The kinases NDR1/2 act downstream of the Hippo homolog MST1 to mediate both egress of thymocytes from the thymus and lymphocyte motility

2015 ◽  
Vol 8 (397) ◽  
pp. ra100-ra100 ◽  
Author(s):  
Fengyuan Tang ◽  
Jason Gill ◽  
Xenia Ficht ◽  
Thomas Barthlott ◽  
Hauke Cornils ◽  
...  
Keyword(s):  
Lymphocyte Motility

scholarly journals Merger of dynamic two-photon and phosphorescence lifetime microscopy reveals dependence of lymphocyte motility on oxygen in solid and hematological tumors

2019 ◽  
Vol 7 (1) ◽  
Author(s):  
Mateusz Rytelewski ◽  
Karine Haryutyunan ◽  
Felix Nwajei ◽  
Meenakshi Shanmugasundaram ◽  
Patrick Wspanialy ◽  
...  
Keyword(s):  
Phosphorescence Lifetime ◽  
Two Photon ◽  
Hematological Tumors ◽  
Lymphocyte Motility

Lymph node chemokines promote sustained T lymphocyte motility without triggering stable integrin adhesiveness in the absence of shear forces

2007 ◽  
Vol 8 (10) ◽  
pp. 1076-1085 ◽  
Author(s):  
Eilon Woolf ◽  
Irina Grigorova ◽  
Adi Sagiv ◽  
Valentin Grabovsky ◽  
Sara W Feigelson ◽  
...  
Keyword(s):  
Lymph Node ◽  
T Lymphocyte ◽  
Shear Forces ◽  
Lymphocyte Motility

Kindlin-3 is required for the stabilization of TCR-stimulated LFA-1:ICAM-1 bonds critical for lymphocyte arrest and spreading on dendritic cells

Blood ◽  
2011 ◽  
Vol 117 (26) ◽  
pp. 7042-7052 ◽  
Author(s):  
Sara W. Feigelson ◽  
Valentin Grabovsky ◽  
Eugenia Manevich-Mendelson ◽  
Ronit Pasvolsky ◽  
Ziv Shulman ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
T Cell ◽  
Leukocyte Adhesion ◽  
Lymphocyte Function ◽  
Leukocyte Adhesion Deficiency ◽  
Tcr Signaling ◽  
Normal Expression ◽  
Lymphocyte Motility ◽  
Tcr Activation

Kindlin-3 is a key lymphocyte function–associated antigen-1 (LFA-1) coactivator deleted in leukocyte adhesion deficiency-III (LAD-III). In the present study, we investigated the involvement of this adaptor in lymphocyte motility and TCR-triggered arrest on ICAM-1 or on dendritic cells (DCs). Kindlin-3–null primary T cells from a LAD-III patient migrated normally on the major lymph node chemokine CCL21 and engaged in normal TCR signaling. However, TCR activation of Kindlin-3–null T lymphocytes failed to trigger the robust LFA-1–mediated T-cell spreading on ICAM-1 and ICAM-1–expressing DCs that is observed in normal lymphocytes. Kindlin-3 was also essential for cytoskeletal anchorage of the LFA-1 heterodimer and for microclustering of LFA-1 within ventral focal dots of TCR-stimulated lymphocytes spread on ICAM-1. Surprisingly, LFA-1 on Kindlin-3–null lymphocytes migrating over CCL21 acquired normal expression of an epitope associated with the conformational activation of the key headpiece domain, β I. This activated LFA-1 was highly responsive to TCR-triggered ICAM-1–driven stop signals in normal T cells locomoting on CCL21, but not in their Kindlin-3–null T-cell counterparts. We suggest that Kindlin-3 selectively contributes to a final TCR-triggered outside-in stabilization of bonds generated between chemokine-primed LFA-1 molecules and cell-surface ICAM-1.

scholarly journals Human lymphocyte motility: normal characteristics and anomalous behavior of chronic lymphocytic leukemia cells

Blood ◽  
1976 ◽  
Vol 48 (5) ◽  
pp. 717-729 ◽  
Author(s):  
SC Jarvis ◽  
R Snyderman ◽  
HJ Cohen
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Human Lymphocyte ◽  
Human Lymphocytes ◽  
Surface Membrane ◽  
Cell Types ◽  
Anomalous Behavior ◽  
Lymphocytic Leukemia ◽  
Boyden Chamber ◽  
Surface Receptor ◽  
Lymphocyte Motility

Abstract The characteristics of human lymphocyte motility and its relationship to the redistribution of surface membrane antigens (capping) are poorly defined. Since chronic lymphocytic leukemia (CLL) cells cap poorly when compared with normal human lymphocytes, this study was undertaken to compare the motility of these two cell types. A modification of the Boyden chamber system was employed to quantify lymphocyte motility by placing lymphocyte suspensions on 8-mum convoluted-pore nitrocellulose filters and measuring the depth of migration of the cells into the filter at 37 degrees C. After 3 hr of incubation, CLL cells migrated significantly less into the filter than normal cells. Incubation in the presence of sodium azide or at 4 degrees C abolished all motility, indicating the active nature of the process. The relative motility of individual CLL patients' cells correlated best with the proportion of abnormal cells present as determined by surface receptor assays. The possibility that decreased cell motility in CLL was a reflection of enrichment by a “bone marrow-derived” (B cell) population was eliminated by the finding that normal B cells purified by gradient separation of rosetted cells migrated faster than normal T cells and considerably faster than CLL cells. Motility of normal and CLL lymphocytes was decreased by cytochalasin B and increased by colchicine, vincristine, and vinblastine. Thus, human lymphocyte motility appears to be dependent on microfilament integrity but not to require the colchicine-sensitive cytoskeleton. The decreased motility of CLL cells is the result of an intrinsic cell abnormality, but this finding cannot fully explain the decreased capping, since in human lymphocytes the latter is not prevented by an inhibitor of motility.

Lymphocyte surface and cytoplasmic changes associated with translational motility and spontaneous capping of Ig

1979 ◽  
Vol 39 (1) ◽  
pp. 137-147
Author(s):  
D.K. Bhalla ◽  
J. Braun ◽  
M.J. Karnovsky
Keyword(s):  
Fluorescence Microscopy ◽  
B Lymphocytes ◽  
Random Distribution ◽  
Thin Sections ◽  
Sequence Of Events ◽  
Opposite Pole ◽  
Translatory Motion ◽  
Surface Immunoglobulins ◽  
Characteristic Features ◽  
Lymphocyte Motility

Murine B-lymphocytes during translatory motion undergo a series of changes with respect to their morphology and distribution of surface immunoglobulins (Ig). The sequence of events comprising these changes was followed by fluorescence microscopy and a correlated detection of surface features by scanning microscopy on exactly the same cell. A round, presumably non-motile lymphocyte exhibited a random distribution of Ig and its surface displayed evenly distributed microvilli. Formation of a ruffled edge at one pole, accompanied by a decreased fluorescence at this pole marked the initial events of lymphocyte motility. In the subsequent stages, the ruffled edge became progressively prominent and displayed a constriction at its base, while the microvilli were displaced to the opposite pole. Ig in such lymphocytes was localized at the trailing, microvilli-rich pole. Thin sections of motile lymphocytes revealed Ig, microtubules, microfilaments and coated vesicles as the characteristic features of the trailing end. These observations may have bearing on the mechanism of lymphocyte motility and spontaneous capping of Ig.

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