278 research outputs found
Immunology of naturally transmissible tumours.
Naturally transmissible tumours can emerge when a tumour cell gains the ability to pass as an infectious allograft between individuals. The ability of these tumours to colonize a new host and to cross histocompatibility barriers contradicts our understanding of the vertebrate immune response to allografts. Two naturally occurring contagious cancers are currently active in the animal kingdom, canine transmissible venereal tumour (CTVT), which spreads among dogs, and devil facial tumour disease (DFTD), among Tasmanian devils. CTVT are generally not fatal as a tumour-specific host immune response controls or clears the tumours after transmission and a period of growth. In contrast, the growth of DFTD tumours is not controlled by the Tasmanian devil's immune system and the disease causes close to 100% mortality, severely impacting the devil population. To avoid the immune response of the host both DFTD and CTVT use a variety of immune escape strategies that have similarities to many single organism tumours, including MHC loss and the expression of immunosuppressive cytokines. However, both tumours appear to have a complex interaction with the immune system of their respective host, which has evolved over the relatively long life of these tumours. The Tasmanian devil is struggling to survive with the burden of this disease and it is only with an understanding of how DFTD passes between individuals that a vaccine might be developed. Further, an understanding of how these tumours achieve natural transmissibility should provide insights into general mechanisms of immune escape that emerge during tumour evolution.This is the final version of the article. It first appeared from Wiley via http://dx.doi.org/10.1111/imm.1237
Identification of a protein encoded in the EB-viral open reading frame BMRF2
Using monospecific rabbit sera against a peptide derived from a potential antigenic region of the Epstein-Barr viral amino acid sequence encoded in the open reading frame BMRF2 we could identify a protein-complex of 53/55 kDa in chemically induced B95-8, P3HR1 and Raji cell lines. This protein could be shown to be membrane-associated, as predicted by previous computer analysis of the secondary structure and hydrophilicity pattern, and may be a member of EBV-induced membrane proteins in lytically infected cells
High titer HIV-1 V3-specific antibodies with broad reactivity but low neutralizing potency in acute infection and following vaccination.
Identifying the earliest neutralizing antibody specificities that are elicited following infection or vaccination
by HIV-1 is an important objective of current HIV/AIDS vaccine research. We have shown previously that
transplantation of HIV-1 V3 epitopes into an HIV-2 envelope (Env) scaffold provides a sensitive and specific
means to detect and quantify HIV-1 V3 epitope specific neutralizing antibodies (Nabs) in human sera. Here,
we employ this HIV-2/HIV-1 V3 scaffolding strategy to study the kinetics of development and breadth of V3-
specific Nabs in longitudinal sera from individuals acutely infected with clade C or clade B HIV-1 and in
human subjects immunized with clade B HIV-1 immunogens. HIV-2/HIV-1 chimeras containing V3
sequences matched to virus type (HIV-2 or HIV-1), subtype (clade B or C), or strain (autologous or
heterologous) were used as test reagents. We found that by 3–8 weeks post infection, 12 of 14 clade C
subjects had a median IC50 V3-specific Nab titer of 1:700 against chimeric viruses containing a heterologous
clade C V3. By 5 months post-infection, all 14 subjects were positive for V3-specific Nabs with median titers
of 1:8000 against heterologous clade C V3 and 1:1300 against clade B V3. Two acutely infected clade B
patients developed heterologous clade B V3-specific Nabs at titers of 1:300 and 1:1800 by 13 weeks of
infection and 1:5000 and 1:11000 by 7 months of infection. Titers were not different against chimeras
containing autologous clade B V3 sequences. Each of 10 uninfected normal human volunteers who were
immunized with clade B HIV-1 Env immunogens, but none of five sham immunized control subjects,
developed V3-specific Nabs titers as high as 1:3000 (median 1:1300; range 1:700–1:3000). None of the HIV-
1 infected or vaccinated subjects had antibodies that neutralized primary HIV-1 virus strains. These results
indicate that high-titer, broadly reactive V3-specific antibodies are among the first to be elicited during acute
and early HIV-1 infection and following vaccination but these antibodies lack neutralizing potency against
primary HIV-1 viruses, which effectively shield V3 from antibody binding to the functional Env trimer
Stacey Palker
ProgramMA, Deaf Education | Fontbonne University
Previous EducationMS, Early Childhood and Elementary Education | New York UniversityBS, Family Studies | Syracuse UniversityMinor in Policy Studies, focusing on Urban Education Reform | Syracuse Universityhttps://griffinshare.fontbonne.edu/fnip-2021/1005/thumbnail.jp
Detection of antibodies to human T-lymphotropic virus type I by using synthetic peptides
Improvement of Gelatin Particle Agglutination Test for Detection of Anti-HTLV-I Antibody
The mitogenic activity of human T-cell leukemia virus type I is T-cell associated and requires the CD2/LFA-3 activation pathway.
The presence of a high number of activated T cells in the bloodstream and spontaneous proliferation of peripheral blood mononuclear cells in vitro are striking characteristics of human T-cell leukemia virus type I (HTLV-I) infection. The HTLV-I regulatory protein Tax and the envelope protein gp46 have been implicated in mediating the activation process. In this study, HTLV-I-producing cell lines and purified virus from the cell lines were examined for the ability to activate peripheral blood lymphocytes (PBLs) and Jurkat cells. Antisera and monoclonal antibodies against several cellular adhesion proteins involved in T-cell activation and against viral proteins were used to identify which molecules may be participating in the activation process. First, neither virus from a T-cell line, MT2, nor virus produced from the human osteosarcoma cell line HOS/PL was able to induce PBLs to proliferate. In contrast, both fixed and irradiated HTLV-I-producing T-cell lines induced proliferation of PBLs; HOS/PL cells did not activate PBLs. Second, HTLV-I-positive T-cell lines were capable of activating interleukin-2 mRNA expression in Jurkat cells. Induction of interleukin-2 expression was inhibited by anti-CD2 and anti-lymphocyte function-associated antigen 3 (LFA-3) monoclonal antibodies but not anti-human leukocyte antigen-DR, anti-CD4, anti-LFA-1, or anti-intercellular adhesion molecule 1. Similar results were obtained with PBLs as the responder cells. Furthermore, monoclonal antibodies and antisera against various regions of the HTLV-I envelope proteins gp46 and gp21 as well as p40tax did not block activation. These data indicate that HTLV-I viral particles are not intrinsically mitogenic and that infection of target T cells is not necessary for activation. Instead, the mitogenic activity is restricted to virus-producing T cells, requires cell-to-cell contact, and may be mediated through the LFA-3/CD2 activation pathway
TUMOR-INFILTRATING LYMPHOCYTES AND P-GLYCOPROTEIN/MELANOMA ANTIGEN A EXPRESSION IN VINCRISTINE-TREATED CANINE TRANSMISSIBLE VENEREAL TUMORS
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