Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Aerobic exercise increases oxidant stress and leads to apoptosis of mouse intestinal lymphocytes (IL). The purpose of this study was to determine whether freewheel running prevents IL loss 24 h after a bout of strenuous exercise. Mice were randomly assigned to in-cage running wheels with 24 h access (WR) or individual cages without running wheels (NR) for 4 months. WR mice accumulated 364 km over 4 months and had higher cytochrome oxidase activity in the plantaris (p < .05), indicative of training. Total intestinal, CD3alphabeta, CD3gammadelta, CD8alpha, and CD8beta lymphocytes and intracellular glutathione were significantly lower in WR and NR mice 24 h post-exercise. The number of CD4 IL decreased 24 h after exercise in NR (p < .01) but not in WR mice relative to their respective no exercise controls. Thus, freewheel running in mice for 4 months prevented CD4 IL loss after acute exercise.
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PMID:Freewheel running selectively prevents mouse CD4+ intestinal lymphocyte death produced after a bout of acute strenuous exercise. 1611 39

Direct intratumoral introduction of therapeutic or regulatory genes is a developing technology with potential application for cancer gene therapy. Macrophage inflammatory protein-1 beta (MIP-1beta) is a chemokine which can chemoattract immune cells such as T cells. In the present study, murine colorectal adenocarcinoma CT26 cells were transfected with a recombinant adenovirus (AdhMIP-1beta) carrying the human MIP-1beta gene. 24 h post-transfection, hMIP-1beta levels reached approximately 980 pg/ml in supernatants of 10(6) hMIP-1beta-transfected CT26 cells. Moreover, the supernatants exhibited chemotactic activity for CD8(+) T cells, CD4(+) T cells, NK cells and immature DCs. Intratumoral injection of AdhMIP-1beta significantly inhibited tumor growth and prolonged the survival time of tumor-bearing mice. Intratumoral hMIP-1beta gene transfer also induced powerful tumor-specific CTL responses in vivo. The therapeutic effects of hMIP-1beta gene therapy were greatly reduced following in vivo depletion of both CD4(+) and CD8(+) T cells, but were unaffected by depletion of single T cell subsets. Immune cell depletion experiments also revealed that NK cells played an important role in hMIP-1beta-induced antitumor responses. These results suggest that intratumoral expression of hMIP-1beta has the potential effect to induce host antitumor immunity and may prove to be a useful form of cancer gene therapy.
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PMID:Intratumoral expression of MIP-1beta induces antitumor responses in a pre-established tumor model through chemoattracting T cells and NK cells. 1621 68

The development of potent adjuvants, conditioning innate and adaptative immunity, particularly CTL responses, has become currently a hot point in the rational design of vaccines for cancer immunotherapy. We have described a new approach, in which gangliosides are incorporated into vesicles from Neisseria meningitidis to form Very Small Size Proteoliposomes (VSSP). VSSP is a good alternative to the existing adjuvants for use in whole cells vaccines since it promotes 80% tumour rejection and growing delay in the CT26 and F3II tumour models respectively. Also VSSP induces activation of CTL responses to co-injected trimmed peptides and soluble proteins. This phenomena is facilitated by the cross-presentation of exogenous antigen and do not need cooperation of CD4 T cells for primary CD8 T cells expansion.
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PMID:Very small size proteoliposomes derived from Neisseria meningitidis: An effective adjuvant for generation of CTL responses to peptide and protein antigens. 1631 10

The aim of the present study was to investigate gender differences in numbers and function of blood immune cells in stressed and non-stressed laboratory rats. Psychosocial stress in adult male or female rats was induced by social confrontation of an intruder rat with a resident opponent for 2 h. Behavioral analysis indicated that intruders of both sexes were clearly defeated and had markedly higher plasma corticosterone concentrations than unstressed home cage controls at the end of the confrontation. Lower numbers of CD4, CD8, and B cells as well as a reduced proliferative response of lymphocytes to ConA were observed in stressed groups of either sex. However, some important gender differences were also observed. Stressed males had higher granulocyte numbers than controls, while granulocyte numbers remained unchanged in stressed females. Similarly, stressed males had higher phagocytic activity than stressed females. Second, there was a gender difference in some basal values. Female controls had lower NK cell numbers than control males. Interestingly, NK numbers in stressed males decreased considerably, reaching the same low levels as in (stressed and control) females. In addition, females exhibited higher basal corticosterone concentrations than males. To summarise, these data do not indicate a superior blood cellular immune function in female rats, neither for the control nor the stress condition. However, the data clearly suggest that male and female rats should not be considered as a uniform group with respect to their immunological response to stress.
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PMID:Gender difference in basal and stress levels of peripheral blood leukocytes in laboratory rats. 1637 19

Protein cages, including viral capsids, ferritins, and heat shock proteins (Hsps), can serve as nanocontainers for biomedical applications. They are genetically and chemically malleable platforms, with potential as therapeutic and imaging agent delivery systems. Here, both genetic and chemical strategies were used to impart cell-specific targeting to the Hsp cage from Methanococcus jannaschii. A tumor vasculature targeting peptide was incorporated onto the exterior surface of the Hsp cage. This protein cage bound to alpha(v)beta(3) integrin-expressing cells. Cellular tropism was also imparted by conjugating anti-CD4 antibodies to the exterior of Hsp cages. These Ab-Hsp cage conjugates specifically bound to CD4(+) cells. Protein cages have the potential to simultaneously incorporate multiple functionalities, including cell-specific targeting, imaging, and therapeutic agent delivery. We demonstrate the simultaneous incorporation of two functionalities, imaging and cell-specific targeting, onto the Hsp protein cage.
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PMID:Melanoma and lymphocyte cell-specific targeting incorporated into a heat shock protein cage architecture. 1649 64

The human CXC chemokine, stromal cell-derived factor 1 (SDF-1alpha), is known to function in vitro as a chemotactic factor for lymphocytes, monocytes, and dendritic cells. In the context that dendritic cells are powerful antigen-presenting cells, we hypothesized that adenoviral gene transfer of SDF-1alpha to tumors might inhibit growth of preexisting tumors through attracting dendritic cells to the tumor. AdSDF-1alpha mediated the expression of SDF-1alpha mRNA and protein in A549 cells in vitro, and the supernatant of the AdSDF-1alpha-infected A549 cells showed chemotactic activity for dendritic cells. When syngeneic murine CT26 colon carcinoma tumors (BALB/c) and B16 melanoma and Lewis lung cell carcinoma (C57Bl/6) were injected with AdSDF-1alpha (5 x 10(8) plaque-forming units), there was an accumulation of dendritic cells and CD8(+) cells within the tumor and significant inhibition of tumor growth compared with tumors injected with PBS or AdNull (control vector). The injection of AdSDF-1alpha into tumors induced the inflammatory enlargement and the accumulation of dendritic cells in the draining lymph node. Intratumoral AdSDF-1alpha administration elicited tumor-specific CTLs and adoptive transfer of splenocytes from AdSDF-1alpha-treated mice resulted in the elongation of survival after tumor challenge. Interestingly, in wild-type and CD4(-/-) mice but not in CD8(-/-) mice, AdSDF-1alpha inhibited the growth of the tumor. These observations suggest that adenoviral gene transfer of SDF-1alpha may be a useful strategy to accumulate dendritic cells in tumors and evoke antitumor immune responses to inhibit tumor growth.
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PMID:Adenoviral gene transfer of stromal cell-derived factor-1 to murine tumors induces the accumulation of dendritic cells and suppresses tumor growth. 1658 75

Raman spectroscopy has exhibited the C-H stretch (A1 mode) frequency nu1 of hydrated methanes at 2915 cm(-1) for the 5(12) cage and 2905 cm(-1) for the 5(12)6(2) cage. These values are lower than the frequency of 2916.5 cm(-1) in gaseous methane. In this paper, we theoretically examine the Raman spectra observed in methane hydrate by normal mode analysis using the independent molecule model. By a breakdown of the symmetry, the four frequencies in modes A1, E, T2 and T2 observed in gaseous methane are separated into nine frequencies in the hydrate. It is necessary to consider the anharmonic potential energy within methane and hydrogen bonding between methane hydrogen and water oxygen in order to get a result in qualitative agreement with experiment. The frequency in the 5(12)6(2) cage is shifted downward in comparison to the one in 5(12), and the frequencies in the both cages are also shifted downward compared with the frequencies in gas. Calculations are also reported for the isotopic methane (CD4, 13CH4) hydrates.
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PMID:Application of the independent molecule model to elucidate the dynamics of structure I methane hydrate. 1703 Jan 34

CD4(+) and CD8(+) T cell responses to endogenous retroviral envelope glycoprotein gp90 generate protective immunity to murine colon carcinoma CT26. A panel of I-A(d)-restricted T cell hybridomas recognize gp90 synthesized by CT26 cells but not by other gp90-expressing tumors. Here we report that antigenicity resides in an incompletely folded form of gp90 that is unique to CT26. In contrast to more compact forms of gp90 that are present in other tumors, this open conformer is captured by recycling I-A(d) on antigen-presenting cells and is processed intracellularly. Thus, gp90 acquires immunodominance via MHC-guided processing, and the generation of an MHC class II-restricted response can be controlled by the intracellular folding environment of antigen-expressing cells.
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PMID:Folding of an MHC class II-restricted tumor antigen controls its antigenicity via MHC-guided processing. 1738 59

Synthetic biomaterials are considered to be nonimmunogenic. Therefore, the role that adaptive immunity may play in the host response to implanted synthetic biomaterials has not been extensively studied. Cardinal features of adaptive immunity include specificity and T cell responses, which are greater and more effective with upregulation of activation receptors upon rechallenge. We compared the primary and secondary in vivo host response to three synthetic biomaterials: Elasthane 80A, silicone rubber, and polyethylene terephthalate using a cage implant model in Sprague Dawley rats. The synthetic biomedical polymers were subcutaneously implanted in cages for 14 days. Following explantation of the cages and a 2 week healing period, rats were implanted with cages containing the biomedical polymers for an additional 2 weeks. The cellular exudates within the cages were analyzed 4, 7, and 14 days post primary and secondary implantation by flow cytometry for the following cell types: T cells (inclusive of CD8(+), CD4(+), and CD4(+)/CD25(+) subsets), B cells, granulocytes, and macrophages. At day 14 following secondary implantation, there was an increase in T cells, granulocytes, and macrophages in the exudates when compared with primary implantation for all groups inclusive of the empty cage control. However, CD4(+)/CD8(+) ratios, the percentage of CD4(+)CD25(+) T cells, and the macrophage surface adhesion/fusion did not vary significantly upon secondary implantation. Despite a quantitative increase in T cells following secondary biomaterial exposure, T cell subset distribution did not change, indicating nonspecific recruitment rather than an adaptive immune response.
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PMID:T cell subset distributions following primary and secondary implantation at subcutaneous biomaterial implant sites. 1772 64

Glucocorticoid-induced TNF receptor family related protein (GITR) is a member of the TNFR superfamily. Previous studies have shown that in vivo administration of a GITR agonistic Ab (DTA-1) is able to overcome tolerance and induce tumor rejection in several murine syngeneic tumor models. However, little is known about the in vivo targets and the mechanisms of how this tolerance is overcome in a tumor-bearing host, nor is much known about how the immune network is regulated to achieve this antitumor response. In this study, we demonstrate that the in vivo ligation of GITR on CD4(+) effector T cells renders them refractory to suppression by regulatory T (T(reg)) cells in the CT26 tumor-bearing mouse. GITR engagement on T(reg) cells does not appear to directly abrogate their suppressive function; rather, it increases the expansion of T(reg) cells and promotes IL-10 production, a cytokine important for their suppressive function. Moreover, CD4(+) effector T cells play a crucial role in mediating DTA-1-induced immune activation and expansion of CD8(+), NK, and B cells in the tumor-draining lymph nodes. This includes increased CD69 expression on all of these subsets. In addition, NK and tumor-specific CD8(+) T cells are generated that are cytolytic, which show increased intracellular IFN-gamma production and CD107a mobilization, the latter a hallmark of cytolytic activities that lead to tumor killing.
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PMID:Pivotal roles of CD4+ effector T cells in mediating agonistic anti-GITR mAb-induced-immune activation and tumor immunity in CT26 tumors. 1802 80


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