Ccr7 t cell activation


















Introduction Inflammation in the central nervous system CNS , whether of infectious or autoimmune etiology, is associated with infiltration of immune cells into the cerebrospinal fluid CSF and brain parenchyma. Materials and Methods 2. Open in a separate window. Results 3. Figure 1. Figure 2. Figure 3. Supplementary Material 01 Click here to view. Footnotes Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication.

J Leukoc Biol. In vivo labeling of blood T cells: rapid traffic into cerebrospinal fluid in multiple sclerosis. Ann Neurol. Migration of hematogenous cells through the blood-brain barrier and the initiation of CNS inflammation.

Brain Pathol. T-lymphocyte entry into the central nervous system. J Neurosci Res. J Neurovirol. T-cell subsets in the cerebrospinal fluid and blood of patients with multiple sclerosis. Soluble and cell surface ICAM-3 in blood and cerebrospinal fluid of patients with multiple sclerosis: influence of methylprednisolone treatment and relevance as markers for disease activity. Acta Neurol Scand. The imbalance in CSF T cell subsets in active multiple sclerosis.

Central nervous system immunity associated with clinical outcome in acute encephalitis. J Neurol Sci. Autoreactive T lymphocytes in multiple sclerosis determined by antigen-induced secretion of interferon-gamma. J Clin Invest. Analysis of lymphocyte subpopulations in cerebrospinal fluid and peripheral blood in patients with multiple sclerosis and inflammatory diseases of the nervous system. Three or more routes for leukocyte migration into the central nervous system.

It is possible that activated T cells activate HRPTEpiC to express adhesion molecules or to secrete inflammatory cytokines or chemokines 23 , The first possible explanation for this finding is that IL levels may reflect not only production from T cells but also from other cell types.

Second, it may be because of measurement differences between flow cytometry and the enzyme-linked immunosorbent assay ELISA. Our study has some limitations. Other studies using vascular endothelial cells and B cells that are also involved in alloimmunity may be necessary to reflect the full spectrum of allograft rejection. However, further investigation may be required for clarification.

Two separate in vitro experiments and an ex vivo studies were designed. Six healthy individuals aged 27—40 years were recruited for blood donation. Seventeen recipients with normal biopsy findings without any evidence of rejection comprised the normal control group NC. All patients were taking tacrolimus and mycophenolate mofetil combination therapy. The baseline characteristics of both groups are presented in Table 1.

All methods were performed in accordance with the relevant guidelines and regulations. Written informed consent was obtained from KT recipients and healthy individuals. We collected peripheral blood for the analysis of immune cell profile and processed as follows. Isotype controls were monitored non-specific binding. The generated melting peak represented the quantity of the specific amplified product.

The crossing point was defined as the maximum of the second derivative from the fluorescence curve. Negative controls that contained all elements of the reaction mixture except from the template DNA were also included.

All samples were processed in duplicate. PBMCs 1. All cultures were set up in triplicate Fig. Briefly, 1. All reagents and buffers were used at room temperature. In the samples used for in vitro experiments, flow cytometry analysis was performed after collection of PBMCs.

In brief, cells were cultured in RPMI media. In the samples used for the ex vivo experiments, flow cytometry analysis was performed after the collection of blood. Statistical analyses were performed using SPSS software. Continuous variables are summarized as the median with range. Independent t-tests were used for continuous variables. A non-parametric, Wilcoxon signed-rank test was used between the control and treatment groups. Sakaguchi, S. Regulatory T cells and immune tolerance.

Campbell, D. Gill, R. An orchestrated dance between differing regulatory T cell phenotypes in allograft tolerance. Safinia, N. Promoting transplantation tolerance; adoptive regulatory T cell therapy. Izawa, A. Journal of immunology , — Derks, R. Dendritic cell type determines the mechanism of bystander suppression by adaptive T regulatory cells specific for the minor antigen HA Coordinate regulation of complex T cell populations responding to bacterial infection.

Foulds, K. Zenewicz, D. Shedlock, J. Jiang, A. Troy, and H. Masopust, D. Vezys, A. Marzo, and L. Preferential localization of effector memory cells in nonlymphoid tissue. Kerksiek, K. Busch, I. Allen, and E.

H2-M3-restricted T cells in bacterial infection: rapid primary but diminished memory responses. Fillatreau, S. T cell accumulation in B cell follicles is regulated by dendritic cells and is independent of B cell activation.

Nakano, H. Gene duplications at the chemokine locus on mouse chromosome 4: multiple strain-specific haplotypes and the deletion of secondary lymphoid-organ chemokine and EBI-1 ligand chemokine genes in the plt mutation.

Sallusto, F. Geginat, and A. Central and effector memory T cell subsets: function, generation, and maintenance. Northrop, J. CD8 T-cell memory: the other half of the story. Microbes Infect. Kaech, J. Wherry, and R. The role of programming in memory T-cell development. Wherry, J. Becker, D. Masopust, S. Kaech, R. Antia, U. Lineage relationship and protective immunity of memory CD8 T cell subsets. Scimone, M. Felbinger, I. Mazo, J. Stein, U. Rolph, M. Ploss, A. Lauvau, B.

Contos, K. Kerksiek, P. Guirnalda, I. Leiner, M. Bevan, and E. Urdahl, K. Sun, and M. Positive selection of MHC class Ib-restricted cells on hematopoietic cells. Hogquist, K. Jameson, W. Heath, J. Howard, M. Bevan, and F. T cell receptor antagonist peptides induce positive selection. Mombaerts, P. Clarke, M. Rudnicki, J. Iacomini, S. Itohara, J. Lafaille, L. Wang, Y. Ichikawa, R. Jaenisch, M. Hooper, and S. Kursar, A. This reference demonstrates that DCs have to express CCR7 to migrate from the skin to peripheral lymph nodes under inflammatory conditions, and reference 13 shows that CCR7 is also indispensable for DC migration in non-inflammatory, steady-state situations.

Worbs, T. Oral tolerance originates in the intestinal immune system and relies on antigen carriage by dendritic cells. This reference and reference 31 show that CCR7-dependent migration of antigen-carrying DCs into the draining lymph nodes is required for the induction of tolerance to ingested and inhaled antigens.

Johansson-Lindbom, B. Jang, M. CCR7 is critically important for migration of dendritic cells in intestinal lamina propria to mesenteric lymph nodes. Mice lacking expression of secondary lymphoid organ chemokine have defects in lymphocyte homing and dendritic cell localization. Marsland, B. Immunity 22 , — Yanagawa, Y.

CCR7 ligands induce rapid endocytosis in mature dendritic cells with concomitant up-regulation of Cdc42 and Rac activities. Bajenoff, M. Stromal cell networks regulate lymphocyte entry, migration, and territoriality in lymph nodes. Immunity 25 , — CCR7-ligands stimulate the intranodal motility of T lymphocytes in vivo. References 40—42 demonstrate that CCR7 influences the motility of lymphocytes in lymph nodes.

In addition, reference 43 shows that, in the absence of shear forces, lymph-node chemokines promote T-cell motility without triggering firm integrin adhesiveness.

Okada, T. CC chemokine receptor 7 contributes to Gi-dependent T cell motility in the lymph node. Huang, J. Requirements for T lymphocyte migration in explanted lymph nodes. Woolf, E. Lymph node chemokines promote sustained T lymphocyte motility without triggering stable integrin adhesiveness in the absence of shear forces.

Hardtke, S. Balanced expression of CXCR5 and CCR7 on follicular T helper cells determines their transient positioning to lymph node follicles and is essential for efficient B-cell help. Arnold, C. Scandella, E. Dendritic cell-independent B cell activation during acute virus infection: a role for early CCR7-driven B—T helper cell collaboration.

Junt, T. Kursar, M. Differential requirements for the chemokine receptor CCR7 in T cell activation during Listeria monocytogenes infection. Schneider, M. This study, along with reference 59, demonstrates that CCR7 is required for the migration of T Reg cells into lymph nodes and that this homing is essential for the unimpaired function of T Reg cells.

Pahuja, A. Experimental autoimmune encephalomyelitis develops in CC chemokine receptor 7-deficient mice with altered T-cell responses. Mori, S. Grinnan, D. Enhanced allergen-induced airway inflammation in paucity of lymph node T cell plt mutant mice. Allergy Clin. Saleh, S. Pron, B. Dendritic cells are early cellular targets of Listeria monocytogenes after intestinal delivery and are involved in bacterial spread in the host.

Baluk, P. Functionally specialized junctions between endothelial cells of lymphatic vessels. Sakaguchi, S. Menning, A. Kocks, J. Regulatory T cells interfere with the development of bronchus-associated lymphoid tissue.

Mueller, S. Regulation of homeostatic chemokine expression and cell trafficking during immune responses. Science , — Kretschmer, K. Inducing and expanding regulatory T cell populations by foreign antigen. Liang, S. Mann, M. Huehn, J. Lee, J. Davalos-Misslitz, A. Generalized multi-organ autoimmunity in CCR7-deficient mice.



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