scholarly journals Regulation of expression of a human intercellular adhesion molecule (ICAM-1) during lymphohematopoietic differentiation

Blood ◽  
1989 ◽  
Vol 73 (7) ◽  
pp. 1896-1903
Author(s):  
AW Boyd ◽  
SM Dunn ◽  
JV Fecondo ◽  
JG Culvenor ◽  
U Duhrsen ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
Lymphocytic Leukemia ◽  
Intercellular Adhesion Molecule ◽  
Cell Contact ◽  
Small Subset ◽  
B Cell Differentiation ◽  
Immune Functions

The intercellular adhesion molecule (ICAM-1) is a cell-surface molecule which binds to leukocyte function antigen-1 (LFA-1) and regulates both leukocyte adhesion to endothelial cells and immune functions requiring cell-cell contact. Membrane expression of ICAM-1 is highly regulated on all hematopoietic lineages. Cell membrane antigen is significantly expressed on a small subset of bone marrow (BM) progenitors but is weak or absent on all cell lineages once they enter the circulation. However, strong expression on tissue macrophages and germinal center B cells suggested that activated cells may show upregulated expression. When B cells, T cells, macrophages, or granulocytes were activated in vitro by suitable mitogens, ICAM-1 expression was induced in all cases. Parallel studies of hematopoietic tumors demonstrated a heterogeneity of expression which correlated with expression on their normal cellular counterparts. In particular, a striking correlation between expression on B-cell tumors and corresponding stages of B-cell differentiation was noted. The widely varying expression of ICAM-1 contrasts with LFA-1 which, while variable, is nevertheless significantly positive at all stages of differentiation. This suggests that the major regulation of homotypic adhesion mediated by the LFA-1/ICAM-1 linkage occurs through control of ICAM-1 expression. In keeping with this notion, ICAM-1 expression was also correlated with the “adhesiveness” of B-lymphoid tumors. Large solitary lymphoma masses showed intense expression of ICAM-1. Conversely, chronic lymphocytic leukemia (CLL) cells and lymphoma cells from tumors exhibiting diffuse, widespread lymph node disease showed weak expression. These observations are discussed in relation to the role of ICAM-1 in regulation of lymphoid recirculation and the biology of lymphoid tumors.

scholarly journals Regulation of expression of a human intercellular adhesion molecule (ICAM-1) during lymphohematopoietic differentiation

Blood ◽  
1989 ◽  
Vol 73 (7) ◽  
pp. 1896-1903 ◽  
Author(s):  
AW Boyd ◽  
SM Dunn ◽  
JV Fecondo ◽  
JG Culvenor ◽  
U Duhrsen ◽  
...  
Keyword(s):  
B Cells ◽  
B Cell ◽  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
Lymphocytic Leukemia ◽  
Intercellular Adhesion Molecule ◽  
Cell Contact ◽  
Small Subset ◽  
B Cell Differentiation ◽  
Immune Functions

Abstract The intercellular adhesion molecule (ICAM-1) is a cell-surface molecule which binds to leukocyte function antigen-1 (LFA-1) and regulates both leukocyte adhesion to endothelial cells and immune functions requiring cell-cell contact. Membrane expression of ICAM-1 is highly regulated on all hematopoietic lineages. Cell membrane antigen is significantly expressed on a small subset of bone marrow (BM) progenitors but is weak or absent on all cell lineages once they enter the circulation. However, strong expression on tissue macrophages and germinal center B cells suggested that activated cells may show upregulated expression. When B cells, T cells, macrophages, or granulocytes were activated in vitro by suitable mitogens, ICAM-1 expression was induced in all cases. Parallel studies of hematopoietic tumors demonstrated a heterogeneity of expression which correlated with expression on their normal cellular counterparts. In particular, a striking correlation between expression on B-cell tumors and corresponding stages of B-cell differentiation was noted. The widely varying expression of ICAM-1 contrasts with LFA-1 which, while variable, is nevertheless significantly positive at all stages of differentiation. This suggests that the major regulation of homotypic adhesion mediated by the LFA-1/ICAM-1 linkage occurs through control of ICAM-1 expression. In keeping with this notion, ICAM-1 expression was also correlated with the “adhesiveness” of B-lymphoid tumors. Large solitary lymphoma masses showed intense expression of ICAM-1. Conversely, chronic lymphocytic leukemia (CLL) cells and lymphoma cells from tumors exhibiting diffuse, widespread lymph node disease showed weak expression. These observations are discussed in relation to the role of ICAM-1 in regulation of lymphoid recirculation and the biology of lymphoid tumors.

scholarly journals Essential Lymphocyte Function Associated 1 (LFA-1): Intercellular Adhesion Molecule Interactions for T Cell–mediated B Cell Apoptosis by Fas/APO-1/CD95

1997 ◽  
Vol 186 (7) ◽  
pp. 1171-1176 ◽  
Author(s):  
Jin Wang ◽  
Michael J. Lenardo
Keyword(s):  
T Cell ◽  
B Cells ◽  
B Cell ◽  
Adhesion Molecule ◽  
Cell Apoptosis ◽  
Fas Ligand ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Lymphocyte Function ◽  
Th1 Cell

B cells are susceptible to Fas ligand (FasL)+ CD4+ Th1 cell–mediated apoptosis. We demonstrate that blocking the interactions between lymphocyte function associated (LFA)-1 and intercellular adhesion molecule(ICAM)-1 and ICAM-2 completely suppresses Fas-dependent B cell lysis. Antibodies to CD2 and CD48 partially suppress B cell apoptosis, whereas anti-B7.1 and anti-B7.2 antibodies have no effect. Also, B cells from ICAM-1–deficient mice are resistant to FasL+ T cell–mediated death. Our results suggest that LFA-1/ICAM interactions are crucial for Th1 cell–mediated B cell apoptosis and may contribute to the maintenance of B cell homeostasis in vivo.

Splenectomy of rats selectively reduces lymphocyte function-associated antigen 1 and intercellular adhesion molecule 1 expression on B-cell subsets in blood and lymph nodes

Blood ◽  
2001 ◽  
Vol 98 (10) ◽  
pp. 3035-3041 ◽  
Author(s):  
Novica M. Milićević ◽  
Birgit Luettig ◽  
Christian Trautwein ◽  
Torsten Wüstefeld ◽  
Michael Mähler ◽  
...  
Keyword(s):  
B Cells ◽  
Lymph Nodes ◽  
B Cell ◽  
Adhesion Molecule ◽  
Intercellular Adhesion ◽  
T Cell Subsets ◽  
Intercellular Adhesion Molecule ◽  
Lymphocyte Function ◽  
Intercellular Adhesion Molecule 1 ◽  
Surface Molecules

Abstract Splenectomy increases the number of B cells in the blood of humans and animals. It is unknown whether this is due to changes in migration, proliferation, or both. The numbers of naı̈ve (IgD+IgM+), memory (IgD−IgMhigh), newly formed (IgMhighCD90high), early recirculating follicular (IgMlowCD90high), recirculating follicular (IgMlowCD90−), and marginal zone (IgMhighCD90−) phenotype B cells were determined in control and splenectomized rats by flow cytometry. All subsets increased significantly in the blood after splenectomy. Because surface molecules are involved in the regulation of migration and proliferation, their expression (lymphocyte function-associated antigen 1 [LFA-1], intercellular adhesion molecule 1 (ICAM-1), L-selectin, α4-integrins, CD44, major histocompatability complex class II, interleukin 2 receptor-α chain) was determined on B- and T-cell subsets of both groups. B cells, but not T cells, showed a significantly reduced LFA-1 and ICAM-1 expression in blood and lymph nodes, whereas the expression of the other surface molecules analyzed remained unchanged. The down-regulation of these molecules did not influence the adherence of B cells to high endothelial venules in vitro. In vivo, however, ICAM-1low–expressing B cells migrated significantly faster through lymph nodes (ICAM-1low 41 ± 5 hours versus ICAM-1high58 ± 3 hours), whereas proliferation of B cells in bone marrow, lymph node, and blood remained unchanged. Thus, the presence of one organ is necessary for appropriate expression of LFA-1 and ICAM-1 on B cells in other, distant organs. The more rapid transit of ICAM-1low B cells through lymph nodes may be responsible for the increased B-cell number in the blood after splenectomy.

A pre-embedding double staining procedure used to observe the effect of fixation on the activity of intercellular adhesion molecule on T and B cells

1990 ◽  
Vol 48 (3) ◽  
pp. 378-379
Author(s):  
Jane E. Ramberg ◽  
Shigeto Tohma ◽  
Peter E. Lipsky
Keyword(s):  
B Cells ◽  
Adhesion Molecule ◽  
Colloidal Gold ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Staining Procedure ◽  
Double Staining ◽  
T And B Cells ◽  
Microtiter Plates ◽  
Streptavidin Peroxidase

Intercellular adhesion molecule (ICAM-1) appears to be a ligand for LFA-1 dependent adhesion in T cell mediated cytotoxcity. It is found on cells of both hematopoietic and non-hematopoietic origin. While observing the activity of ICAM-1 on the surfaces of interacting T and B cells, we found that we could successfully carry out a pre-embedding double staining procedure utilizing both colloidal gold and peroxidase conjugated reagents.On 24-well microtiter plates, mitomycin-treated T4 cells were stimulated with 64.1 (anti-CD3) for one hour before the addition, in some instances, of B cells. Following a 12-48 hour incubation at 38°C, the cells were washed and then immunostained with a colloidal gold conjugated RFB-4 (anti-CD22); biotinylated R6.5 (anti-ICAM-1); followed by streptavidin/peroxidase. This method allowed us to observe two different antigens without concern about possible cross-reaction of reagents. Because we suspected ICAM-1 and R6.5 were sensitive to fixation, we tried varying concentrations of fresh paraformaldehyde before R6.5, after R6.5 and after streptavidin/peroxidase. All immunostaining and washing was done on ice with ice cold reagents.

scholarly journals The immunomodulatory functions and molecular mechanism of a new bursal heptapeptide (BP7) in immune responses and immature B cells

2019 ◽  
Vol 50 (1) ◽  
Author(s):  
Xiu Li Feng ◽  
Yang Zheng ◽  
Man Man Zong ◽  
Shan Shan Hao ◽  
Guang Fang Zhou ◽  
...  
Keyword(s):  
B Cells ◽  
Immune Responses ◽  
B Cell ◽  
Molecular Mechanisms ◽  
Bursa Of Fabricius ◽  
Biological Factor ◽  
Mrna Levels ◽  
B Cell Differentiation ◽  
Immune Functions ◽  
Wehi 231

Abstract The bursa of Fabricius (BF) is the acknowledged central humoural immune organ unique to birds and plays a vital role in B lymphocyte development. In addition, the unique molecular immune features of bursal-derived biological peptides involved in B cell development are rarely reported. In this paper, a novel bursal heptapeptide (BP7) with the sequence GGCDGAA was isolated from the BF and was shown to enhance the monoclonal antibody production of a hybridoma. A mouse immunization experiment showed that mice immunized with an AIV antigen and BP7 produced strong antibody responses and cell-mediated immune responses. Additionally, BP7 stimulated increased mRNA levels of sIgM in immature mouse WEHI-231 B cells. Gene microarray results confirmed that BP7 regulated 2465 differentially expressed genes in BP7-treated WEHI-231 cells and induced 13 signalling pathways and various immune-related functional processes. Furthermore, we found that BP7 stimulated WEHI-231 cell autophagy and AMPK-ULK1 phosphorylation and regulated Bcl-2 protein expression. Finally, chicken immunization showed that BP7 enhanced the potential antibody and cytokine responses to the AIV antigen. These results suggested that BP7 might be an active biological factor that functions as a potential immunopotentiator, which provided some novel insights into the molecular mechanisms of the effects of bursal peptides on immune functions and B cell differentiation.

Circulating forms of intercellular adhesion molecule (ICAM)-1 in mice lacking membranous ICAM-1

Blood ◽  
2000 ◽  
Vol 95 (4) ◽  
pp. 1350-1355 ◽  
Author(s):  
Natasja K. van den Engel ◽  
Edmund Heidenthal ◽  
Antje Vinke ◽  
Hubert Kolb ◽  
Stephan Martin
Keyword(s):  
Adhesion Molecule ◽  
Transmembrane Domain ◽  
Flow Cytometric Analysis ◽  
Intercellular Adhesion ◽  
Intercellular Adhesion Molecule ◽  
Enzyme Linked Immunosorbent Assay ◽  
Immune Functions ◽  
Wild Type ◽  
Spleen Cells ◽  
Intercellular Adhesion Molecule 1

Mice deficient in intercellular adhesion molecule-1 (ICAM-1), lacking membranous ICAM-1, show a normal development but abnormalities of inflammatory and immune functions. Although the membrane-bound form of ICAM-1 is not detectable in the mutant strain, circulating ICAM-1 (cICAM) is present in serum from ICAM-1-deficient mice in similar amounts as in serum from wild-type mice. These findings were confirmed in vitro by flow cytometric analysis of lipopolysaccharide-stimulated spleen cells, and cICAM-enzyme-linked immunosorbent assay analysis of supernatants of cultured spleen cells. To analyze for the source of cICAM-1, spleen cell RNA was isolated and ICAM-1 RNA was amplified by reverse transcriptase-polymerase chain reaction using primers binding in the 5′ and 3′ untranslated regions. Different fragments were cloned and sequenced. In wild-type RNA the common 5 domain form of ICAM-1 was identified. In RNA from ICAM-1 mutant mice only 3 smaller fragments were found. Sequencing these fragments identified 3 alternatively spliced isoforms of ICAM-1, lacking 2 or 3 extracellular domains. However, in all spliced fragments the transmembrane domain was included. Therefore, we postulate that circulating forms of ICAM-1 are generated by proteolytic cleavage of membranous ICAM-1. The data indicate that the expression of membranous ICAM-1 and the appearance of circulating forms in serum are independently regulated mechanisms.

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