Disease relevance of Sell

• To determine the primary structure of A.11 and examine its expression in lymphoid cells, we constructed an expression phage cDNA library of rat thoracic duct lymphocytes (TDL) and performed screening by immunoselection (utilizing an anti-A.11 polyclonal antiserum) as well as by hybridization selection [1].
• These results indicated that ATL cells constitutively overexpress the L-selectin gene that can be transactivated by HTLV-1 Tax [2].
• Constitutive overexpression of the L-selectin gene in fresh leukemic cells of adult T-cell leukemia that can be transactivated by human T-cell lymphotropic virus type 1 Tax [2].
• The role of the inducible L-selectin ligand was studied in complement-dependent acute dermatitis in rats [3].
• By using a rat ureteral obstruction model, we showed previously that L-selectin plays an important role in leukocyte infiltration into the kidney [4].

High impact information on Sell

• Painful stimulation suppresses joint inflammation by inducing shedding of L-selectin from neutrophils [5].
• Initial leukocyte tethering via the alpha 4-integrin could not be demonstrated in this model, whereas L-selectin did support leukocyte tethering [6].
• Concomitant with the enhanced lymphocyte adhesion, the cardiac endothelium begins to de novo express sialyl Lewis(a) and sialyl Lewis(x) (sLea and sLex) epitopes, which have been shown to be sequences of L-selectin counterreceptors [7].
• The endothelium of allografts, but not that of syngeneic grafts or normal controls, also reacted with the L-selectin-immunoglobulin G fusion protein, giving further proof of inducible L-selectin counterreceptors [7].
• De novo expression of endothelial sialyl Lewis(a) and sialyl Lewis(x) during cardiac transplant rejection: superior capacity of a tetravalent sialyl Lewis(x) oligosaccharide in inhibiting L-selectin-dependent lymphocyte adhesion [7].

Chemical compound and disease context of Sell

• These data suggest that PMNs from LPS-treated rats do not exacerbate ischemia-reperfusion injury as do control PMNs, possibly, due to impaired PMN adhesion to endothelium as a result of decreased L-selectin receptors [8].
• In summary, endotoxin protection from O2 toxicity was associated with reduced neutrophils in the lung and a loss of L-selectin from peripheral blood neutrophils [9].
• To understand the mechanism of erythromycin (EM) on otitis media with effusion, we examined its effects on leukocyte accumulation and expression of adhesion molecules L-selectin and Mac-1, using a rat experimental model Administration of EM inhibited leukocyte (neutrophil) accumulation in the middle ear cavity after LPS stimulation [10].

Biological context of Sell

• Evidence of post-transcriptional regulation of L-selectin gene expression in rat lymphoid cells [1].
• Transfection of RS-2 cDNA into 70Z/3 cells conferred binding to HEV concomitant with expression of A.11, providing direct evidence that A.11 is rat L-selectin [1].
• A rat cDNA clone encoding an adhesion molecule, LECAM-1, has been isolated from the SD rat and the partial nucleotide sequence was determined [11].
• Shedding of L-selectin may mediate endogenous downregulation of inflammation by limiting neutrophil accumulation at inflammatory sites [5].
• Leukocyte-endothelial cell interactions were studied in colonic venules by using intravital microscopy under basal conditions and after P-, E-, or L-selectin immunoblockade [12].

Anatomical context of Sell

• During development of fast contracting skeletal muscle in the rat hindleg, embryonic and neonatal forms of the myosin heavy chain are present prior to the accumulation of the adult fast type ( Whalen , R. G., Sell, S. M., Butler-Browne, G.S., Schwartz, K., Bouveret, P., and Pinset -H arstr öm, I. (1981) Nature (Lond.) 292, 805-809) [13].
• Metabolic radiolabelling studies revealed that thymocytes synthesize markedly less L-selectin than do TDL or LN lymphocytes [1].
• Early investigations of lymphocyte migration in the rat operationally identified a lymphocyte membrane protein, designated 'A.11', which mediates lymphocyte adherence to lymph node (LN) high endothelial venules (HEV) [1].
• One of the major characteristics of HEV endothelial cells (HEVEC) is their capacity to incorporate large amounts of sulfate into sialomucin-type counter-receptors for the lymphocyte homing receptor L-selectin [14].
• Intravenous injection of a rat T-cell line that overexpresses L-selectin showed increased organ infiltration [2].

Associations of Sell with chemical compounds

• Olive oil enhanced the expression of both alpha4-integrin and L-selectin on lymphocytes, whereas octanoic acid only increased the expression of L-selectin [15].
• Covalent cross-linking of the oxidized ligand to L-selectin can be demonstrated, suggesting Schiff base formation between lysine residues of the selectin and the newly formed aldehydes [16].
• Enhanced interaction of L-selectin with the high endothelial venule ligand via selectively oxidized sialic acids [16].
• L-selectin is an adhesion molecule of the selectin family that mediates the initial step of leukocyte adhesion to vascular endothelium [2].
• The sulfated fucose polymer fucoidin and the polyphosphomannan PPME bind to L-selectin and inhibit L-selectin-mediated lymphocyte adhesion to lymph node high endothelial venules (LN-HEV) [17].

Regulatory relationships of Sell

• P-selectin and PECAM-1 were constitutively expressed on endothelia of noninflamed lymph nodes and subcutaneous tissue and were upregulated in inflammation. beta-endorphin positive cells expressed L-selectin in lymph nodes and subcutaneous tissue [18].
• L-Selectin is shed from these cells allowing them to adhere to the microvasculature via constitutively expressed ICAM-1 [19].

Other interactions of Sell

• In addition, Sertoli cell L-selectin is shown to interact with actin binding proteins, potentially providing a link between L-selectin and Rac1 signaling [20].
• In animals treated i.v. with Abs to CD11a, L-selectin, or ICAM-1 lung injury was significantly attenuated in parallel with reduced lung content of MPO [21].
• This ligand has been named GlyCAM 1 (Gly-cosylation-dependent Cell Adhesion Molecule 1) because its adhesive interactions with the L selectin lectin domain require that the GlyCAM 1 polypeptide chain be appropriately modified with carbohydrates [22].
• Ex vivo assessment of blood neutrophils showed significant upregulation of CD11a and CD11b and significant downregulation of L-selectin within five hours of TNF-alpha administration [23].
• However, inhibition of L-selectin sheddase activity with KD-IX-73-4 had no effect on the number of neutrophils mobilized in response to rat MIP-2 [24].

Analytical, diagnostic and therapeutic context of Sell

• However, Northern blot studies using RS-2 as a probe indicate that thymocytes possess more L-selectin RNA than does TDL [1].
• Expression of P- and E-selectin was assessed by the radiolabeled antibody technique, and L-selectin by flow cytometry [12].
• Studies using in situ hybridization showed expression of the L-selectin mRNA in the infiltrating leukemic cells in the liver of two ATL patients [2].
• Binding of lymphocytes to LN HEV on frozen sections was blocked by either rLEC-IgG or the anti-rat LECAM-1 mAb [25].
• L-selectin requirements in three models of acute lung injury in rats have been identified: systemic activation of complement after intravenous infusion of cobra venom factor (CVF) and intrapulmonary deposition of IgG or IgA immune complexes [26].

References