Regulation of Tissue-selective T-Lymphocyte Homing Receptors during the Virgin to Memory/Effector Cell Transition in Human Secondary Lymphoid Tissues

1993 ◽  
Vol 148 (6_pt_2) ◽  
pp. S47-S54 ◽  
Author(s):  
Louis J. Picker
Keyword(s):  
T Lymphocyte ◽  
Effector Cell ◽  
Lymphoid Tissues ◽  
Lymphocyte Homing ◽  
Lymphocyte Homing Receptors ◽  
Cell Transition

Localization of T-Lymphocyte Areas in Human Lymphoid Tissues by Fluorochrome-Labelled Helix pomatia A Haemagglutinin

1982 ◽  
Vol 16 (2) ◽  
pp. 83-90 ◽  
Author(s):  
J. ZEROMSKI ◽  
S. HAMMARSTROM ◽  
U. HELLSTROM ◽  
P. BIBERFELD ◽  
P. PERLMANN
Keyword(s):  
T Lymphocyte ◽  
Helix Pomatia ◽  
Lymphoid Tissues

Expression of lymphocyte homing receptors α4β7 and MAdCAM-l in young and old rats

2002 ◽  
Vol 37 (8-9) ◽  
pp. 1089-1095 ◽  
Author(s):  
Douglas L Schmucker ◽  
Trevor M Owen ◽  
Thomas B Issekutz ◽  
Loida Gonzales ◽  
Rose K Wang
Keyword(s):  
Lymphocyte Homing ◽  
Lymphocyte Homing Receptors ◽  
Old Rats

scholarly journals Colony forming T lymphocyte deficit in the development of feline retrovirus induced immunodeficiency syndrome

Blood ◽  
1989 ◽  
Vol 73 (2) ◽  
pp. 509-516 ◽  
Author(s):  
SL Quackenbush ◽  
JI Mullins ◽  
EA Hoover
Keyword(s):  
T Lymphocyte ◽  
Leukemia Virus ◽  
Feline Leukemia Virus ◽  
Lymphoid Tissues ◽  
Prodromal Phase ◽  
Time Period ◽  
Immunodeficiency Disease ◽  
Immunodeficiency Syndrome ◽  
Colony Forming Assay ◽  
Prospective Investigation

Abstract The identification and molecular cloning of a feline leukemia virus (FeLV) isolate (FeLV-FAIDS) that consistently produces immunodeficiency syndrome has allowed prospective investigation of events that occur in the prodromal phase of disease. Using a T-lymphocyte colony forming assay (T-CFU-Ic) we have demonstrated that a drastic depletion of circulating T-CFU-Ic prefigures the development of clinical immunodeficiency disease in inoculated cats and correlates with the appearance and replication of the FeLV-FAIDS variant genome in serially collected bone marrow samples. During the same presymptomatic time period, no significant alterations in conventional mitogen-induced lymphocyte blastogenic responses or in circulating lymphocyte numbers were evident. Thus T-CFU-Ic assay but not conventional mitogen-driven blastogenesis identified animals destined to develop immunodeficiency syndrome. The correlation among T-CFU-Ic depletion, the replication of the lymphocytopathic FeLV-FAIDS variant genome in hematopoietic and lymphoid tissues, and the onset of clinical disease, infers that ablation of a colony-forming T lymphocyte progenitor subset is important in the early pathogenesis of feline retrovirus-induced immunodeficiency syndrome.

Human Conjunctiva Contains High Endothelial Venules That Express Lymphocyte Homing Receptors

1999 ◽  
Vol 69 (4) ◽  
pp. 397-403 ◽  
Author(s):  
RICHARD JOHN HAYNES ◽  
PATRICK JASON TIGHE ◽  
ROBERT ALASTAIR HOWIE SCOTT ◽  
HARMINDER SINGH DUA
Keyword(s):  
Lymphocyte Homing ◽  
High Endothelial Venules ◽  
Lymphocyte Homing Receptors ◽  
Human Conjunctiva

Lymphocyte-Homing Receptors and Preferential Migration Pathways

1991 ◽  
Vol 196 (4) ◽  
pp. 374-380 ◽  
Author(s):  
Y.-H. Chin ◽  
R. Sackstein ◽  
J.-P. Cai
Keyword(s):  
Lymphocyte Homing ◽  
Lymphocyte Homing Receptors ◽  
Migration Pathways

scholarly journals CC Chemokine Receptor 7–dependent and –independent Pathways for Lymphocyte Homing

2001 ◽  
Vol 194 (12) ◽  
pp. 1875-1881 ◽  
Author(s):  
Golo Henning ◽  
Lars Ohl ◽  
Tobias Junt ◽  
Phillip Reiterer ◽  
Volker Brinkmann ◽  
...  
Keyword(s):  
B Cells ◽  
Chemokine Receptor ◽  
Peripheral Blood ◽  
Lymphoid Tissues ◽  
Lymphocyte Homing ◽  
High Endothelial Venules ◽  
Peripheral Lymph ◽  
Independent Mechanism ◽  
Secondary Lymphoid Organs ◽  
Deficient Mice

Cognate interaction of chemokine receptor CCR7 on lymphocytes with its ligands CCL19 and CCL21 expressed on high endothelial venules (HEVs) is essential for effective migration of T and B cells across HEVs into secondary lymphoid organs. Plt mice, which lack expression of CCL19 and CCL21-ser, both ligands for CCR7 on HEVs, as well as CCR7-deficient mice, have a defective cell migration and reduced homing of lymphocytes. FTY720, a novel immunosuppressant, causes a reduction of lymphocytes in peripheral blood and tissues and their sequestration into lymphoid tissues. In this study we demonstrate that FTY720 rescues the homing defect in both CCR7−/− mice and plt mice. After FTY720 treatment, the number of CD4+ and CD8+ T cells as well as B cells in peripheral blood is reduced while pertussis toxin–sensitive homing into peripheral lymph nodes, mesenteric lymph node, and Peyer's patches is increased. Immunohistology demonstrates that FTY720 enables these cells to enter lymphoid tissue through HEVs. Thus, our data suggest an alternative G-αi-dependent, CCR7-CCL19/CCL21-independent mechanism for lymphocyte homing through HEVs which is strongly augmented in the presence of FTY720.

Lymphocyte homing receptors

Cell ◽  
1986 ◽  
Vol 44 (5) ◽  
pp. 673-680 ◽  
Author(s):  
Michael Gallatin ◽  
Thomas P. St. John ◽  
Mark Siegelman ◽  
Roger Reichert ◽  
Eugene C. Butcher ◽  
...  
Keyword(s):  
Lymphocyte Homing ◽  
Lymphocyte Homing Receptors

scholarly journals Infection of lymphocytes by a virus that aborts cytotoxic T lymphocyte activity and establishes persistent infection.

1991 ◽  
Vol 174 (1) ◽  
pp. 203-212 ◽  
Author(s):  
P Borrow ◽  
A Tishon ◽  
M B Oldstone
Keyword(s):  
Immune System ◽  
T Lymphocytes ◽  
T Lymphocyte ◽  
Persistent Infection ◽  
Infectious Virus ◽  
Cytotoxic T Lymphocyte ◽  
Lymphoid Tissues ◽  
Wild Type ◽  
Ctl Response ◽  
Adult Mice

For viruses to establish persistent infections in their hosts, they must possess some mechanism for evading clearance by the immune system. When inoculated into adult immunocompetent mice, wild-type lymphocytic choriomeningitis virus (LCMV ARM) induces a CD8(+)-mediated cytotoxic T lymphocyte (CTL) response that clears the infection within 7-14 d (CTL+ [P-]). By contrast, variant viruses isolated from lymphoid tissues of persistently infected mice fail to induce a CTL response and are thus able to establish a persistent infection in adult mice (CTL- [P+]). This report compares the interaction of CTL+ (P-) and CTL- (P+) viruses with cells of the immune system. Both types of virus initially bind to 2-4% of CD4+ and CD8+ T lymphocytes and replicate within cells of both subsets. The replication of CTL- (P+) and CTL+ (P-) viruses in lymphocytes in vivo is similar for the first 5 d after initiating infection. Thereafter, in mice infected with CTL- (P+) variants, lymphocytes retain viral genetic information, and infectious virus can be recovered throughout the animals' lives. In contrast, when adult mice are infected with wild-type CTL+ (P-) LCMV ARM, virus is not recovered from lymphocytes for greater than 7 d after infection. A CD8(+)-mediated anti-LCMV CTL response is induced in such mice. Clearance of infected lymphocytes is produced by these LCMV-specific CTLs, as shown by their ability to lyse lymphocytes expressing LCMV determinants in vitro and the fact that depletion of CD8+ lymphocytes before infection with CTL+ (P-) viruses results in levels of infected lymphocytes similar to those found in undepleted CTL- (P+)-infected mice. Hence, CTL-mediated lysis of T lymphocytes carrying infectious virus is a critical factor determining whether virus persists or the infection is terminated.

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