ovalbumin and Encephalitis--Viral

ovalbumin has been researched along with Encephalitis--Viral* in 2 studies

Other Studies

2 other study(ies) available for ovalbumin and Encephalitis--Viral

ArticleYear
Viral-induced encephalitis initiates distinct and functional CD103+ CD11b+ brain dendritic cell populations within the olfactory bulb.
    Proceedings of the National Academy of Sciences of the United States of America, 2012, Apr-17, Volume: 109, Issue:16

    Dendritic cells (DC) are antigen-presenting cells found in both lymphoid and nonlymphoid organs, including the brain (bDC) of Cd11c/eyfp transgenic C57BL/6 mice. Using an intranasal vesicular stomatitis virus infection, we demonstrated that EYFP(+) cells amass in areas associated with viral antigens, take on an activated morphology, and project their processes into infected neuronal tissue within the olfactory bulb. These bDC separated into three EYFP(+) CD45(+) CD11b(+) populations, all but one being able to functionally promote both T lymphocyte proliferation and T(H)1 cytokine production. One population was shown to emanate from the brain and a second population was peripherally derived. The third population was of indeterminate origin, being both radiosensitive and not replenished by donor bone marrow. Finally, each EYFP(+) population contained CD11b(+) CD103(+) subpopulations and could be distinguished in terms of CD115, Gr-1, and Ly-6C expression, highlighting mucosal and monocyte-derived DC lineages.

    Topics: Animals; Antigen Presentation; Antigens, CD; Antigens, Ly; Brain; CD11b Antigen; Cells, Cultured; Dendritic Cells; Encephalitis, Viral; Flow Cytometry; Integrin alpha Chains; Leukocyte Common Antigens; Luminescent Proteins; Mice; Mice, Inbred C57BL; Mice, Transgenic; Microscopy, Confocal; Olfactory Bulb; Ovalbumin; Receptor, Macrophage Colony-Stimulating Factor; Receptors, Chemokine; Rhabdoviridae Infections; T-Lymphocytes; Vesicular stomatitis Indiana virus

2012
Lymphotoxin alpha-/- mice develop functionally impaired CD8+ T cell responses and fail to contain virus infection of the central nervous system.
    Journal of immunology (Baltimore, Md. : 1950), 2001, Jan-15, Volume: 166, Issue:2

    Recent observations have indicated that viral persistence and tumor spreading could occur because of effector function-defective CD8(+) T cells. Although chronic exposure to Ag, lack of CD4 help, and epitope dominance are suggested to interfere with CTL differentiation, mechanisms underlying the defective effector function remain obscure. We demonstrate in this report that lymphotoxin alpha-deficient mice develop CD8(+) T cells at normal frequencies when infected with HSV or immunized with OVA Ag but show impaired cytotoxic and cytokine-mediated effector functions resulting in enhanced susceptibility to HSV-induced encephalitis. Although these cells display near normal levels of perforin and Fas ligand, they remain largely at a naive state as judged by high expression of CD62 ligand and failure to up-regulate activation or memory markers. In particular, these CD8(+) T cells revealed inadequate expression of the IL-12 receptor, thus establishing a link between CTL differentiation and LTalpha possibly through regulation of IL-12 receptor. Viruses and tumors could evade immunity by targeting the same pathway.

    Topics: Amino Acid Sequence; Animals; Biomarkers; CD8-Positive T-Lymphocytes; Cells, Cultured; Cytotoxicity, Immunologic; Encephalitis, Viral; Epitopes, T-Lymphocyte; Female; Genetic Predisposition to Disease; Herpes Simplex; Herpesvirus 1, Human; Immunophenotyping; Lymphocyte Activation; Lymphotoxin-alpha; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Mice, SCID; Molecular Sequence Data; Ovalbumin; Spleen; T-Lymphocytes, Cytotoxic

2001
chemdatabank.com