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Lymphocyte Migration (lymphocyte + migration)
Selected AbstractsT lymphocyte rolling and recruitment into peripheral lymph nodes is regulated by a saturable density of L-selectin (CD62L)EUROPEAN JOURNAL OF IMMUNOLOGY, Issue 5 2007Elena Galkina Dr. Abstract L-selectin mediates tethering and rolling of lymphocytes in high endothelial venules (HEV) of lymph nodes (LN) and of leukocytes at inflammatory sites. We used transgenic mice expressing varying levels of wild-type or a non-cleavable mutant form of L-selectin on T cells to determine the relationship between L-selectin density, tethering and rolling, and migration into LN. T cells expressing supraphysiological levels of either wild-type or non-cleavable L-selectin showed rolling parameters similar to C57BL/6 T cells in hydrodynamic flow assays and during rolling in Peyer's patch HEV. In contrast, PMA- or antigen-activated T cells and L-selectin+/, T cells expressing subphysiological levels of L-selectin showed reduced numbers of rolling cells with increased rolling velocity. Short-term homing studies showed that elevated expression of L-selectin above physiological levels had no effect on T cell migration to LN; however, low L-selectin expression resulted in reduced T cell homing to LN. Thus, T lymphocyte migration into LN is regulated by the density of cell surface L-selectin. In addition, there is a saturable density of L-selectin required for optimal homing to PLN in C57BL/6 mice, the L-selectin level on circulating naive T cells promotes optimal homing, and increased expression above saturating levels promotes no further increase in T cell recruitment. [source] Structure, lymphatic vascularization and lymphocyte migration in mucosa-associated lymphoid tissueIMMUNOLOGICAL REVIEWS, Issue 1 2003Giacomo Azzali Summary:, In this review, we consider the morphological aspects and topographical arrangement of gut-associated lymphoid tissue (GALT) (solitary and aggregate lymph nodules or Peyer's patches) and of vermiform appendix in the human child and in some mammals. The spatial arrangement of the vessels belonging to apparatus lymphaticus periphericus absorbens (ALPA) and of blood vessels within each lymphoid follicle as well as the ultrastructural characteristics of the lymphatic endothelium with high absorption capacity are considered. Particular attention is also paid to the morphological and biomolecular mechanisms inducing lymphocyte transendothelial migration to the bloodstream by means of lymphatic vessels as well as their passage from blood into lymphoid tissue through the high endothelial venules (HEVs). The preferential transendothelial passage of lymphocytes and polymorphonuclear neutrophils within ALPA vessels of the interfollicular area does not occur following the opening of intercellular contacts, but rather it occurs by means of ,intraendothelial channels'. In HEVs, on the contrary, the hypothesis is plausible that lymphocyte transendothelial migration into lymphoid tissue occurs through a channel-shaped endothelial invagination entirely independent of interendothelial contacts. The lymph of ALPA vessels of the single Peyer's patch is conveyed into precollector lymphatic vessels and into prelymph nodal collectors, totally independent of the ALPA vessels of the gut segments devoid of lymphoid tissue. The quantitative distribution of T lymphocytes in the lymph of mucosal ALPA vessels suggests a prevalent function of fluid uptake, whereas a reservoir and supply function is implicated for the vessels of interfollicular area. The precollector lymphatic vessels and prelymph nodal collectors are considered to be vessels with low absorption capacity, whose main function is lymph conduction and flow. [source] Astilbin suppresses delayed-type hypersensitivity by inhibiting lymphocyte migrationJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 5 2003Yu Cai This study examined the effects of astilbin, a flavanone, on delayed-type hypersensitivity reactions and its mechanisms of action on cell migration. Astilbin significantly inhibited the sheep-red-blood-cell-induced footpad reaction and picryl-chloride-induced ear dermatitis without affecting the organ weights, when administered during the effector phase but not the induction phase. The flavanone also significantly inhibited the migration to gelatin of spleen cells isolated from mice with ear dermatitis in a transwell system. Furthermore, the isolated spleen cells from normal mice were incubated with astilbin in the presence of concanavalin A, or those from mice with ear dermatitis were cultured with astilbin. In the supernatants collected, the activity of matrix metalloproteinases (MMPs) MMP-2 and MMP-9 was remarkably inhibited by astilbin. These results suggest that astilbin may inhibit delayed-type hypersensitivity reactions through selectively suppressing the lymphocyte functions, including cell migration, via down-regulating MMP activity. [source] Thermal Facilitation of Lymphocyte Trafficking Involves Temporal Induction of Intravascular ICAM-1MICROCIRCULATION, Issue 2 2009QING CHEN ABSTRACT Objective: Fever is associated with improved survival, although its beneficial mechanisms are poorly understood. Previous studies indicate that the thermal element of fever augments lymphocyte migration across high endothelial venules (HEVs) of lymphoid organs by increasing the intravascular display of a gatekeeper trafficking molecule, intercellular adhesion molecule-1 (ICAM-1). Here, we evaluated the spatio-temporal relationship between the thermal induction of intravascular ICAM-1 and lymphocyte trafficking. Methods: Intravascular ICAM-1 density was quantified by immunofluorescence staining in mice exposed to fever-range whole-body hyperthermia (39.5±0.5°C). ICAM-1,dependent lymphocyte trafficking was measured in short-term homing assays. Results: A linear relationship was observed between the duration of heat treatment and intravascular ICAM-1 density in HEVs with maximal responses requiring sustained (i.e., five hours) thermal stress. Circulating lymphocytes were found to sense incremental changes in ICAM-1 on HEVs, such that trafficking is proportional to the intravascular density of ICAM-1. We further identified a hydroxamate-sensitive shedding mechanism that restores ICAM-1 expression to homeostatic levels following the cessation of thermal stress. Conclusions: The time-dependent response to thermal stress indicates that ICAM-1 density governs the efficiency of lymphocyte interactions with HEVs in vivo. These studies highlight the dynamic role of the microcirculation in promoting immune surveillance during febrile inflammatory responses. [source] Are serum levels of CD44 relevant in children with pediatric sarcomas?,PEDIATRIC BLOOD & CANCER, Issue 1 2006Rejin Kebudi MD Abstract Background Variation in serum levels of CD44, which acts as an adhesion receptor involved in lymphocyte migration and binding, have been reported in some malignancies. The aim of this study is to compare serum levels of CD44 in children with sarcomas with those in healthy children. Procedure CD44 levels were measured by enzyme-linked immunosorbent assay (ELISA) in serum samples taken at diagnosis from 55 children with sarcomas and from 27 healthy children of similar age, sex, and socioeconomic status. Results There was no statistically significant difference between CD44 serum levels of children with sarcomas and those of healthy children. No significant difference was observed between CD44 serum levels of each patient group and those of control group (P,>,0.05). There was no significant difference among CD44 serum levels of patient groups according to stage or outcome. Conclusions In this study, serum CD44 levels were not found to be of value in the diagnosis or prognosis in children with sarcomas. © 2005 Wiley-Liss, Inc. [source] Acceleration of the onset of collagen-induced arthritis by a deficiency of platelet endothelial cell adhesion molecule 1ARTHRITIS & RHEUMATISM, Issue 11 2003Yoshifumi Tada Objective Platelet endothelial cell adhesion molecule 1 (PECAM-1; CD31) is a member of the immunoglobulin superfamily that is expressed in platelets, leukocytes, and endothelial cells. PECAM-1 has been shown to play a role in transendothelial migration of leukocytes and contains immunoreceptor tyrosine-based inhibitory motifs in its cytoplasmic tail and inhibits cellular responses. We examined the role of PECAM-1 in the development of collagen-induced arthritis (CIA). Methods CIA was induced in PECAM-1,deficient DBA/1 mice. The incidence of arthritis and the arthritis index were examined. Anti,type II collagen (anti-CII) antibody levels and interferon-, (IFN,) production by lymph node cells and spleen cells were determined. Lymphocytes from arthritic PECAM-1,deficient and wild-type mice were labeled with dye, transferred to arthritic PECAM-1+/, mice, and cell migration to inflamed joints was examined. Results PECAM-1,deficient mice showed accelerated onset of arthritis and increased severity only during the early phase. Anti-CII antibody levels were also increased during the early phase. IFN, production by lymph node cells and spleen cells from PECAM-1,deficient mice in response to CII was higher than that in wild-type mice. Lymphocytes from arthritic PECAM-1,deficient mice showed accelerated migration to inflamed joints, but not lymph nodes or spleen. The development of anti-CII antibody,induced arthritis was similar in PECAM-1,deficient and wild-type mice. Conclusion These results indicate that PECAM-1 negatively regulates humoral and cell-mediated immune responses and lymphocyte migration into joints and, consequently, the development of CIA. In addition, the role of PECAM-1 in the transendothelial migration of leukocytes appears to be redundant in this model. [source] The changing face of treatment for Crohn's diseaseBRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 4 2006S. Vermeire Blocking lymphocyte migration holds promise [source] Tumour necrosis factor-alpha (TNF- ,) enhances lymphocyte migration into rheumatoid synovial tissue transplanted into severe combined immunodeficient (SCID) miceCLINICAL & EXPERIMENTAL IMMUNOLOGY, Issue 1 2000S. Wahid Adhesion mechanisms play a major role in the recruitment of peripheral blood lymphocytes (PBL) which characteristically infiltrate rheumatoid arthritis (RA) synovium and other chronically inflamed tissues. Through a sequential series of complex integrated adhesion and signalling events, ,multistep model of migration', specific subsets of PBL are recruited into inflamed tissues. In this process both leucocyte receptors and microvascular endothelial (MVE) counter-receptors play a critical role. The MVE in particular, during an inflammatory state, is the target of various inflammatory mediators that cause the up-regulation of several cell adhesion molecules (CAM). One of the most important factors known to be a powerful inducer of MVE CAM is TNF- ,. Conversely, blocking TNF- , causes a down-modulation of CAM expression. To test directly the capacity of TNF- , to induce cell migration into RA synovium we adapted a model in which synovial grafts were implanted into SCID mice subcutaneously. Using this model we demonstrate that: (i) transplants remain viable and become vascularized and fed by mouse subdermal vessels; (ii) the mouse vasculature connects to the transplant vasculature which maintains the ability to express human CAM; (iii) intragraft injections of TNF- , up-regulate the expression of human CAM, following the down-regulation which occurred 4 weeks post-transplantation; and (iv) the up-regulation of graft CAM is associated with increased human PBL migration into the transplants. This study provides direct evidence in vivo of the capacity of TNF- , to induce cell migration. In addition, it provides the experimental background for the optimal use of this model. [source] | ||||||||||