressed primarily on myeloid cells including monocytes/macrophages, dendritic cells, NK cells, and neutrophils. However, little is known about the regulation of their expression during host antimicrobial responses. We have investigated the effect of pulmonary mycobacterial infection and type 1 cytokines on the expression of these molecules both in vivo and in vitro. While DAP12 was constitutively expressed at high levels in the lungs, the MDL-1, TREM-1, and TREM-2 molecules were inducible during mycobacterial infection. Their kinetic expression was correlated with that of the type 1 cytokines tumor necrosis factor alpha (TNF-α) and gamma interferon (IFN-γ). In primary lung macrophage cultures, high constitutive levels of DAP12 and TREM-2 were not modulated by mycobacterial or type 1 cytokine exposure. In contrast, expression of both MDL-1 and TREM-1 was markedly induced by mycobacterial infection and such induction was inhibited by concurrent exposure to IFN-γ. On mycobacterial infection of TNF-α(−/−) and IFN-γ(−/−) mice in vivo or their lung macrophages in vitro, TNF-α was found to be critical for mycobacterially induced MDL-1, but not TREM-1, expression whereas IFN-γ negatively regulated mycobacterially induced MDL-1 and TREM-1 expression. Our findings thus suggest that DAP12 and its associating molecules are differentially regulated by mycobacterial infection and type 1 cytokines and that MDL-1- and TREM-1-triggered DAP12 signaling may play an important role in antimicrobial type 1 immunity

Intranasal Boosting with an Adenovirus-Vectored Vaccine Markedly Enhances Protection by Parenteral Mycobacterium bovis BCG Immunization against Pulmonary Tuberculosis

Parenterally administered Mycobacterium bovis BCG vaccine confers only limited immune protection from pulmonary tuberculosis in humans. There is a need for developing effective boosting vaccination strategies. We examined a heterologous prime-boost regimen utilizing BCG as a prime vaccine and our recently described adenoviral vector expressing Ag85A (AdAg85A) as a boost vaccine. Since we recently demonstrated that a single intranasal but not intramuscular immunization with AdAg85A was able to induce potent protection from pulmonary Mycobacterium tuberculosis challenge in a mouse model, we compared the protective effects of parenteral and mucosal booster immunizations following subcutaneous BCG priming. Protection by BCG prime immunization was not effectively boosted by subcutaneous BCG or intramuscular AdAg85A. In contrast, protection by BCG priming was remarkably boosted by intranasal AdAg85A. Such enhanced protection by intranasal AdAg85A was correlated to the numbers of gamma interferon-positive CD4 and CD8 T cells residing in the airway lumen of the lung. Our study demonstrates that intranasal administration of AdAg85A represents an effective way to boost immune protection by parenteral BCG vaccination

Gamma Interferon Responses of CD4 and CD8 T-Cell Subsets Are Quantitatively Different and Independent of Each Other during Pulmonary Mycobacterium bovis BCG Infection

Gamma interferon (IFN-γ) is a key cytokine in host defense against intracellular mycobacterial infection. It has been believed that both CD4 and CD8 T cells are the primary sources of IFN-γ. However, the relative contributions of CD4 and CD8 T-cell subsets to IFN-γ production and the relationship between CD4 and CD8 T-cell activation have not been examined. By using a model of pulmonary mycobacterial infection and various immunodetection assays, we found that CD4 T cells mounted a much stronger IFN-γ response than CD8 T cells at various times after mycobacterial infection, and this pronounced IFN-γ production by CD4 T cells was attributed to both greater numbers of antigen-specific CD4 T cells and a greater IFN-γ secretion capacity of these cells. By using major histocompatibility complex class II-deficient or CD4-deficient mice, we found that the lack of CD4 T cells did not negatively affect primary or secondary CD8 T-cell IFN-γ responses. The CD8 T cells activated in the absence of CD4 T cells were capable of immune protection against secondary mycobacterial challenge. Our results suggest that, whereas both CD4 and CD8 T cells are capable of IFN-γ production, the former represent a much greater cellular source of IFN-γ. Moreover, during mycobacterial infection, CD8 T-cell IFN-γ responses and activation are independent of CD4 T-cell activation

Memory T cells in the lung and spleen of infant and adult mice following BCG immunization.

<p>Infant and adult mice were BCG immunized and sacrificed at 8 or 16 weeks. Cells from the lung (A) and spleen (B) were stained with extracellular antibodies for memory CD4 T cell markers and analyzed by flow cytometry. Absolute numbers of CD4⁺CD44⁺ cells that are T_eff/T_EM (CD127^-/+CD62L^-) or T_CM (CD127⁺CD62L⁺) in the tissues were calculated. Results are from one experiment per timepoint, n = 4/group/timepoint. Data are expressed as Mean ± SEM. *, p < 0.05.</p