scholarly journals P-selectin mediates Ca(2+)-dependent adhesion of activated platelets to many different types of leukocytes: detection by flow cytometry

Blood ◽  
1992 ◽  
Vol 80 (1) ◽  
pp. 134-142 ◽  
Author(s):  
LG de Bruijne-Admiraal ◽  
PW Modderman ◽  
AE Von dem Borne ◽  
A Sonnenberg
Keyword(s):  
T Cells ◽  
Divalent Cations ◽  
Phosphatidyl Inositol ◽  
Cell Types ◽  
Inhibitory Effect ◽  
Immunofluorescence Assay ◽  
Cd8 Cells ◽  
Activated Platelets ◽  
Selectin Ligands ◽  
Different Types

Abstract Previous studies have shown that thrombin-activated platelets interact through the P-selectin with neutrophils and monocytes. To identify other types of leukocytes capable of such an interaction, eosinophils, basophils, and lymphocytes were isolated from whole blood. Binding of these cells to activated platelets was examined in a double immunofluorescence assay and the results show that activated platelets not only bind to neutrophils and monocytes, but also to eosinophils, basophils, and subpopulations of T lymphocytes. Using monoclonal antibodies (MoAbs) specific for subsets of T cells, we could further demonstrate that the T cells which bind activated platelets are natural killer (NK) cells and an undefined subpopulation of CD4+ and CD8+ cells. All these interactions were dependent on divalent cations and were completely inhibited by an MoAb against P-selectin. Thus, P- selectin mediates the binding of activated platelets to many different types of leukocytes. Studies with leukocytes treated with proteases or neuraminidase have shown that the structures recognized by P-selectin are glycoproteins carrying sialic acid residues. Because the loss of binding of activated platelets to neuraminidase-treated neutrophils was almost complete, but only partial to treated eosinophils, basophils, and monocytes, the latter cell types may have different P-selectin ligands in addition to those present on neutrophils. We found that two previously identified ligands for P-selectin, the oligosaccharides Le(x) and sialyl-Le(x), had little or no inhibitory effect on adhesion of activated platelets to leukocytes and that binding was not inhibited by MoAbs against these oligosaccharides. In addition, there was no correlation between the expression of Le(x) on several cell types and their capacity to bind activated platelets. In contrast, the expression of sialyl-Le(x) on cells was almost perfectly correlated with their ability to bind activated platelets. Thus, while Le(x) cannot be a major ligand for P-selectin, a possible role for sialyl-Le(x) in P- selectin-mediated adhesion processes cannot be dismissed. Finally, activated platelets were found to bind normally to monocytes and neutrophils of patients with paroxysmal nocturnal hemoglobulinuria (PNH) and to neutrophils from which phosphatidyl inositol (PI)-linked proteins had been removed by glycosylphosphatidyl inositol-specific phospholipase C (GPI-PLC) digestion. This suggests that at least part of the P-selectin ligands on these cells are not GPI-anchored.

scholarly journals P-selectin mediates Ca(2+)-dependent adhesion of activated platelets to many different types of leukocytes: detection by flow cytometry

Blood ◽  
1992 ◽  
Vol 80 (1) ◽  
pp. 134-142 ◽  
Author(s):  
LG de Bruijne-Admiraal ◽  
PW Modderman ◽  
AE Von dem Borne ◽  
A Sonnenberg
Keyword(s):  
T Cells ◽  
Divalent Cations ◽  
Phosphatidyl Inositol ◽  
Cell Types ◽  
Inhibitory Effect ◽  
Immunofluorescence Assay ◽  
Cd8 Cells ◽  
Activated Platelets ◽  
Selectin Ligands ◽  
Different Types

Previous studies have shown that thrombin-activated platelets interact through the P-selectin with neutrophils and monocytes. To identify other types of leukocytes capable of such an interaction, eosinophils, basophils, and lymphocytes were isolated from whole blood. Binding of these cells to activated platelets was examined in a double immunofluorescence assay and the results show that activated platelets not only bind to neutrophils and monocytes, but also to eosinophils, basophils, and subpopulations of T lymphocytes. Using monoclonal antibodies (MoAbs) specific for subsets of T cells, we could further demonstrate that the T cells which bind activated platelets are natural killer (NK) cells and an undefined subpopulation of CD4+ and CD8+ cells. All these interactions were dependent on divalent cations and were completely inhibited by an MoAb against P-selectin. Thus, P- selectin mediates the binding of activated platelets to many different types of leukocytes. Studies with leukocytes treated with proteases or neuraminidase have shown that the structures recognized by P-selectin are glycoproteins carrying sialic acid residues. Because the loss of binding of activated platelets to neuraminidase-treated neutrophils was almost complete, but only partial to treated eosinophils, basophils, and monocytes, the latter cell types may have different P-selectin ligands in addition to those present on neutrophils. We found that two previously identified ligands for P-selectin, the oligosaccharides Le(x) and sialyl-Le(x), had little or no inhibitory effect on adhesion of activated platelets to leukocytes and that binding was not inhibited by MoAbs against these oligosaccharides. In addition, there was no correlation between the expression of Le(x) on several cell types and their capacity to bind activated platelets. In contrast, the expression of sialyl-Le(x) on cells was almost perfectly correlated with their ability to bind activated platelets. Thus, while Le(x) cannot be a major ligand for P-selectin, a possible role for sialyl-Le(x) in P- selectin-mediated adhesion processes cannot be dismissed. Finally, activated platelets were found to bind normally to monocytes and neutrophils of patients with paroxysmal nocturnal hemoglobulinuria (PNH) and to neutrophils from which phosphatidyl inositol (PI)-linked proteins had been removed by glycosylphosphatidyl inositol-specific phospholipase C (GPI-PLC) digestion. This suggests that at least part of the P-selectin ligands on these cells are not GPI-anchored.

scholarly journals Activated Platelets Induce an Anti-Inflammatory Response of Monocytes/Macrophages through Cross-Regulation of PGE2and Cytokines

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Bona Linke ◽  
Yannick Schreiber ◽  
Bettina Picard-Willems ◽  
Patrick Slattery ◽  
Rolf M. Nüsing ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Cell Types ◽  
Inhibitory Effect ◽  
Innate Immune ◽  
Prostaglandin E ◽  
Murine Bone Marrow ◽  
Activated Platelets ◽  
Monocytes And Macrophages ◽  
Inflammatory Processes ◽  
Necrosis Factor

Platelets are well known for their role in hemostasis and are also increasingly recognized for their roles in the innate immune system during inflammation and their regulation of macrophage activation. Here, we aimed to study the influence of platelets on the production of inflammatory mediators by monocytes and macrophages. Analyzing cocultures of platelets and murine bone marrow-derived macrophages or human monocytes, we found that collagen-activated platelets release high amounts of prostaglandin E2(PGE2) that leads to an increased interleukin- (IL-) 10 release and a decreased tumor necrosis factor (TNF)αsecretion out of the monocytes or macrophages. Platelet PGE2mediated the upregulation of IL-10 in both cell types via the PGE2receptor EP2. Notably, PGE2-mediated IL-10 synthesis was also mediated by EP4 in murine macrophages. Inhibition of TNFαsynthesis via EP2 and EP4, but not EP1, was mediated by IL-10, since blockade of the IL-10 receptor abolished the inhibitory effect of both receptors on TNFαrelease. This platelet-mediated cross-regulation between PGE2and cytokines reveals one mechanism how monocytes and macrophages can attenuate excessive inflammatory responses induced by activated platelets in order to limit inflammatory processes.

scholarly journals Targeting Selectins Mediated Biological Activities With Multivalent Probes

2021 ◽  
Vol 9 ◽  
Author(s):  
Deepak Ganesh ◽  
Prashant Jain ◽  
Chethan Devanur Shanthamurthy ◽  
Suraj Toraskar ◽  
Raghavendra Kikkeri
Keyword(s):  
Tumor Metastasis ◽  
Inflammatory Diseases ◽  
Biological Activities ◽  
Type I ◽  
Blood Capillaries ◽  
Activated Platelets ◽  
Selectin Ligands ◽  
Different Types ◽  
Selectin Binding ◽  
Sialyl Lewisa

Selectins are type-I transmembrane glycoproteins that are ubiquitously expressed on activated platelets, endothelial cells, and leukocytes. They bind to cell surface glycoproteins and extracellular matrix ligands, regulate the rolling of leukocytes in the blood capillaries, and recruit them to inflammatory sites. Hence, they are potential markers for the early detection and inhibition of inflammatory diseases, thrombosis, cardiovascular disorders, and tumor metastasis. Fucosylated and sialylated glycans, such as sialyl Lewisx, its isoform sialyl Lewisa, and heparan sulfate, are primary selectin ligands. Functionalization of these selectin-binding ligands on multivalent probes, such as nanoparticles, liposomes, and polymers, not only inhibits selectin-mediated biological activity but is also involved in direct imaging of the inflammation site. This review briefly summarizes the selectin-mediated various diseases such as thrombosis, cancer and recent progress in the different types of multivalent probes used to target selectins.

scholarly journals Crosstalk Between Tumor-Associated Microglia/Macrophages and CD8-Positive T Cells Plays a Key Role in Glioblastoma

2021 ◽  
Vol 12 ◽  
Author(s):  
Sheng Tu ◽  
Xu Lin ◽  
Jili Qiu ◽  
Jiaqi Zhou ◽  
Hui Wang ◽  
...  
Keyword(s):  
T Cells ◽  
Cd8 T Cells ◽  
Immune Cells ◽  
Malignant Disease ◽  
Immune Therapy ◽  
Cell Types ◽  
Different Types ◽  
The Central Nervous System ◽  
And Function ◽  
The Relationship

Glioblastoma is considered to be the most malignant disease of the central nervous system, and it is often associated with poor survival. The immune microenvironment plays a key role in the development and treatment of glioblastoma. Among the different types of immune cells, tumor-associated microglia/macrophages (TAM/Ms) and CD8-positive (CD8+) T cells are the predominant immune cells, as well as the most active ones. Current studies have suggested that interaction between TAM/Ms and CD8+ T cells have numerous potential targets that will allow them to overcome malignancy in glioblastoma. In this review, we summarize the mechanism and function of TAM/Ms and CD8+ T cells involved in glioblastoma, as well as update on the relationship and crosstalk between these two cell types, to determine whether this association alters the immune status during glioblastoma development and affects optimal treatment. We focus on the molecular factors that are crucial to this interaction, and the role that this crosstalk plays in the biological processes underlying glioblastoma treatment, particularly with regard to immune therapy. We also discuss novel therapeutic targets that can aid in resolving reticular connections between TAM/Ms and CD8+ T cells, including depletion and reprogramming TAM/Ms and novel TAM/Ms-CD8+ T cell cofactors with potential translational usage. In addition, we highlight the challenges and discuss future perspectives of this crosstalk between TAM/Ms and CD8+ T cells.

scholarly journals Distinct mechanisms of neonatal tolerance induced by dendritic cells and thymic B cells.

1991 ◽  
Vol 173 (3) ◽  
pp. 549-559 ◽  
Author(s):  
M Inaba ◽  
K Inaba ◽  
M Hosono ◽  
T Kumamoto ◽  
T Ishida ◽  
...  
Keyword(s):  
T Cells ◽  
Dendritic Cells ◽  
B Cells ◽  
Cell Types ◽  
Cell Sorter ◽  
Histocompatibility Complex ◽  
Different Types ◽  
Induced Tolerance ◽  
Antigen Presenting

To assess the role of different types of antigen-presenting cells (APC) in the induction of tolerance, we isolated B cells, macrophages, and dendritic cells from thymus and spleen, and injected these into neonatal BALB/c mice across an Mls-1 antigenic barrier. One week after injection of APC from Mls-1-incompatible mice or from control syngeneic mice, we measured the number of thymic, Mls-1a-reactive, V beta 6+ T cells and the capacity of thymocytes to induce a graft-vs.-host (GVH) reaction in popliteal lymph nodes of Mls-1a mice. Injection of thymic but not spleen B cells deleted thymic, Mls-1a-reactive V beta 6+ T cells and induced tolerance in the GVH assay. The thymic B cells were primarily of the CD5+ type, and fluorescence-activated cell sorter-purified CD5+ thymic B cells were active. Injection of dendritic cells from spleen or thymus also induced tolerance, but the V beta 6 cells were anergized rather than deleted. Macrophages from thymus did not induce tolerance. Dendritic cells and thymic B cells were also effective in inducing tolerance even when injected into Mls-, major histocompatibility complex-incompatible, I-E- mice, but only thymic B cells depleted V beta 6-expressing T cells. Therefore, different types of bone marrow-derived APC have different capacities for inducing tolerance, and the active cell types (dendritic cells and CD5+ thymic B cells) can act by distinct mechanisms.

Activated Platelets Release Two Types of Membrane Vesicles: Microvesicles by Surface Shedding and Exosomes Derived From Exocytosis of Multivesicular Bodies and -Granules

Blood ◽  
1999 ◽  
Vol 94 (11) ◽  
pp. 3791-3799 ◽  
Author(s):  
Harry F.G. Heijnen ◽  
Anja E. Schiel ◽  
Rob Fijnheer ◽  
Hans J. Geuze ◽  
Jan J. Sixma
Keyword(s):  
Platelet Activation ◽  
Annexin V ◽  
Membrane Vesicles ◽  
Cell Types ◽  
Multivesicular Bodies ◽  
Factor X ◽  
Activated Platelets ◽  
Immuno Electron Microscopy ◽  
Different Types ◽  
Platelet Aggregates

Platelet activation leads to secretion of granule contents and to the formation of microvesicles by shedding of membranes from the cell surface. Recently, we have described small internal vesicles in multivesicular bodies (MVBs) and -granules, and suggested that these vesicles are secreted during platelet activation, analogous to the secretion of vesicles termed exosomes by other cell types. In the present study we report that two different types of membrane vesicles are released after stimulation of platelets with thrombin receptor agonist peptide SFLLRN (TRAP) or -thrombin: microvesicles of 100 nm to 1 μm, and exosomes measuring 40 to 100 nm in diameter, similar in size as the internal vesicles in MVBs and -granules. Microvesicles could be detected by flow cytometry but not the exosomes, probably because of the small size of the latter. Western blot analysis showed that isolated exosomes were selectively enriched in the tetraspan protein CD63. Whole-mount immuno-electron microscopy (IEM) confirmed this observation. Membrane proteins such as the integrin chains IIb-β3 and β1, GPIb, and P-selectin were predominantly present on the microvesicles. IEM of platelet aggregates showed CD63+ internal vesicles in fusion profiles of MVBs, and in the extracellular space between platelet extensions. Annexin-V binding was mainly restricted to the microvesicles and to a low extent to exosomes. Binding of factor X and prothrombin was observed to the microvesicles but not to exosomes. These observations and the selective presence of CD63 suggest that released platelet exosomes may have an extracellular function other than the procoagulant activity, attributed to platelet microvesicles.

On Our Way to a Better Understanding of CD8 T Cell Differentiation and Memory T Cell Development.

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. sci-52-sci-52 ◽  
Author(s):  
Susan Kaech
Keyword(s):  
T Cells ◽  
T Cell ◽  
Bacterial Infections ◽  
T Cell Development ◽  
Cell Types ◽  
Cell Potential ◽  
Effector Cells ◽  
Memory T Cell ◽  
Different Types ◽  
Two Populations

Abstract As certain acute viral or bacterial infections resolve, two types of effector CD8 T cells are formed that differ in their longevity and memory T-cell potential. These cell types can be distinguished from one another by surface markers, namely IL-7R and KLRG1. Memory precursor effector cells are enriched in the IL-7Rhi KLRG1lo cell population, and short-lived effector cells are enriched in the KLRGhi IL-7Rlo population. These two populations become discernible during the peak of clonal expansion. Upon expression of KLRG1, the effector cells are committed to becoming short-lived. Our recent progress toward identifying the signals and genetic pathways that control the formation of these different types of effector T cells will be discussed.

scholarly journals Oligoclonal Expansion of Cd8+ T Cells during Idiopathic Multicentric Castleman Disease Flares Suggests an Antigen Driven Process

Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 2411-2411
Author(s):  
Dustin Shilling ◽  
Jason E Stadanlick ◽  
Wenzhao Meng ◽  
Abhishek Rao ◽  
Vera P Krymskaya ◽  
...  
Keyword(s):  
T Cells ◽  
Lymph Nodes ◽  
Cd8 T Cells ◽  
Partial Remission ◽  
Cell Types ◽  
Castleman Disease ◽  
Disease Flare ◽  
Cd8 Cells ◽  
Hla Dr ◽  
Cd8 Cell

Abstract Castleman disease (CD) describes a group of heterogeneous diseases defined by shared characteristic lymph node histopathology and is classified based on the number of regions of enlarged lymph nodes. Multicentric CD (MCD) involves multiple regions of lymphadenopathy as well as systemic inflammation, cytopenias, and vital organ dysfunction due to a cytokine storm that often includes interleukin-6. In ~50% of patients, the pathogenic driver is Kaposi sarcoma-associated/human herpesvirus-8 (HHV-8) in the context of immunosuppression. In contrast, the etiologic driver in HHV8-negative MCD (idiopathic or iMCD) is unknown. To date, most research has focused on descriptive characterization of the enlarged lymph nodes, and the pathological cell types driving iMCD pathogenesis remain unidentified. Given that lymphoid cells circulate through the blood and lymph nodes, are able to produce high levels of cytokines upon activation, and are the primary cell types responsible for the enlarged lymph nodes in iMCD and other related diseases, we first performed a detailed immunophenotyping of peripheral blood mononuclear cells (PBMCs) obtained from iMCD patients in remission (n=16), iMCD patients during disease flare (n=6) and healthy donors (HD) (n=15). PBMCs were isolated by density gradient and either stained immediately or cryopreserved for future analyses. A HD sample was drawn at the same time as each experimental sample and processed and analyzed in parallel. Our initial hypothesis was that analysis of iMCD flare PBMCs would reveal an abnormal myeloid or lymphocyte subset. Thus, we stained and analyzed PBMCs for standard lineage markers: CD11b, CD15, CD19, CD3, CD56 and CD14. However, we observed no gross differences in population frequencies during either remission or flare compared to HD. Additionally, no differences in the proportions of natural killer T cells (CD3+CD56+), or CD4+ or CD8+ lymphocytes were observed. However, more refined examinations of the lymphocyte sub-sets based upon activation status revealed an increased proportion of activated memory (CD62LlowHLA-DR+) CD8+ cells during iMCD flare compared to HD and iMCD patients in remission and a decreased proportion of naïve (CD62L+CD45RA+) CD8+ cells compared to HD (p<0.05 for each comparison, Bonferroni corrected 2-tailed t-test). Interestingly, for one patient followed over a 7-month period, during which time he experienced two disease flares, the proportion of activated memory CD8+ cells mirrored the re-emergence of clinical disease symptoms, rising to 80% of all CD8+ lymphocytes during disease flare and waning as flares subsided. We next questioned whether the expansion of memory CD8+ T cells represented a diverse population of T cells with unique TCRs or alternatively, reflected the expansion of one or a few dominate TCR clones. Thus, we performed bulk TCRβ sequencing on genomic DNA from peripheral CD8+ cells obtained during the patient's partial remission between his two flares and at the start of his second disease flare (flare 2). Interestingly, we found that TCRs from CD8+ cells showed an overrepresentation of only a few clonotypes, indicating increased oligoclonality; the top 20 clones accounted for 45% (partial remission) and 52% (flare 2) of bulk CD8+ reads. Furthermore, the top copy number rearrangement comprised 7.5% (partial remission) and 10% (flare 2) of the CD8+ cell repertoires (healthy subjects' CD8+ T cell top copy number rearrangement is typically below 5%). Sequencing of activated (HLA-DR+) and memory (CD45RO+) CD8+ populations also revealed increased clonality. In these populations, the top 20 clones accounted for 45% (CD45RO+) and 33% (HLA-DR+) of sequencing reads during the patient's partial remission and increased to 61% (CD45RO+) and 54% (HLA-DR+) of sequencing reads during flare 2. Further, the top TCRβ sequences persisted over time, being identified in both the partial remission and flare 2 samples. This study identifies quantitative and phenotypic differences in CD8+ cell populations during iMCD disease flare. Furthermore, we present evidence suggesting a role for oligoclonal T cells in iMCD, as our TCRβ sequencing findings reveal a substantial accumulation of only a few TCR clonotypes in CD8+ populations during disease flare. Cumulatively, these results suggest that TCR signaling, due to antigen stimulation or T cell dysregulation may be involved in iMCD pathogenesis. Disclosures Fajgenbaum: Janssen Pharmaceuticals, Inc.: Research Funding.

Activated Platelets Release Two Types of Membrane Vesicles: Microvesicles by Surface Shedding and Exosomes Derived From Exocytosis of Multivesicular Bodies and -Granules

Blood ◽  
1999 ◽  
Vol 94 (11) ◽  
pp. 3791-3799 ◽  
Author(s):  
Harry F.G. Heijnen ◽  
Anja E. Schiel ◽  
Rob Fijnheer ◽  
Hans J. Geuze ◽  
Jan J. Sixma
Keyword(s):  
Platelet Activation ◽  
Annexin V ◽  
Membrane Vesicles ◽  
Cell Types ◽  
Multivesicular Bodies ◽  
Factor X ◽  
Activated Platelets ◽  
Immuno Electron Microscopy ◽  
Different Types ◽  
Platelet Aggregates

Abstract Platelet activation leads to secretion of granule contents and to the formation of microvesicles by shedding of membranes from the cell surface. Recently, we have described small internal vesicles in multivesicular bodies (MVBs) and -granules, and suggested that these vesicles are secreted during platelet activation, analogous to the secretion of vesicles termed exosomes by other cell types. In the present study we report that two different types of membrane vesicles are released after stimulation of platelets with thrombin receptor agonist peptide SFLLRN (TRAP) or -thrombin: microvesicles of 100 nm to 1 μm, and exosomes measuring 40 to 100 nm in diameter, similar in size as the internal vesicles in MVBs and -granules. Microvesicles could be detected by flow cytometry but not the exosomes, probably because of the small size of the latter. Western blot analysis showed that isolated exosomes were selectively enriched in the tetraspan protein CD63. Whole-mount immuno-electron microscopy (IEM) confirmed this observation. Membrane proteins such as the integrin chains IIb-β3 and β1, GPIb, and P-selectin were predominantly present on the microvesicles. IEM of platelet aggregates showed CD63+ internal vesicles in fusion profiles of MVBs, and in the extracellular space between platelet extensions. Annexin-V binding was mainly restricted to the microvesicles and to a low extent to exosomes. Binding of factor X and prothrombin was observed to the microvesicles but not to exosomes. These observations and the selective presence of CD63 suggest that released platelet exosomes may have an extracellular function other than the procoagulant activity, attributed to platelet microvesicles.

scholarly journals Activated CD8 T cells express two distinct P-Selectin Ligands

2017 ◽  
Author(s):  
Douglas A. Carlow ◽  
Michelle C. Tra ◽  
Hermann J. Ziltener
Keyword(s):  
T Cells ◽  
Cd8 T Cells ◽  
High Endothelial Venules ◽  
Original Source ◽  
Activated Platelets ◽  
Selectin Ligands ◽  
Peripheral Lymph ◽  
Donor Cells ◽  
A Cell

One sentence summaryMurine primary in-vivo activated CD8+ T cells express two ligands for P-selectin, canonical PSGL-1 and a cell-extrinsic ligand docked on L-selectin.AbstractP-selectin (PSel) expressed on activated endothelia and platelets supports recruitment of leukocytes expressing PSel ligand (PSelL) to sites of inflammation. While monitoring PSelL expression on activated CD8+T cells (Tact) in adoptive transfer models, we observed two distinct PSelL on responding donor cells, the canonical cell-intrinsic PSelL PSGL1 and a second undocumented PSelL provisionally named PSL2. PSL2 is unusual among selectin ligands in that it is cell-extrinsic, loaded onto L-selectin (LSel) expressed by Tact but not LSel on resting naïve CD8+T cells. PSL2 expression is highest on Tact responding in peripheral lymph nodes and low on Tact responding in spleen suggesting that the original source of PSL2 is high endothelial venules, cells known to produce LSelL. When both PSGL1 and PSL2 were absent from the surface of Tact, no significant residual PSelL activity was detected. PSL2 is a ligand for both PSel and LSel and can physically bridge the two selectins. The LSel/PSL2 complex can mediate PSel-dependent adherence of Tact to immobilized PSel-hIgG or to activated platelets, either independently or cooperatively with PSGL1. PSel engagement of PSGL1 and LSel/PSL2 would likely deliver distinct signals known to be relevant in leukocyte recruitment.

Sign in / Sign up

Export Citation Format

Share Document