The Experts below are selected from a list of 9495 Experts worldwide ranked by ideXlab platform
Jason G Cyster - One of the best experts on this subject based on the ideXlab platform.
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cyclical modulation of sphingosine 1 phosphate receptor 1 surface expression during lymphocyte recirculation and relationship to lymphoid organ transit
Journal of Experimental Medicine, 2005Co-Authors: Charles G Lo, Richard L Proia, Ying Xu, Jason G CysterAbstract:Sphingosine-1-phosphate receptor 1 (S1P 1 ) was recently shown to be required for lymphocyte egress from lymphoid organs. Here we have examined the relationship between S1P 1 abundance on the cell and egress efficiency. Using an integrin neutralization approach to separate the processes of entry and exit, we show that pertussis toxin treatment reduces lymphocyte egress from lymph nodes. Retrovirally mediated S1P 1 overexpression is sufficient to reduce B cell accumulation in the splenic White Pulp and to promote egress of activated T cells from lymph nodes, whereas S1P 1 +/ − cells have reduced lymph node exit efficiency. Furthermore, lymphocyte S1P 1 is down-regulated in the blood, up-regulated in lymphoid organs, and down-regulated again in the lymph. We propose that cyclical ligand-induced modulation of S1P 1 on circulating lymphocytes contributes to establishing their lymphoid organ transit time.
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sphingosine 1 phosphate receptor 1 promotes b cell localization in the splenic marginal zone
Nature Immunology, 2004Co-Authors: Guy Cinamon, Richard L Proia, Mehrdad Matloubian, Matthew Lesneski, Caroline Low, Jason G CysterAbstract:The factors directing marginal zone B cells to the splenic marginal zone are not well understood. Here we report that FTY720, a drug that targets sphingosine 1-phosphate (S1P) receptors, induced marginal zone B cell migration into follicles. Marginal zone B cells expressed S1P receptors 1 and 3 (S1P(1) and S1P(3), respectively). Using gene-targeted mice, we show that S1P(1) but not S1P(3) was required for localization in the marginal zone. In mice lacking the chemokine CXCL13, S1P(1)-deficient marginal zone B cells reacquired a marginal zone distribution. Exposure to lipopolysaccharide or antigen caused marginal zone B cells to downregulate S1P(1) and S1P(3) and to migrate into the splenic White Pulp. These data suggest that marginal zone B cell localization to the marginal zone depends on responsiveness to the blood lysophospholipid S1P, with S1P(1) signaling overcoming the recruiting activity of CXCL13.
Andrew Wotherspoon - One of the best experts on this subject based on the ideXlab platform.
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histopathology of the spleen in t cell large granular lymphocyte leukemia and t cell prolymphocytic leukemia a comparative review
The American Journal of Surgical Pathology, 2005Co-Authors: Nnenna Osuji, Estella Matutes, Daniel Catovsky, Irvin A Lampert, Andrew WotherspoonAbstract:We review retrospectively the spleen histology in 8 patients with T-cell large granular lymphocyte (LGL) leukemia and 4 with T-cell prolymphocytic leukemia (T-PLL) to identify characteristic patterns of involvement and to distinguish such patterns from those described in other low grade B- and T-cell malignancies. Moderate splenic enlargement with red Pulp expansion due to lymphocytic infiltration was characteristic of LGL leukemia. Abnormal lymphocytes expressed cytotoxic granule proteins and were consistently CD45RO and CD5 negative in contrast to normal red Pulp T cells. This infiltration respected anatomic boundaries with encroachment but no invasion of White Pulp areas. Unlike in hairy cell leukemia, the main differential diagnosis for red Pulp lymphocytosis, the White Pulp was not only preserved in T-cell LGL leukemia but showed germinal center hyperplasia with expansion of the mantle zones. By comparison, T-PLL spleens showed marked red Pulp lymphoid infiltration by medium-sized cells with irregular nuclei and prominent eosinophilic nucleoli. T-PLL lymphocytes, unlike LGLs, were more invasive, infiltrating the spleen capsule as well as White Pulp areas. T-cell prolymphocytes did not express cytotoxic granule proteins or NK-cell markers, were CD5+, CD45RO+ like normal spleen T cells, were CD2+, CD3+, CD45+, CD43+, TCRbeta+, but CD25-, CD30-, ALK-1-, TRAP-, DBA44-, and TdT-. Expression of CD4 and CD8 in these cells mirrored that of circulating T-PLL cells. These observations on the morphologic and immunohistochemical appearances of the spleen in T-cell LGL leukemia and T-PLL may aid diagnosis of these uncommon T-cell disorders, particularly T-cell LGL leukemia, where presentation may be cryptic and where unique pathognomonic features, are absent.
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histopathology of the spleen in t cell large granular lymphocyte leukemia and t cell prolymphocytic leukemia a comparative review
The American Journal of Surgical Pathology, 2005Co-Authors: Nnenna Osuji, Estella Matutes, Daniel Catovsky, Irvin A Lampert, Andrew WotherspoonAbstract:We review retrospectively the spleen histology in 8 patients with T-cell large granular lymphocyte (LGL) leukemia and 4 with T-cell prolymphocytic leukemia (T-PLL) to identify characteristic patterns of involvement and to distinguish such patterns from those described in other low grade B- and T-cell malignancies. Moderate splenic enlargement with red Pulp expansion due to lymphocytic infiltration was characteristic of LGL leukemia. Abnormal lymphocytes expressed cytotoxic granule proteins and were consistently CD45RO and CD5 negative in contrast to normal red Pulp T cells. This infiltration respected anatomic boundaries with encroachment but no invasion of White Pulp areas. Unlike in hairy cell leukemia, the main differential diagnosis for red Pulp lymphocytosis, the White Pulp was not only preserved in T-cell LGL leukemia but showed germinal center hyperplasia with expansion of the mantle zones. By comparison, T-PLL spleens showed marked red Pulp lymphoid infiltration by medium-sized cells with irregular nuclei and prominent eosinophilic nucleoli. T-PLL lymphocytes, unlike LGLs, were more invasive, infiltrating the spleen capsule as well as White Pulp areas. T-cell prolymphocytes did not express cytotoxic granule proteins or NK-cell markers, were CD5+, CD45RO+ like normal spleen T cells, were CD2+, CD3+, CD45+, CD43+, TCRbeta+, but CD25-, CD30-, ALK-1-, TRAP-, DBA44-, and TdT-. Expression of CD4 and CD8 in these cells mirrored that of circulating T-PLL cells. These observations on the morphologic and immunohistochemical appearances of the spleen in T-cell LGL leukemia and T-PLL may aid diagnosis of these uncommon T-cell disorders, particularly T-cell LGL leukemia, where presentation may be cryptic and where unique pathognomonic features, are absent.
Nnenna Osuji - One of the best experts on this subject based on the ideXlab platform.
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histopathology of the spleen in t cell large granular lymphocyte leukemia and t cell prolymphocytic leukemia a comparative review
The American Journal of Surgical Pathology, 2005Co-Authors: Nnenna Osuji, Estella Matutes, Daniel Catovsky, Irvin A Lampert, Andrew WotherspoonAbstract:We review retrospectively the spleen histology in 8 patients with T-cell large granular lymphocyte (LGL) leukemia and 4 with T-cell prolymphocytic leukemia (T-PLL) to identify characteristic patterns of involvement and to distinguish such patterns from those described in other low grade B- and T-cell malignancies. Moderate splenic enlargement with red Pulp expansion due to lymphocytic infiltration was characteristic of LGL leukemia. Abnormal lymphocytes expressed cytotoxic granule proteins and were consistently CD45RO and CD5 negative in contrast to normal red Pulp T cells. This infiltration respected anatomic boundaries with encroachment but no invasion of White Pulp areas. Unlike in hairy cell leukemia, the main differential diagnosis for red Pulp lymphocytosis, the White Pulp was not only preserved in T-cell LGL leukemia but showed germinal center hyperplasia with expansion of the mantle zones. By comparison, T-PLL spleens showed marked red Pulp lymphoid infiltration by medium-sized cells with irregular nuclei and prominent eosinophilic nucleoli. T-PLL lymphocytes, unlike LGLs, were more invasive, infiltrating the spleen capsule as well as White Pulp areas. T-cell prolymphocytes did not express cytotoxic granule proteins or NK-cell markers, were CD5+, CD45RO+ like normal spleen T cells, were CD2+, CD3+, CD45+, CD43+, TCRbeta+, but CD25-, CD30-, ALK-1-, TRAP-, DBA44-, and TdT-. Expression of CD4 and CD8 in these cells mirrored that of circulating T-PLL cells. These observations on the morphologic and immunohistochemical appearances of the spleen in T-cell LGL leukemia and T-PLL may aid diagnosis of these uncommon T-cell disorders, particularly T-cell LGL leukemia, where presentation may be cryptic and where unique pathognomonic features, are absent.
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histopathology of the spleen in t cell large granular lymphocyte leukemia and t cell prolymphocytic leukemia a comparative review
The American Journal of Surgical Pathology, 2005Co-Authors: Nnenna Osuji, Estella Matutes, Daniel Catovsky, Irvin A Lampert, Andrew WotherspoonAbstract:We review retrospectively the spleen histology in 8 patients with T-cell large granular lymphocyte (LGL) leukemia and 4 with T-cell prolymphocytic leukemia (T-PLL) to identify characteristic patterns of involvement and to distinguish such patterns from those described in other low grade B- and T-cell malignancies. Moderate splenic enlargement with red Pulp expansion due to lymphocytic infiltration was characteristic of LGL leukemia. Abnormal lymphocytes expressed cytotoxic granule proteins and were consistently CD45RO and CD5 negative in contrast to normal red Pulp T cells. This infiltration respected anatomic boundaries with encroachment but no invasion of White Pulp areas. Unlike in hairy cell leukemia, the main differential diagnosis for red Pulp lymphocytosis, the White Pulp was not only preserved in T-cell LGL leukemia but showed germinal center hyperplasia with expansion of the mantle zones. By comparison, T-PLL spleens showed marked red Pulp lymphoid infiltration by medium-sized cells with irregular nuclei and prominent eosinophilic nucleoli. T-PLL lymphocytes, unlike LGLs, were more invasive, infiltrating the spleen capsule as well as White Pulp areas. T-cell prolymphocytes did not express cytotoxic granule proteins or NK-cell markers, were CD5+, CD45RO+ like normal spleen T cells, were CD2+, CD3+, CD45+, CD43+, TCRbeta+, but CD25-, CD30-, ALK-1-, TRAP-, DBA44-, and TdT-. Expression of CD4 and CD8 in these cells mirrored that of circulating T-PLL cells. These observations on the morphologic and immunohistochemical appearances of the spleen in T-cell LGL leukemia and T-PLL may aid diagnosis of these uncommon T-cell disorders, particularly T-cell LGL leukemia, where presentation may be cryptic and where unique pathognomonic features, are absent.
Marc Bajenoff - One of the best experts on this subject based on the ideXlab platform.
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fibroblastic reticular cells guide t lymphocyte entry into and migration within the splenic t cell zone
Journal of Immunology, 2008Co-Authors: Marc Bajenoff, Nicolas Glaichenhaus, Ronald N GermainAbstract:Although a great deal is known about T cell entry into lymph nodes, much less is understood about how T lymphocytes access the splenic White Pulp (WP). We show in this study that, as recently described for lymph nodes, fibroblastic reticular cells (FRCs) form a network in the T cell zone (periarteriolar lymphoid sheath, PALS) of the WP on which T lymphocytes migrate. This network connects the PALS to the marginal zone (MZ), which is the initial site of lymphocyte entry from the blood. T cells do not enter the WP at random locations but instead traffic to that site using the FRC-rich MZ bridging channels (MZBCs). These data reveal that FRCs form a substrate for T cells in the spleen, guiding these lymphocytes from their site of entry in the MZ into the PALS, within which they continue to move on the same network.
Oliver Smithies - One of the best experts on this subject based on the ideXlab platform.
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a tetraethylene glycol coat gives gold nanoparticles long in vivo half lives with minimal increase in size
International Journal of Nanomedicine, 2017Co-Authors: Julian D Willett, Marlon G Lawrence, Jennifer Wilder, Oliver SmithiesAbstract:In this study, we describe the experiments determining whether coating gold nanoparticles with tetraethylene glycol (TEG) provides pharmacologically relevant advantages, such as increased serum half-life and resistance to protein adsorption. Monodisperse TEG-coated, NaBH4-reduced gold nanoparticles with a hydrodynamic size comparable to albumin were synthesized by reducing gold chloride with NaBH4 under alkaline conditions in the presence of TEG-SH. The particles were characterized by gel electrophoresis, column chromatography, and transmission electron microscopy. The nanoparticles were subsequently injected intravenously into mice, and their half-lives and final destinations were determined via photometric analysis, light microscopy (LM), and transmission electron microscopy. The TEG particles had a long half-life (~400 minutes) that was not influenced by splenectomy. After 500 minutes of injection, TEG particles were found in kidney proximal tubule cell vesicles and in spleen red and White Pulp. The particles induced apoptosis in the spleen red Pulp but not in White Pulp or the kidney. Some of the TEG particles appeared to have undergone ligand exchange reactions that increased their charge. The TEG particles were shown to be resistant to nonspecific protein adsorption, as judged by gel electrophoresis and column chromatography. These results demonstrate that naturally monodisperse, small-sized gold nanoparticles coated with TEG have long in vivo plasma half-lives, are minimally toxic, and are resistant to protein adsorption. This suggests that a TEG coating should be considered as an alternative to a polyethylene glycol coating, which is polydisperse and of much larger size.
