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p120-Catenin is required for mouse vascular development.
Oas RG, Xiao K, Summers S, Wittich KB, Chiasson CM, Martin WD, Grossniklaus HE, Vincent PA, Reynolds AB, Kowalczyk AP
(2010) Circ Res 106: 941-51
MeSH Terms: Animals, Antigens, CD, Blood Vessels, Body Patterning, CD8 Antigens, Cadherins, Catenins, Cell Proliferation, Cells, Cultured, Embryo Loss, Endothelial Cells, Gestational Age, Hemorrhage, Immunoglobulins, Integrases, Mice, Mice, Inbred C57BL, Mice, Knockout, Microvessels, Pericytes, Promoter Regions, Genetic, Receptor Protein-Tyrosine Kinases, Receptor, TIE-2
Show Abstract · Added March 5, 2014
RATIONALE - p120-catenin (p120) is an armadillo family protein that binds to the cytoplasmic domain of classical cadherins and prevents cadherin endocytosis. The role of p120 in vascular development is unknown.
OBJECTIVE - The purpose of this study is to examine the role of p120 in mammalian vascular development by generating a conditionally mutant mouse lacking endothelial p120 and determining the effects of the knockout on vasculogenesis, angiogenic remodeling, and the regulation of endothelial cadherin levels.
METHODS AND RESULTS - A conditional Cre/loxP gene deletion strategy was used to ablate p120 expression, using the Tie2 promoter to drive endothelial Cre recombinase expression. Mice lacking endothelial p120 died embryonically beginning at embryonic day 11.5. Major blood vessels appeared normal at embryonic day 9.5. However, both embryonic and extraembryonic vasculature of mutant animals were disorganized and displayed decreased microvascular density by embryonic day 11.5. Importantly, both vascular endothelial cadherin and N-cadherin levels were significantly reduced in vessels lacking p120. This decrease in cadherin expression was accompanied by reduced pericyte recruitment and hemorrhaging. Furthermore, p120-null cultured endothelial cells exhibited proliferation defects that could be rescued by exogenous expression of vascular endothelial cadherin.
CONCLUSIONS - These findings reveal a fundamental role for p120 in regulating endothelial cadherin levels during vascular development, as well as microvascular patterning, vessel integrity, and endothelial cell proliferation. Loss of endothelial p120 results in lethality attributable to decreased microvascular density and hemorrhages.
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23 MeSH Terms
Differential effect of imipenem treatment on wild-type and NK cell-deficient CD8 knockout mice during acute intra-abdominal injury.
Enoh VT, Fairchild CD, Lin CY, Varma TK, Sherwood ER
(2006) Am J Physiol Regul Integr Comp Physiol 290: R685-93
MeSH Terms: Abdominal Injuries, Animals, Anti-Bacterial Agents, Bacterial Infections, CD8 Antigens, CD8-Positive T-Lymphocytes, Cecum, Cytokines, Female, Imipenem, Killer Cells, Natural, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Peritonitis, Treatment Outcome
Show Abstract · Added October 18, 2015
CD8 knockout mice depleted of natural killer (NK) cells by treatment with anti-asialoGM1 (CD8KO/alphaAsGM1 mice) are resistant to injury caused by cecal ligation and puncture (CLP). However, CLP-induced injury is complex. Potential sources of injury include bacterial dissemination, cecal ischemia, and translocation of bacterial toxins. We treated wild-type and CD8KO/alphaAsGM1 mice with imipenem after CLP to decrease bacterial dissemination. Additional mice were subjected to cecal ligation without puncture of the cecal wall or cecal ligation and removal of cecal contents. Imipenem treatment decreased bacterial counts by at least two orders of magnitude. However, all wild-type mice, whether treated with saline or imipenem, died by 42 h after CLP and exhibited significant hypothermia, metabolic acidosis, and high plasma cytokine concentrations. Wild-type mice subjected to cecal ligation without puncture also died, despite very low bacterial counts in blood, but wild-type mice subjected to cecal ligation and washout of cecal contents survived. In CD8KO/alphaAsGM1 mice subjected to CLP, imipenem treatment increased survival from 50% to 100%. After cecal ligation without puncture, long-term survival was 80-90% in CD8KO/alphaAsGM1 mice. Hypothermia, metabolic acidosis, and cytokine production were attenuated in CD8KO/alphaAsGM1 mice compared with wild-type controls. These results indicate that bacterial dissemination is not a major source of injury in wild-type mice after CLP, but the presence of gut flora in the cecal lumen is required for induction of systemic inflammation after cecal injury. CD8KO/alphaAsGM1 mice are resistant to the systemic manifestations of cecal injury.
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17 MeSH Terms
Cardiovascular dysfunction caused by cecal ligation and puncture is attenuated in CD8 knockout mice treated with anti-asialoGM1.
Tao W, Enoh VT, Lin CY, Johnston WE, Li P, Sherwood ER
(2005) Am J Physiol Regul Integr Comp Physiol 289: R478-R485
MeSH Terms: Acid-Base Equilibrium, Animals, Antibodies, CD8 Antigens, Cardiovascular Diseases, Cecum, Cytokines, Female, G(M1) Ganglioside, Hemodynamics, Inflammation Mediators, Ligation, Mice, Mice, Inbred C57BL, Mice, Knockout, Myocardial Contraction, Myocardium, Punctures
Show Abstract · Added October 18, 2015
The present study was designed to assess hemodynamics and myocardial function at 18 h after injury caused by cecal ligation and puncture (CLP) in CD8-knockout mice treated with anti-asialoGM1 (CD8KO/alphaAsGM1 mice). Arterial pressure was measured by carotid artery cannulation, and left ventricular pressure-volume measurements were obtained by use of a 1.4-Fr conductance catheter. Blood acid-base balance and indexes of hepatic, renal, and pulmonary injury were also measured. CD8KO/alphaAsGM1 mice exhibited higher mean arterial pressure and increased systemic vascular resistance compared with wild-type mice. Cardiac output was significantly decreased in wild-type, but not CD8KO/alphaAsGM1, mice compared with sham controls. Myocardial function was better preserved in CD8KO/alphaAsGM1 mice as indicated by less impairment of left ventricular pressure development over time, time varying maximum elastance, end-systolic pressure-volume relationship, and preload recruitable stroke work. The impairment in myocardial function was associated with induction of proinflammatory cytokine mRNAs in the hearts of wild-type mice. The hemodynamic derangements in wild-type mice were coupled with significant metabolic acidosis and elevated serum creatinine levels. Overall, this study shows that cardiovascular collapse and shock characterized by hypotension, myocardial depression, low systemic vascular resistance, and metabolic acidosis occurs after CLP in wild-type mice but is attenuated in CD8KO/alphaAsGM1 mice. These observations likely explain, in part, the previously observed survival advantage of CD8KO/alphaAsGM1 mice following CLP.
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18 MeSH Terms
Mice depleted of CD8+ T and NK cells are resistant to injury caused by cecal ligation and puncture.
Sherwood ER, Enoh VT, Murphey ED, Lin CY
(2004) Lab Invest 84: 1655-65
MeSH Terms: Acidosis, Animals, CD8 Antigens, CD8-Positive T-Lymphocytes, Cecum, Cytokines, Female, Hypothermia, Killer Cells, Natural, Lymphocyte Depletion, Mice, Mice, Inbred C57BL, Mice, Knockout, Sepsis, beta 2-Microglobulin
Show Abstract · Added October 18, 2015
We previously showed that beta 2 microglobulin knockout mice depleted of NK cells by treatment with anti-asialoGM1 (beta2MKO/alphaAsGM1 mice) are resistant to sepsis caused by cecal ligation and puncture (CLP). beta2MKO mice possess multiple immunological defects including depletion of CD8+ T cells. This study was designed to determine the contribution of CD8+ T and NK cell deficiency to the resistance of beta2MKO/alphaAsGM1 mice to CLP-induced injury. beta2MKO/alphaAsGM1 mice and CD8 knockout mice treated with anti-asialoGM1 (CD8KO/alphaAsGM1 mice) survived significantly longer than wild-type mice following CLP. Improved long-term survival was also observed in wild-type mice rendered CD8+ T/NK cell-deficient by treatment with both anti-CD8alpha and anti-asialoGM1. Blood gas analysis and body temperature measurements showed that CD8+ T and NK cell-deficient mice have significantly reduced metabolic acidosis and less hypothermia compared to control mice at 18 h after CLP. CD8+ T/NK cell-deficient mice also showed an attenuated proinflammatory response as indicated by decreased expression of mRNAs for IL-1, IL-6 and MIP-2 in spleen and heart. IL-6, KC and MIP-2 levels in blood and peritoneal fluid were also significantly decreased CD8+ T/NK cell-deficient mice compared to controls. CD8+ T/NK cell-deficient mice exhibited decreased bacterial concentrations in blood, but not in peritoneal fluid or lung, compared to wild-type controls. These data show that mice depleted of CD8+ T and NK cells exhibit survival benefit, improved physiologic function and an attenuated proinflammatory response following CLP that is comparable to beta2M/alphaAsGM1 mice.
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15 MeSH Terms
Peyer's patch dendritic cells process viral antigen from apoptotic epithelial cells in the intestine of reovirus-infected mice.
Fleeton MN, Contractor N, Leon F, Wetzel JD, Dermody TS, Kelsall BL
(2004) J Exp Med 200: 235-45
MeSH Terms: Animals, Antigens, Viral, Apoptosis, CD11b Antigen, CD11c Antigen, CD4-Positive T-Lymphocytes, CD8 Antigens, Cell Division, Cell Line, Dendritic Cells, Epithelial Cells, Female, Immunity, Mucosal, Intestinal Mucosa, Intestines, Keratins, Mice, Mice, Inbred BALB C, Microscopy, Confocal, Microscopy, Fluorescence, Orthoreovirus, Mammalian, Peyer's Patches
Show Abstract · Added December 10, 2013
We explored the role of Peyer's patch (PP) dendritic cell (DC) populations in the induction of immune responses to reovirus strain type 1 Lang (T1L). Immunofluorescence staining revealed the presence of T1L structural (sigma1) and nonstructural (sigmaNS) proteins in PPs of T1L-infected mice. Cells in the follicle-associated epithelium contained both sigma1 and sigmaNS, indicating productive viral replication. In contrast, sigma1, but not sigmaNS, was detected in the subepithelial dome (SED) in association with CD11c(+)/CD8alpha(-)/CD11b(lo) DCs, suggesting antigen uptake by these DCs in the absence of infection. Consistent with this possibility, PP DCs purified from infected mice contained sigma1, but not sigmaNS, and PP DCs from uninfected mice could not be productively infected in vitro. Furthermore, sigma1 protein in the SED was associated with fragmented DNA by terminal deoxy-UTP nick-end labeling staining, activated caspase-3, and the epithelial cell protein cytokeratin, suggesting that DCs capture T1L antigen from infected apoptotic epithelial cells. Finally, PP DCs from infected mice activated T1L-primed CD4(+) T cells in vitro. These studies show that CD8alpha(-)/CD11b(lo) DCs in the PP SED process T1L antigen from infected apoptotic epithelial cells for presentation to CD4(+) T cells, and therefore demonstrate the cross-presentation of virally infected cells by DCs in vivo during a natural viral infection.
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22 MeSH Terms
Aberrant expression of T-cell-associated antigens on B-cell non-Hodgkin lymphomas.
Kaleem Z, White G, Zutter MM
(2001) Am J Clin Pathol 115: 396-403
MeSH Terms: Aged, Aged, 80 and over, Antigens, CD, Antigens, CD7, B-Lymphocytes, CD2 Antigens, CD4 Antigens, CD8 Antigens, Female, Flow Cytometry, Humans, Leukemia, Lymphocytic, Chronic, B-Cell, Lymphoma, B-Cell, Lymphoma, Follicular, Lymphoma, Large B-Cell, Diffuse, Lymphoma, Mantle-Cell, Male, Middle Aged, T-Lymphocytes
Show Abstract · Added February 16, 2014
We describe 9 well-characterized cases of B-cell non-Hodgkin lymphoma (NHL) that showed aberrant expression of T-cell-associated antigens by 2-color flow cytometry. Cases were as follows: chronic lymphocytic leukemia/small lymphocytic lymphoma, 4; follicle center cell lymphoma, 2; mantle cell lymphoma, 1; and diffuse large B-cell lymphoma, 2. CD2 was the most commonly expressed antigen (5 cases). CD8 and CD7 were identified in 2 cases each, including 1 case that expressed both CD7 and CD4. The disease course and response to treatment were compatible with the type and stage of lymphoma. No unusually aggressive behavior was noted in any case. A control group of 59 cases of benign lymph nodes analyzed during the same period showed no aberrant expression of T-cell-associated antigens; thus, such expression is not a feature of benign lymphoid proliferations. Study of these B-cell lymphomas may prove invaluable to study aberrant activation of silent or repressed T-cell differentiation genes. CD2-expressing B-cell NHLs may represent clonal expansion of CD2+ B lymphocytes that normally constitute a small fraction of peripheral B lymphocytes and should not be confused with composite B- and T-cell lymphomas. Unless aggressive behavior is noted consistently, no aggressive treatment is justified.
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19 MeSH Terms
Non-depleting anti-CD4, but not anti-CD8, antibody induces long-term survival of xenogeneic and allogeneic hearts in alpha1,3-galactosyltransferase knockout (GT-Ko) mice.
Chong AS, Ma L, Yin D, Shen J, Blinder L, XiuLong X, Williams JW, Byrne G, Diamond LE, Logan JS
(2000) Xenotransplantation 7: 275-83
MeSH Terms: Animals, Antibodies, CD4 Antigens, CD8 Antigens, Galactosyltransferases, Graft Survival, Heart Transplantation, Mice, Mice, Inbred C57BL, Mice, Inbred DBA, Mice, Inbred Strains, Mice, Knockout, Rats, Transplantation, Heterologous, Transplantation, Homologous
Show Abstract · Added December 10, 2013
The anti-galactose-alpha1,3-galactose (Gal) antibody (Ab) response following pig-to-human transplantation is vigorous and largely resistant to currently available immunosuppression. The recent generation of GT-Ko mice provides a unique opportunity to study the immunological basis of xenograft-elicited anti-Gal Ab response in vivo, and to test the efficacy of various strategies at controlling this Ab response [1]. In this study, we compared the ability of non-depleting anti-CD4 and anti-CD8 to control rejection and antibody production in GT-Ko mice following xenograft and allograft transplantation. Hearts from baby Lewis rat or C3H mice were transplanted heterotopically into GT-Ko. Non-depleting anti-CD4 (YTS177) and anti-CD8 (YTS105) Abs were used at 1 mg/mouse, and given as four doses daily from day -2 to 1 then q.o.d. till day 21. Xenograft rejection occurred at 3 to 5 days post-transplantation in untreated GT-Ko recipients, and was histologically characterized as vascular rejection. Anti-CD4, but not anti-CD8, Ab treatment prolonged xenograft survival to 68 to 74 days and inhibited anti-Gal Ab as well as xeno-Ab production. In four of the five hearts from anti-CD4 mAbs-treated GT-Ko mice, we observed classic signs of chronic rejection, namely, thickened intima in the lumen of vessels, significant IgM deposition, fibrosis and modest mononuclear cell infiltrate of Mac-1+ macrophages and scattered T cells (CD8>CD4). Xenograft rejection in untreated, as well as anti-CD4- and anti-CD8-treated, recipients was associated with increased intragraft IL-6, IFN-gamma and IL-10 mRNA. C3H allografts were rejected in 7 to 9 days by untreated GT-Ko mice and were histologically characterized as cellular rejection. Treatment with anti-CD4 and anti-CD8 mAb resulted in graft survivals of >94.8 and 11.8 days, respectively. Anti-CD4 mAb treatment resulted in a transient inhibition of alloreactive and anti-Gal Ab production. The presence of circulating alloreactive and anti-Gal Abs at >50 days post-transplant was associated with significant IgM and IgG deposition in the graft. Yet, in the anti-CD4 mAb-treated group, the allografts showed no signs of rejection at the time of sacrifice (>100 days post-transplantation). All rejected allografts had elevated levels of intragraft IL-6, IFN-gamma and IL-10 mRNA, while the long-surviving anti-CD4-treated allografts had reduced mRNA levels of these cytokines. Collectively, our studies suggest that the elicited xeno-antibody production and anti-Gal Ab production in GT-Ko mice are CD4+ T-cell dependent. The majority of xenografts succumbed to chronic rejection, while allografts survived with minimal histological change, despite elevated levels of circulating alloAbs. Thus, immunosuppression with anti-CD4 mAb therapy induces long-term survival of allografts more effectively than to xenografts.
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15 MeSH Terms
Hedgehog signaling regulates differentiation from double-negative to double-positive thymocyte.
Outram SV, Varas A, Pepicelli CV, Crompton T
(2000) Immunity 13: 187-97
MeSH Terms: Animals, CD4 Antigens, CD8 Antigens, Cell Differentiation, Hedgehog Proteins, Mice, Mice, Inbred BALB C, Proteins, Signal Transduction, T-Lymphocyte Subsets, Thymus Gland, Trans-Activators
Show Abstract · Added November 5, 2010
The hedgehog (Hh) signaling pathway is involved in the development of many tissues. Here we show that sonic hedgehog (Shh) is involved in thymocyte development. Our data suggest that termination of Hh signaling is necessary for differentiation from CD4-CD8-double-negative (DN) to CD4+CD8+ double-positive (DP) thymocyte. Shh is produced by the thymic stroma, and Patched and Smoothened (Smo), the transmembrane receptors for Shh, are expressed in DN thymocytes. A neutralizing monoclonal antibody against Shh increases differentiation of DN to DP thymocytes, and Shh protein arrests thymocyte differentiation at the CD25+ DN stage, after T cell receptor beta (TCRbeta) gene rearrangement. We show that one consequence of pre-TCR signaling is downregulation of Smo, allowing DN thymocytes to proliferate and differentiate.
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12 MeSH Terms
Lineage-specific differences among CD8+ T cells in their dependence of NF-kappa B/Rel signaling.
Mora AL, Chen D, Boothby M, Rubin DH
(1999) Eur J Immunol 29: 2968-80
MeSH Terms: Animals, CD8 Antigens, CD8-Positive T-Lymphocytes, Cell Lineage, Cells, Cultured, Mice, Mice, Inbred C57BL, Mice, Transgenic, NF-kappa B, Oncogene Proteins v-rel, Phosphoproteins, Protein Isoforms, Protein-Tyrosine Kinases, Receptors, Antigen, T-Cell, alpha-beta, Signal Transduction, Transcription Factors
Show Abstract · Added December 10, 2013
Whereas most CD8+ T cells in lymph nodes and spleen express the CD8alpha beta heterodimer and depend absolutely on thymic competence for their development, a substantial population of T cells expressing CD8alpha alpha matures extrathymically. Although the existence of these CD8 sublineages is well established, relatively little is known about differences that might exist among CD8 cells in their requirement for particular transcriptional pathways during the development and maintenance of normal populations. Transgenic mice whose T lineage expresses an IkappaBalpha mutant exhibited decreased NF-kappaB signaling and a diminution in mature CD8 T cells. We now have determined that although TCR-dependent CD69 induction by CD8alpha alpha and CD8alpha beta T cells was unaffected by inhibition of NF-kappaB, TCRalpha beta CD8alpha beta T cells were preferentially reduced compared to their TCRalpha beta CD8alpha alpha or TCRgamma delta counterparts. This finding was most prominent in spleen, but was also apparent in Peyer's patches of transgenic mice. In addition, diminished antiviral cytotoxic responses of CD8alpha beta intraepithelial lymphocytes were observed after enteric reovirus infection. Taken together, these results indicate that NF-kappaB signaling is more important for the thymus-dependent TCRalpha beta CD8alpha beta population than for other CD8 lineages, and thus regulates the number, function, and normal balance of CD8 subsets in the periphery.
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16 MeSH Terms
The HIV-1 Nef protein acts as a connector with sorting pathways in the Golgi and at the plasma membrane.
Mangasarian A, Foti M, Aiken C, Chin D, Carpentier JL, Trono D
(1997) Immunity 6: 67-77
MeSH Terms: CD4 Antigens, CD8 Antigens, Cell Compartmentation, Cell Membrane, Coated Pits, Cell-Membrane, Cytoplasm, Down-Regulation, Endocytosis, Gene Products, nef, Golgi Apparatus, HIV-1, Humans, Microscopy, Confocal, Recombinant Fusion Proteins, nef Gene Products, Human Immunodeficiency Virus
Show Abstract · Added February 19, 2015
The HIV Nef protein down-regulates the cell surface expression of CD4 and of MHC I at least in part through accelerated endocytosis. To investigate further the mechanism of this effect, we created chimeric integral membrane proteins comprising the extracellular and transmembrane regions of CD4 or CD8 and Nef as the cytoplasmic domain. These fusion molecules could down-modulate CD4 in trans in a dileucine-dependent manner. Furthermore, in spite of lacking receptor-derived internalization signals, the Nef-containing chimeras underwent both Golgi retention and rapid endocytosis via clathrin-coated pits. Taken together, these data suggest that Nef down-regulates CD4 and probably MHC I by physically connecting these receptors with sorting pathways in the Golgi and at the plasma membrane.
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15 MeSH Terms