CD44-Hyaluronate Interaction Mediates In Vitro Lymphocyte Binding to the White Matter of the Central Nervous System

Aho, Riitta; Jalkanen, Sirpa; Kalimo, Hannu

doi:10.1097/00005072-199405000-00011

Cited by 14 publications

(10 citation statements)

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“…Furthermore, we have screened the TLD-4A2 mAb against recombinant rat PECAM-1 and did not find reactivity by ELISA-although other monoclonal antibodies of the TLD series were CD31-specific (Male et al, 1995). Similar to the expression of PECAM-1, CD44 is expressed on astrocytes in the brain but is not reportedly expressed on microglia (Aho et al, 1994;Moretto et al, 1993). Thus, the bulk of currently available evidence suggests that this is a novel cell surface molecule (Barclay et al, 1994;Pigott and Power, 1994).…”

Section: Williams Et Almentioning

confidence: 97%

Inhibition of Experimental Allergic Encephalomyelitis with an Antibody that Recognizes a Novel Antigen Expressed on Lymphocytes, Endothelial Cells, and Microglia

Williams

Zhao

Politopoulou³

et al. 2000

Laboratory Investigation

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SUMMARY:Experimental allergic encephalomyelitis (EAE) is a frequently employed animal model of the human disease multiple sclerosis. EAE can be induced by adoptive transfer of CD4 ϩ T cells that are specific for central nervous system (CNS) antigens, typically myelin proteins. Although the pathogenic mechanism or mechanisms responsible for the clinical signs and histological changes in EAE and multiple sclerosis are not fully defined, the entry of T lymphocytes and antigen recognition within the CNS are required. The present study describes the participation of a novel cell surface molecule with properties suggesting a role in cell-cell adhesion or co-stimulation, or both, in the development of EAE in the rat. The molecule is defined by the unique monoclonal antibody (mAb) TLD-4A2. The TLD-4A2 antigen is present on resting and activated T lymphocytes, activated CNS endothelial cells, and microglia. The antigen is normally distributed in many tissues including lymph node, thymus, and spleen, as well as in the inflamed CNS. Both its pattern of tissue distribution and immunoprecipitation and immunoblotting studies suggest that the TLD-4A2 antigen is a novel molecule. Treatment of rats with the purified 4A2 mAb resulted in the inhibition of the clinical signs of EAE and also decreased the number T cells and macrophages accumulating in the CNS parenchyma. TLD-4A2 antibody did not seem to directly interfere with T cell viability in vivo, as demonstrated by the ability to recover and stimulate CD4 ϩ encephalitogenic T cells from cervical lymph nodes of 4A2-treated animals. In vitro, the antibody partially blocked T cell proliferation assays. These data suggest that the TLD-4A2 mAb recognizes a novel molecule expressed on lymphocytes, endothelial cells, and macrophages that may play a role in hematogenous cell traffic and the initiation of CNS inflammation. (Lab Invest 2000, 80:313-326).

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Section: Williams Et Almentioning

confidence: 97%

Inhibition of Experimental Allergic Encephalomyelitis with an Antibody that Recognizes a Novel Antigen Expressed on Lymphocytes, Endothelial Cells, and Microglia

Williams

Zhao

Politopoulou³

et al. 2000

Laboratory Investigation

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“…Since the endothelial ligand of leukocyte CD44 is hyaluronate (12), the function of which cannot be inhibited by mAbs, its role was analyzed by digesting the target sections with a hyaluronate degrading enzyme, as described (13). Briefly, the synovial sections were incubated with a buffer containing hyaluronidase from Streptococcus dysgalactiae (Seikagaku Corporation, Tokyo, Japan) and a cocktail of protease in- hibitors for 30 min at room temperature.…”

Section: Introductionmentioning

confidence: 99%

Homing of mucosal leukocytes to joints. Distinct endothelial ligands in synovium mediate leukocyte-subtype specific adhesion.

Salmi¹,

Rajala²,

Jalkanen³

1997

J. Clin. Invest.

124

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Inflammation and infection of the gut can be followed by reactive arthritis at a distant joint. Leukocyte recruitment into synovium is essential for this process, but nothing is known about the endothelial adhesion molecules in synovial membrane which direct the homing of activated, gut-derived leukocytes to joints. Here we analyzed the expression of the known endothelial adhesion molecules in inflamed syno1 1vium and their function in binding of mucosal leukocytes. Intercellular adhesion molecule-1 (ICAM-1/CD54) and vascular adhesion protein-1 (VAP-1) were most prominently expressed in synovial vessels. All other adhesion molecules were found at lower levels in inflamed synovia, except mucosal addressin which was absent. Binding of macrophages isolated from lamina propria of the gut to synovial endothelium was almost entirely P-selectin-dependent. In contrast, small intestinal lymphocytes and immunoblasts both relied mainly on VAP-1 in recognition of synovial vessels. Thus, endothelial P-selectin and VAP-1 mediate binding of mucosal effector cells to synovium in a leukocyte subtype-selective manner. Antiadhesive therapy against these inducible molecules should ablate the pathogenetic cascade leading to inappropriate homing of leukocytes to joints in arthritis. ( J. Clin. Invest. 1997. 99:2165-2172).

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“…In other experimental systems, anti-CD44 antibodies can block the migration of murine pro-T cells into the thymus [36,37] and prevent leucocyte extravasation at sites of inflammation [38]. Moreover, they can also stimulate leucocyte adhesion [39] and augment T cell activation [40], suggesting that CD44 does indeed signal within the cell. This idea is supported further by the discovery that CD44 plays a role in cell spreading [41], and cross-linking of CD44 on T cells is known to activate the tyrosine kinase p56 lck [42].…”

Section: Figure 3 Diagrammatic Representation Of Cd44mentioning

confidence: 99%

Role of macrophage CD44 in the disposal of inflammatory cell corpses

VIVERS¹,

DRANSFIELD²,

HART³

2002

Clinical Science

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CD44-Hyaluronate Interaction Mediates In Vitro Lymphocyte Binding to the White Matter of the Central Nervous System

Cited by 14 publications

References 0 publications

Inhibition of Experimental Allergic Encephalomyelitis with an Antibody that Recognizes a Novel Antigen Expressed on Lymphocytes, Endothelial Cells, and Microglia

Inhibition of Experimental Allergic Encephalomyelitis with an Antibody that Recognizes a Novel Antigen Expressed on Lymphocytes, Endothelial Cells, and Microglia

Homing of mucosal leukocytes to joints. Distinct endothelial ligands in synovium mediate leukocyte-subtype specific adhesion.

Role of macrophage CD44 in the disposal of inflammatory cell corpses

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