Different cd3/t cell receptor monoclonal antibodies have distinct capacities to induce adhesion of T lymphocytes to endothelium

Buysmann, S.; Schellekens, P. T. A.; Tax, W.J.M.; Berge, P.J.M. ten

doi:10.1016/s0022-2143(97)90063-9

Cited by 4 publications

(3 citation statements)

References 29 publications

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“…Culture of PBMC was performed in 24-well plates (2.10 6 /ml per well), using RPMI culture medium (RPMI supplemented with 10% heat-inactivated fetal calf serum, 100 IU/ml penicillin, 100 g/ml streptomycin, and 2 mM glutamine), for 18 h at 37°C. Cell culture was performed in the presence or absence of a monoclonal antibody (mAb) anti-human CD3 (1XA, purified mouse IgA) (35), which was previously coated on the culture wells during 2 h at 37°C. Nonbound mAb were washed away before addition of the cells.…”

Section: Cell Isolation and Cell Culturementioning

confidence: 99%

Strong and Selective Glomerular Localization of CD134 Ligand and TNF Receptor-1 in Proliferative Lupus Nephritis

Aten¹,

Roos²,

Claessen³

et al. 2000

Journal of the American Society of Nephrology

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Abstract. CD134 (OX40) is a member of the tumor necrosis factor (TNF) receptor (TNFR) family that can be expressed on activated T lymphocytes. Interaction between CD134 and its ligand (CD134L) is involved in costimulation of T and B lymphocyte activation, and in T cell adhesion to endothelium. To examine the possible role of this interaction in the pathogenesis of systemic lupus erythematosus (SLE), expression of CD134 and CD134L on peripheral blood leukocytes was studied, and no significant differences between SLE patients and control individuals were found. Immunohistology on renal biopsies from patients with lupus nephritis or other renal disorders, using a recombinant human CD134-containing chimeric molecule to detect CD134L, demonstrated the abundant presence of CD134L in all cases of proliferative lupus nephritis in a granular distribution predominantly along the epithelial side of the glomerular capillary wall. Confocal laser scanning microscopy indicated colocalization with subepithelial immune deposits. In none of the other renal disorders examined, including nonproliferative forms of lupus nephritis, was glomerular staining for CD134L detected in a similar pattern. Endothelial CD134L expression was frequently observed in different types of vasculitis. CD134 was detected on perivascular infiltrating leukocytes and on part of the tubular epithelium, but not on glomerular resident cells. Immunohistology for several other TNF(R) family members revealed in proliferative lupus nephritis a similar distribution for TNFR1 as was observed for CD134L. In contrast, glomerular expression of TNFR2 was similar in all cases examined. The glomerular presence of CD134L and TNFR1 in proliferative lupus nephritis in association with subepithelial immune deposits may be of pathogenetic significance and have diagnostic value.

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Section: Cell Isolation and Cell Culturementioning

confidence: 99%

Strong and Selective Glomerular Localization of CD134 Ligand and TNF Receptor-1 in Proliferative Lupus Nephritis

Aten¹,

Roos²,

Claessen³

et al. 2000

Journal of the American Society of Nephrology

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“…7-10 On lymphocytes, CD11b is required for adhesion to and migration through the endothelium. 11 In addition, it mediates adhesion to some parasites. 12,13 On phagocytes, CD11b mediates diapedesis through the endothelium via generation of a high-affinity binding site for intercellular adhesion molecule-1.…”

mentioning

confidence: 99%

Expression of CD3 and CD11b antigens on blood and mammary gland leukocytes and bacterial survival in milk of cows with experimentally induced Staphylococcus aureus mastitis

Rivas

Quimby²,

Coksaygan³

et al. 2001

ajvr

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“…It causes peripheral lymphocytopenia immediately after the first administration, as does IgG2a‐CD3 [5]. This transient peripheral lymphocytopenia is probably mediated by upregulation and activational transformation of adhesion molecules on the surface of peripheral blood T lymphocytes in response to TCR/CD3‐complex triggering [32]. In addition, although significantly reduced as compared to IgG2a‐CD3, IgA‐CD3 causes side‐effects and induces release of TNF α , with a serum peak level being approximately 20% of the level induced by IgG2a‐CD3.…”

Section: Discussionmentioning

confidence: 99%

Non FcR-binding murine antihuman CD3 monoclonal antibody is capable of productive TCR signalling and induces proliferation in the presence of costimulation

Meijer

Yong

Berge

et al. 2001

Clinical and Experimental Immunology

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SUMMARYCLB T3/4.A is a non FcR-binding CD3 mAb of the murine IgA isotype, which may be used as an alternative for the mitogenic OKT3 mAb in the treatment of acute cellular rejection after organ transplantation. We studied TCR signalling and T cell activation in response to T3/4.A in normal human PBMC in vitro. T3/4.A induced a rapid rise in free cytoplasmic Ca 21 , not different from the response to mitogenic CD3 mAb. However, protein tyrosine phosphorylation and, particularly, MAPK activation, were reduced as compared to mitogenic CD3 mAb. T3/4.A enhanced expression of both CD69 and CD25, but proliferation and detectable cytokine production did not occur. Addition of either CD28 mAb or IL-2 induced a strong proliferative response, which was accompanied by cytokine production. At higher mAb concentrations, T cell activation decreased, which correlated with TCR downmodulation. To exclude the possibility that activation by T3/4.A depends on interaction of murine IgA Fc with as yet unknown FcR, we showed that also with CD3 mAb F(ab H ) 2 fragments upregulation of activation molecules occurred, as well as proliferation in the presence of costimulation. We conclude that the non FcR-binding murine IgA mAb T3/4.A acts as a partial agonist and leads to proliferation and cytokine production only in the presence of appropriate costimuli. These findings may explain the mitigated cytokine release syndrome observed in vivo with some nonmitogenic CD3 mAbs.

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Different cd3/t cell receptor monoclonal antibodies have distinct capacities to induce adhesion of T lymphocytes to endothelium

Abstract: Please be advised that this information was generated on 2018-05-09 and may be subject to change.Different CD3/T cell receptor monoclonal antibodies have distinct capacities to induce adhesion of T lymphocytes to endothelium

Cited by 4 publications

References 29 publications

Strong and Selective Glomerular Localization of CD134 Ligand and TNF Receptor-1 in Proliferative Lupus Nephritis

Strong and Selective Glomerular Localization of CD134 Ligand and TNF Receptor-1 in Proliferative Lupus Nephritis

Expression of CD3 and CD11b antigens on blood and mammary gland leukocytes and bacterial survival in milk of cows with experimentally induced Staphylococcus aureus mastitis

Non FcR-binding murine antihuman CD3 monoclonal antibody is capable of productive TCR signalling and induces proliferation in the presence of costimulation

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