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  • 1
    Keywords: APOPTOSIS ; CELLS ; EXPRESSION ; GROWTH ; INHIBITOR ; proliferation ; tumor ; Germany ; KINASE ; CDNA ; PROTEIN ; PROTEINS ; ADHESION MOLECULES ; NF-KAPPA-B ; ACTIVATION ; COMPLEX ; RESPONSES ; COMPLEXES ; MECHANISM ; ANTIGEN ; T-CELL ; T-CELLS ; C-JUN ; PHOSPHORYLATION ; signal transduction ; ALPHA ; IMMUNE-RESPONSES ; MOUSE ; LINE ; MONOCLONAL-ANTIBODIES ; RHO-ASSOCIATED KINASE ; KAPPA-B ; CROSS-LINKING ; MAP KINASES ; FAS-MEDIATED APOPTOSIS ; rodent ; T lymphocytes ; INDUCED CELL-DEATH ; STANDARD ; ABSENCE ; secretion ; HYALURONAN RECEPTOR ; DELAYED-TYPE HYPERSENSITIVITY ; JNK ; KINASES ; TRANSMEMBRANE DOMAIN ; PHOSPHOINOSITIDE 3-KINASE/AKT
    Abstract: CD44v6 is transiently expressed during T cell activation, and constitutively CD44v4-v7 expressing transgenic T cells show accelerated responses towards nominal antigens. The underlying mechanism is unknown. The mouse thymoma EL4 was transfected with CD44 standard isoform (CD44s) or CD44v6 cDNA (EL4-s, EL4-v6). Only EL4-v6 cells proliferated at an over 10-fold higher rate than untransfected cells, displayed up-regulated expression of CD69, CD25, and IL-2, and were protected from apoptosis by CD44v6 cross-linking. In the absence of any stimulus, ERK1/2 was partly phosphorylated, and phosphorylation was significantly increased by CD44v6 cross-linking. The same accounted for JNK, c-jun, and I kappa B alpha. Moreover, NF-kappa B was partly translocated into the nucleus. Instead, CD44s cross-linking induced ERK1/2, JNK, c-jun, and I kappa B alpha phosphorylation only in the context of TCR engagement. No selectively CD44v6 associated transmembrane proteins were uncovered in EL4 cells. However, CD44v6, as opposed to CD44s, did not colocalise with the TCR/CD3 complex after CD3 cross-linking. Furthermore, a CD44-associated 85-kDa protein became hypophosphorylated only after CD44v6 cross-linking. Threonine hypophosphorylation of this protein coincided with the activation of MAP and SAP kinases, which was prohibited in the presence of a phosphatase inhibitor. Thus, CD44v6, distinct to CD44s, stimulates autonomously growth and IL-2 secretion of a thymoma line and rescues cells from apoptosis. (c) 2004 Elsevier Inc. All rights reserved
    Type of Publication: Journal article published
    PubMed ID: 15894169
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  • 2
    Keywords: RECEPTOR ; CELLS ; EXPRESSION ; IN-VITRO ; tumor ; Germany ; THERAPY ; VITRO ; DISEASE ; DISEASES ; MICE ; ACTIVATION ; MECHANISM ; REDUCTION ; ANTIGEN ; DENDRITIC CELLS ; SKIN ; T cell activation ; T cells ; T-CELLS ; treatment ; MIGRATION ; RECRUITMENT ; ANTIGEN-PRESENTING CELLS ; C3H/HEJ MICE ; FOLLICLE ; SUBSET ; RE ; HAIR FOLLICLE ; LYMPHOID ORGANS ; REGULATORY T-CELLS ; DELAYED-TYPE HYPERSENSITIVITY ; RECOVERY ; HAIR LOSS ; lymph node ; LYMPH-NODE ; RELEVANCE ; AA ; autoimmune disease ; PROGRESS ; ACID DIBUTYLESTER SADBE ; ACTIVATED T-CELLS ; ATOPIC-DERMATITIS ; SKIN-ASSOCIATED CHEMOKINE
    Abstract: Long-lasting allergen treatment is the most efficient therapy in alopecia areata (AA). The underlying mechanism is unknown. We here asked whether treatment with a contact sensitizer influences leukocyte migration such that dendritic cell (DC) migration or the recruitment of activated T-cells towards the skin become hampered. Allergen treatment of AA mice was not accompanied by a decrease in skin- infiltrating leukocytes or draining lymph node cells (LNC). However, the distribution of leukocyte subsets was changed with a dominance of monocytes in the skin and a reduced percentage of DCs in draining nodes. Chemokine and chemokine receptor expression in skin and draining nodes was strikingly increased and LNC from untreated and allergen-treated AA mice showed high migratory activity in vitro and readily homed in draining nodes and skin after intravenous injection. However, FITC labelling of the skin and subcutaneous transfer of dye-labelled DC revealed that allergen treatment created a chemokine milieu severely hampering DC migration from the skin towards the draining node. An allergic eczema. Induced reduction in DC migration and antigen transfer could well contribute to insufficient T-cell activation and the recovery of hair follicle in AA and possibly be of relevance for other skin- related autoimmune diseases
    Type of Publication: Journal article published
    PubMed ID: 16675965
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  • 3
    Keywords: ENVIRONMENT ; ANGIOGENESIS ; CELLS ; EXPRESSION ; GROWTH ; IN-VITRO ; tumor ; CELL ; evaluation ; Germany ; IN-VIVO ; tumor growth ; VITRO ; VIVO ; SUPPORT ; DRUG ; MICE ; IMPACT ; INDUCTION ; ALPHA ; resistance ; CANCER-CELLS ; BETA ; ADHESION ; RECRUITMENT ; IMMUNE-RESPONSE ; DRUG-RESISTANCE ; SARCOMA ; chemokine ; inflammation ; CROSS-TALK ; MATRIX ; ONCOLOGY ; RE ; TUMOR-GROWTH ; TUMORIGENICITY ; INFLAMMATORY CYTOKINES ; USA ; MOTILITY ; IL-1 receptor antagonist ; fibrosarcoma ; matrix metalloproteinase ; host ; MATRIX-METALLOPROTEINASE ; systemic ; LEWIS LUNG-CARCINOMA ; myeloid cells ; SUPPRESSOR-CELLS ; TUMOR-HOST INTERACTIONS ; ANCHORAGE-INDEPENDENT GROWTH ; SYSTEMIC INFLAMMATION
    Abstract: Analyzing the growth of fibrosarcoma lines derived from IL-1 alpha-, IL-1 beta-, or IL-1 alpha beta-knockout((-/-)) mice in the immunocompetent host revealed that tumor-derived IL-1 alpha and IL-1 beta exert strong and opposing effects on immune response induction, which prohibited the evaluation of a potential impact on tumorigenicity. Therefore, in vivo growth of IL-1-deficient tumor lines was evaluated in nu/nu mice and was compared with in vitro growth characteristics. All IL-1-deficient fibrosarcoma lines grow in immunocompromised mice. However, IL-1 alpha(-/-)beta-competent ( comp) lines grow more aggressively, efficiently induce angiogenesis, and recruit inflammatory cells. Despite stronger tumorigenicity of IL-1 beta(comp) lines, IL-1 alpha strengthens anchorage-independent growth, but both IL-1a and IL-1 beta support drug resistance. Corresponding to the aggressive growth, IL-1 beta(comp) cells display increased matrix adhesion, motility, and cable formation on matrigel, likely supported by elevated alpha(v)/beta(3) and matrix metalloproteinase expression. Recruitment of myeloid cells requires IL-1 beta but is regulated by IL-1 alpha, because inflammatory chemokine and cytokine expression is stronger in IL-1 alpha(-/-)beta(comp) than in IL-1(wt) lines. This regulatory effect of tumor-derived IL-1 alpha is restricted to the tumor environment and does not affect systemic inflammatory response induction by tumor-derived IL-1 beta. Both sarcoma cell-derived IL-1 alpha and IL-1 beta promote tumor growth. However, IL- 1 alpha exerts regulatory activity on the tumor cell-matrix cross-talk, and only IL-1 beta initiates systemic inflammation
    Type of Publication: Journal article published
    PubMed ID: 18516292
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  • 4
    Keywords: APOPTOSIS ; CELLS ; EXPRESSION ; SURVIVAL ; tumor ; CELL ; Germany ; SUPPORT ; DEATH ; DISEASE ; GENE ; GENE-EXPRESSION ; PROTEIN ; PROTEINS ; MICE ; ACTIVATION ; CELL ACTIVATION ; CUTTING EDGE ; MECHANISM ; REDUCTION ; INDUCTION ; RAT ; T cell ; T cell activation ; T cells ; T-CELL ; T-CELLS ; PHOSPHORYLATION ; MOLECULE ; STIMULATION ; ISOFORM ; gene expression ; resistance ; activation-induced cell death ; CELL-DEATH ; UP-REGULATION ; NUMBER ; LIPID RAFT ; LYMPHOCYTES ; T-LYMPHOCYTES ; T lymphocyte ; Bcl-2 ; ACTIN CYTOSKELETON ; CD4(+) T-CELLS ; HOMING RECEPTOR CD44 ; IMMUNOLOGICAL SYNAPSE ; INDUCED COLITIS ; INFLAMMATORY-BOWEL-DISEASE ; INTESTINAL INFLAMMATION ; MEMBRANE-MICROFILAMENT LINKER ; rodent,autoimmunity,adhesion molecules,apoptosis,signal transduction ; T lymphocytes
    Abstract: Blockade of CD44v7 was described to cure trinitrobenzene sulfonic acid-induced colitis, a disease not developed by mice with targeted deletion of the CD44v7 exon. There was evidence for a reduction in activation-induced cell death on lamina propria lymphocytes of control as compared with CD44v7-deficient mice. To elucidate the mechanism underlying the relative apoptosis resistance of CD44v7-competent as compared with CD44v7-deficient lymphocytes, T cell activation and induction of apoptosis were analyzed on mesenteric lymph node cells and Peyer's patch lymphocytes of CD44v7-deficient and CD44v4-v7-trangenic mice, which overexpress rat CD44v4-v7 on T lymphocytes. CD44v7 deficiency was characterized by an increase in the percentage of apoptotic cells after stimulation, increased numbers of CD95L- and CD152-positive cells, low levels of the anti-apoptotic proteins Bcl-2 and Bcl-XI, and decreased phosphorylation of the pro-apoptotic protein BAD.Also, lymphocytes from CD44v4-v7-transgenic mice displayed reduced levels of CD95L, low numbers of apoptotic cells, and constitutively elevated levels of Bel-XI. When stimulating lymphocytes by CD3 cross-finking, CD44v7 was not recruited toward the immunological synapse and preferentially associated with the cytoskeletal-linker protein ezrin. Thus, as opposed to the CD44 standard isoform, CD44v7 does not function as an accessory molecule; instead, it supports survival of activated T cells by interfering with activation-induced cell death
    Type of Publication: Journal article published
    PubMed ID: 12832452
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  • 5
    Keywords: CANCER ; CELLS ; GROWTH ; GROWTH-FACTOR ; proliferation ; SURVIVAL ; CELL ; Germany ; ENZYMES ; ADHESION MOLECULES ; MOLECULES ; TISSUE ; ACTIVATION ; COMPLEX ; LIGAND ; COMPLEXES ; FAMILY ; TISSUES ; tumour ; BINDING ; ASSOCIATION ; SIGNAL ; MOLECULE ; GLYCOPROTEIN ; CELL-SURVIVAL ; ELEMENT ; NO ; PROGRESSION ; ELEMENTS ; METASTASIS ; REQUIRES ; STEPS ; EXTRACELLULAR-MATRIX ; ADHESION ; MIGRATION ; LIGANDS ; DEGRADATION ; NETHERLANDS ; RHO-ASSOCIATED KINASE ; ADHESION MOLECULE ; HUMAN EPIDERMAL-KERATINOCYTES ; OF-FUNCTION ; growth factors ; LIGAND-BINDING ; CD44 ; MATRIX ; FEATURES ; TASK ; GLYCOPROTEINS ; ANKYRIN-BINDING DOMAIN ; CYTOSKELETAL ELEMENTS ; HEPARAN-SULFATE PROTEOGLYCANS ; LYMPHOCYTE-HOMING RECEPTOR ; PHORBOL-MYRISTATE ACETATE ; PROTEIN-TYROSINE KINASES ; SIGNAL-TRANSDUCTION PATHWAYS ; SRC FAMILY KINASES ; TUMOR-CELL-MIGRATION
    Abstract: It is well established that the large array of functions that a tumour cell has to fulfil to settle as a metastasis in a distant organ requires cooperative activities between the tumour and the surrounding tissue and that several classes of molecules are involved, such as cell-cell and cell-matrix adhesion molecules and matrix degrading enzymes, to name only a few. Furthermore, metastasis formation requires concerted activities between tumour cells and surrounding cells as well as matrix elements and possibly concerted activities between individual molecules of the tumour cell itself. Adhesion molecules have originally been thought to be essential for the formation of multicellular organisms and to tether cells to the extracellular matrix or to neighbouring cells. CD44 transmembrane glycoproteins belong to the families of adhesion molecules and have originally been described to mediate lymphocyte homing to peripheral lymphoid tissues. It was soon recognized that the molecules, under selective conditions, may suffice to initiate metastatic spread of tumour cells. The question remained as to how a single adhesion molecule can fulfil that task. This review outlines that adhesion is by no means a passive task. Rather, ligand binding, as exemplified for CD44 and other similar adhesion molecules, initiates a cascade of events that can be started by adherence to the extracellular matrix. This leads to activation of the molecule itself, binding to additional ligands, such as growth factors and matrix degrading enzymes, complex formation with additional transmembrane molecules and association with cytoskeletal elements and signal transducing molecules. Thus, through the interplay of CD44 with its ligands and associating molecules CD44 modulates adhesiveness, motility, matrix degradation, proliferation and cell survival, features that together may well allow a tumour cell to proceed through all steps of the metastatic cascade
    Type of Publication: Journal article published
    PubMed ID: 15339042
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  • 6
    Keywords: APOPTOSIS ; CELLS ; EXPRESSION ; proliferation ; SURVIVAL ; CELL ; Germany ; PATHWAY ; ADHESION MOLECULES ; ACTIVATION ; signal transduction ; SIGNAL ; BONE-MARROW ; MATURATION ; DELETION ; SIGNAL-TRANSDUCTION ; BONE-MARROW-TRANSPLANTATION ; AKT ; rodent ; THYMOCYTES ; CD44 ; homing ; VARIANT ; HEMATOPOIESIS ; BONE ; PRECURSOR ; RECONSTITUTION ; MARROW ; HYALURONATE ; LEUKEMIC STEM-CELLS ; LYMPHOCYTE PROGENITORS ; VARIANT ISOFORMS
    Abstract: Regain of immunocompetence after myeloablation and bone marrow cell (BMC) reconstitution essentially depends on T progenitor homing into the thymus and intrathymic T cell maturation. CD44 facilitates progenitor homing and settlement in the bone marrow and is known as a T progenitor marker. In search for improving regain of immunocompetence after BMC reconstitution, we explored whether the CD44 standard (CD44 s) and/or variant isoforms CD44v6 and CD44v7 contribute to thymus repopulation and thymocyte maturation. Antibody-blocking studies and cells/mice with a targeted deletion of CD44v6/7 or CD44v7 revealed that CD44s, but not CD44v6 and CD44v7, has a major impact on progenitor cell homing into the thymus. Instead, CD44v6 strengthens apoptosis resistance and expansion of early thymocytes. CD44v6-induced apoptosis resistance, most strong in double-negative (DN) thymocytes, is accompanied by Akt activation. CD44v6-induced proliferation of DN cells proceeds via activation of the MAPK pathway. At later stages of T cell maturation, CD44 acts as an accessory molecule, initiating and supporting TCR/CD3 complex-mediated signal transduction in double-positive and single-positive thymocytes. Thus, CD44 plays a major role in thymus homing. In addition, CD44v6 is important for survival and expansion of early thymocytes. These findings suggest that strengthening CD44v6 expression on lymphoid progenitors could well contribute to accelerated regain of immunocompetence. J. Leukoc. Biol. 85: 251-261; 2009
    Type of Publication: Journal article published
    PubMed ID: 18955544
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  • 7
    Keywords: CELLS ; EXPRESSION ; proliferation ; tumor ; Germany ; IN-VIVO ; DISEASE ; ADHESION MOLECULES ; MICE ; ACTIVATION ; MECHANISM ; mechanisms ; T-CELL ; signal transduction ; ASSOCIATION ; bone marrow ; BONE-MARROW ; PROMOTER ; NUMBER ; ADHESION ; MONOCLONAL-ANTIBODIES ; PROGENITOR CELLS ; BONE-MARROW-TRANSPLANTATION ; rodent ; cord blood ; thymus ; PROMISCUOUS GENE-EXPRESSION ; MOLECULAR-MECHANISMS ; progenitor ; CELL BIOLOGY ; LEUKEMIC STEM-CELLS ; Molecular mechanisms ; ADHESION CASCADE ; thymocyte maturation
    Abstract: Re-acquisition of immunocompetence after allogeneic bone marrow cell (BMC) transplantation depends on intrathymic maturation of the allogeneic T progenitor cells. We recently reported that CD44 promotes progenitor homing into the thymus and T-cell maturation and now elucidate the molecular mechanisms of CD44-supported thymocyte maturation. Lethally irradiated, tumor-bearing mice, allogeneically reconstituted with T-cell-depleted BMC and a small number of common lymphoid progenitor 2 cells (CLP2) from transgenic (TG) mice, that express ratCD44v4-v7 under the Thy1 promoter, showed accelerated immunocompetent T-cell recovery compared with mice reconstituted with non-transgenic (NTG) CLP2. In addition, graft-versus-host disease was strongly reduced after tumor vaccination. TG, but not NTG double-negative (DN) thymocytes showed high proliferative potential, accompanied by constitutive association of lck with CD44. Importantly, when thymocyte adhesion was strengthened by anti-CD44, co-cultures of DN thymocytes with thymic stroma supported DN thymocyte maturation. The close contact between DN thymocytes and thymic stroma promoted persisting activation of lck and ERK1/2, particularly in CD44v6(+) DN thymocytes. Thus, intrathymic T-cell maturation in allogeneically reconstituted, leukemia-bearing hosts can be considerably accelerated by high CD44v6 expression in early thymocytes, in which proliferation-supporting signals are initiated by a crosstalk between CD44v6 on thymocytes and panCD44 on the thymic stroma. Immunology and Cell Biology (2010) 88, 136-147; doi:10.1038/icb.2009.70; published online 29 September 2009
    Type of Publication: Journal article published
    PubMed ID: 19786978
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  • 8
    Keywords: RECEPTOR ; APOPTOSIS ; CANCER ; CELLS ; EXPRESSION ; IN-VITRO ; proliferation ; tumor ; CELL ; CELL-PROLIFERATION ; Germany ; IN-VIVO ; THERAPY ; VITRO ; VIVO ; SUPPORT ; POPULATION ; PROTEIN ; MICE ; ACTIVATION ; NITRIC-OXIDE ; IFN-GAMMA ; REDUCTION ; INDUCTION ; CD8(+) T-CELLS ; SKIN ; T cell ; T cells ; T-CELL ; T-CELLS ; DOWN-REGULATION ; PHOSPHORYLATION ; cytokines ; NO ; DECREASE ; EFFICIENT ; CD8(+) ; sensitization ; chemokine ; protein expression ; HIGH-LEVEL ; EFFECTOR ; Bcl-2 ; C3H/HEJ MICE ; EFFECTOR-CELLS ; ANTIGEN RECEPTOR ; CYTOKINE ; RE ; THERAPIES ; HAIR FOLLICLE ; regulation ; IMMUNE SUPPRESSION ; cell proliferation ; chemokines ; LEVEL ; SUPPRESSOR ; USA ; LYMPH-NODE ; in vivo ; immunology ; regulatory T cells ; spleen ; EXPANSION ; CONTACT ; ALOPECIA-AREATA ; DOMINANCE
    Abstract: Induction of a chronic eczema is a most efficient therapy for alopecia areata (AA). We had noted a reduction in regulatory T cells during AA induction and wondered whether regulatory T cells may become recruited or expanded during repeated skin sensitization or whether additional regulatory cells account for hair regrowth. AA could not be cured by the transfer of CD4(+)CD25(high) lymph node cells from mice repeatedly treated with a contact sensitizer. This obviously is a consequence of a dominance of freshly activated cells as compared with regulatory CD4(+)D25(+) T cells. Instead, a population of Gr1(+)D11b(+) cells was significantly increased in skin and spleen of AA mice repeatedly treated with a contact sensitizer. Gr-1(+)11b(+) spleen cells mostly expressed CD31. Expression of several proinflammatory cytokines as well as of the IFN-gamma receptor and the TNF receptor I were increased. Particularly in the skin, Gr-1(+) cells expressed several chemokines and CCR8 at high levels. Gr-1(+)CD11b(+) cells most potently suppressed AA effector cell proliferation in vitro and promoted partial hair regrowth in vivo. When cocultured with CD4(+) or CD8(+) cells from AA mice, the Gr-1(+)CD11b(+) cells secreted high levels of NO. However, possibly due to high level Bcl-2 protein expression in AA T cells, apoptosis induction remained unaltered. Instead, zeta-chain expression was strongly down-regulated, which was accompanied by a decrease in ZAP70 and ERK1/2 phosphorylation. Thus, a chronic eczema supports the expansion and activation of myeloid suppressor cells that, via zeta-chain down-regulation, contribute to autoreactive T cell silencing in vitro and in vivo
    Type of Publication: Journal article published
    PubMed ID: 17911592
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  • 9
    Keywords: CANCER ; CELLS ; GROWTH ; IN-VITRO ; proliferation ; tumor ; CELL ; CELL-PROLIFERATION ; Germany ; tumor growth ; SUPPORT ; MOLECULES ; TUMORS ; MICE ; MACROPHAGES ; IMPACT ; INDUCTION ; T cell ; T-CELL ; DOWN-REGULATION ; SUSCEPTIBILITY ; MOLECULE ; ALPHA ; BONE-MARROW ; MOUSE ; EFFICIENT ; BETA ; CLASS-I ; RECRUITMENT ; IMMUNE-RESPONSE ; GROWTH-FACTOR-BETA ; SARCOMA ; CTL ; T-cell response ; ONCOLOGY ; RE ; TUMOR-GROWTH ; cell proliferation ; REGULATORY T-CELLS ; LEVEL ; SUPPRESSOR ; chronic inflammation ; USA ; IL-1 receptor antagonist ; EXPANSION ; fibrosarcoma ; host ; systemic ; LEWIS LUNG-CARCINOMA ; myeloid-derived suppressor cells ; SUPPRESSES ; MYELOID SUPPRESSOR-CELLS ; TUMOR-HOST INTERACTIONS
    Abstract: There is evidence that cell-associated IL-1 alpha supports immune response induction. Here we explored the impact of malignant cell-derived IL-1 on immunogenicity, immune response induction and tumor-induced immunosuppression using 3-methylcholanthrene-induced fibrosarcoma lines derived from wild-type (wt), IL-1 alpha-, IL-1 beta- or IL-1a beta-knockout (IL-1 alpha(-/-), IL-1 beta(-/-), IL-1a beta(-/-)) C57BL6 mice. The wt, IL-1 alpha(-/-), IL-1 beta(-/-) and IL-1a beta(-/-) fibrosarcoma lines express MHC class I molecules at a high level. The lines do not differ in their susceptibility toward NK cells, macrophages, and allogeneic CTL, or in their capacity as stimulators of an allogeneic response. However, IL-1 beta(-/-) tumors rarely grow in the syngeneic host, which is the consequence of a strong T helper and CTL response induction by IL-1 alpha-competent, IL-1 beta(-/-) tumors. On the other hand, IL-1 beta-competent, IL-1 alpha(-/-) tumors strongly assist CD11b(+)Gr-1(+) myeloid-derived suppressor cell and regulatory T cell expansion, which both suppress with high efficacy activated T helper cell proliferation and CTL lysis. In tumors, the absence of IL-1 alpha becomes decisive, i.e. despite reduced suppressor cell recruitment, tumor growth was unimpaired due to inefficient immune response induction. Thus, sarcoma cell-derived IL-1 alpha and IL-1 beta do not act in concert. Induction of a strong immune response by IL-1 alpha demands therapeutic exploitation, which may become more efficient if systemic induction of immunosuppression by IL-10 can also be circumvented. (C) 2008 Wiley-Liss, Inc
    Type of Publication: Journal article published
    PubMed ID: 18412246
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  • 10
    Keywords: T-CELL ; T cell ; TRANSPLANTATION ; CELL ; BONE-MARROW ; bone marrow ; MATURATION ; BONE-MARROW-TRANSPLANTATION ; thymus ; MARROW ; PROMOTES ; MEDICINE ; BONE
    Type of Publication: Meeting abstract published
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