MHC class II ligation induces CD58 (LFA-3)-mediated adhesion in human T cells

Research output: Contribution to journalJournal articleResearchpeer-review

Standard

MHC class II ligation induces CD58 (LFA-3)-mediated adhesion in human T cells. / Nielsen, M; Gerwien, J; Geisler, C; Röpke, C; Svejgaard, A; Odum, N.

In: Experimental and Clinical Immunogenetics, Vol. 15, No. 2, 1998, p. 61-8.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Nielsen, M, Gerwien, J, Geisler, C, Röpke, C, Svejgaard, A & Odum, N 1998, 'MHC class II ligation induces CD58 (LFA-3)-mediated adhesion in human T cells', Experimental and Clinical Immunogenetics, vol. 15, no. 2, pp. 61-8.

APA

Nielsen, M., Gerwien, J., Geisler, C., Röpke, C., Svejgaard, A., & Odum, N. (1998). MHC class II ligation induces CD58 (LFA-3)-mediated adhesion in human T cells. Experimental and Clinical Immunogenetics, 15(2), 61-8.

Vancouver

Nielsen M, Gerwien J, Geisler C, Röpke C, Svejgaard A, Odum N. MHC class II ligation induces CD58 (LFA-3)-mediated adhesion in human T cells. Experimental and Clinical Immunogenetics. 1998;15(2):61-8.

Author

Nielsen, M ; Gerwien, J ; Geisler, C ; Röpke, C ; Svejgaard, A ; Odum, N. / MHC class II ligation induces CD58 (LFA-3)-mediated adhesion in human T cells. In: Experimental and Clinical Immunogenetics. 1998 ; Vol. 15, No. 2. pp. 61-8.

Bibtex

@article{16666f80b0a411ddb538000ea68e967b,
title = "MHC class II ligation induces CD58 (LFA-3)-mediated adhesion in human T cells",
abstract = "MHC class II positive T cells found in areas of inflammation are believed to play an important pathogenetic role in autoimmunity. In experimental models , class II molecules have been shown to regulate adhesion between human T cells. It is, however, not known in detail how class II molecules are functionally linked to adhesion molecules. Some data suggest that beta2 integrin (CD11a/CD18) molecules play a role in class-II-induced homotypic adhesion in B cells, monocytes, and virus-transformed or neoplastic cell lines. We have previously obtained evidence that adhesion molecules other than beta2 integrins might play a role in class-II-mediated adhesion in T cells. To study further class-II-mediated adhesion in T cells, we have taken advantage of (allo)antigen-specific beta2-integrin-negative, CD4-positive T cell lines obtained from a leukocyte adhesion deficiency patient. We show that class II ligation induces homotypic adhesion in both beta2-integrin-positive and negative, CD4-positive T cell lines. Anti-CD18 monoclonal antibody (mAb) weakly inhibited the adhesion response in beta2-integrin-positive T cells and had no effect on beta2-integrin-negative T cells. In contrast, an anti-CD58 (LFA-3) mAb almost completely inhibited the adhesion response in beta2-integrin-negative T cells. Antibodies against the CD58 ligand, CD2, partly inhibited the adhesion response in beta2-integrin-negative T cells whereas antibodies against other adhesion molecules did not. The adhesion response in beta2-integrin-positive T cells was partly inhibited by antibodies against CD58 and CD2. Taken together, these data provide the first evidence that CD58 molecules are involved in class-II-induced homotypic adhesion between T cells.",
author = "M Nielsen and J Gerwien and C Geisler and C R{\"o}pke and A Svejgaard and N Odum",
note = "Keywords: Antibodies, Monoclonal; Antigens, CD18; Antigens, CD2; Antigens, CD58; Benzoquinones; Cell Adhesion; Cell Line; Enzyme Inhibitors; Histocompatibility Antigens Class II; Humans; Lactams, Macrocyclic; Protein-Tyrosine Kinases; Quinones; T-Lymphocytes",
year = "1998",
language = "English",
volume = "15",
pages = "61--8",
journal = "Experimental and Clinical Immunogenetics",
issn = "0254-9670",
publisher = "S Karger AG",
number = "2",

}

RIS

TY - JOUR

T1 - MHC class II ligation induces CD58 (LFA-3)-mediated adhesion in human T cells

AU - Nielsen, M

AU - Gerwien, J

AU - Geisler, C

AU - Röpke, C

AU - Svejgaard, A

AU - Odum, N

N1 - Keywords: Antibodies, Monoclonal; Antigens, CD18; Antigens, CD2; Antigens, CD58; Benzoquinones; Cell Adhesion; Cell Line; Enzyme Inhibitors; Histocompatibility Antigens Class II; Humans; Lactams, Macrocyclic; Protein-Tyrosine Kinases; Quinones; T-Lymphocytes

PY - 1998

Y1 - 1998

N2 - MHC class II positive T cells found in areas of inflammation are believed to play an important pathogenetic role in autoimmunity. In experimental models , class II molecules have been shown to regulate adhesion between human T cells. It is, however, not known in detail how class II molecules are functionally linked to adhesion molecules. Some data suggest that beta2 integrin (CD11a/CD18) molecules play a role in class-II-induced homotypic adhesion in B cells, monocytes, and virus-transformed or neoplastic cell lines. We have previously obtained evidence that adhesion molecules other than beta2 integrins might play a role in class-II-mediated adhesion in T cells. To study further class-II-mediated adhesion in T cells, we have taken advantage of (allo)antigen-specific beta2-integrin-negative, CD4-positive T cell lines obtained from a leukocyte adhesion deficiency patient. We show that class II ligation induces homotypic adhesion in both beta2-integrin-positive and negative, CD4-positive T cell lines. Anti-CD18 monoclonal antibody (mAb) weakly inhibited the adhesion response in beta2-integrin-positive T cells and had no effect on beta2-integrin-negative T cells. In contrast, an anti-CD58 (LFA-3) mAb almost completely inhibited the adhesion response in beta2-integrin-negative T cells. Antibodies against the CD58 ligand, CD2, partly inhibited the adhesion response in beta2-integrin-negative T cells whereas antibodies against other adhesion molecules did not. The adhesion response in beta2-integrin-positive T cells was partly inhibited by antibodies against CD58 and CD2. Taken together, these data provide the first evidence that CD58 molecules are involved in class-II-induced homotypic adhesion between T cells.

AB - MHC class II positive T cells found in areas of inflammation are believed to play an important pathogenetic role in autoimmunity. In experimental models , class II molecules have been shown to regulate adhesion between human T cells. It is, however, not known in detail how class II molecules are functionally linked to adhesion molecules. Some data suggest that beta2 integrin (CD11a/CD18) molecules play a role in class-II-induced homotypic adhesion in B cells, monocytes, and virus-transformed or neoplastic cell lines. We have previously obtained evidence that adhesion molecules other than beta2 integrins might play a role in class-II-mediated adhesion in T cells. To study further class-II-mediated adhesion in T cells, we have taken advantage of (allo)antigen-specific beta2-integrin-negative, CD4-positive T cell lines obtained from a leukocyte adhesion deficiency patient. We show that class II ligation induces homotypic adhesion in both beta2-integrin-positive and negative, CD4-positive T cell lines. Anti-CD18 monoclonal antibody (mAb) weakly inhibited the adhesion response in beta2-integrin-positive T cells and had no effect on beta2-integrin-negative T cells. In contrast, an anti-CD58 (LFA-3) mAb almost completely inhibited the adhesion response in beta2-integrin-negative T cells. Antibodies against the CD58 ligand, CD2, partly inhibited the adhesion response in beta2-integrin-negative T cells whereas antibodies against other adhesion molecules did not. The adhesion response in beta2-integrin-positive T cells was partly inhibited by antibodies against CD58 and CD2. Taken together, these data provide the first evidence that CD58 molecules are involved in class-II-induced homotypic adhesion between T cells.

M3 - Journal article

C2 - 9691200

VL - 15

SP - 61

EP - 68

JO - Experimental and Clinical Immunogenetics

JF - Experimental and Clinical Immunogenetics

SN - 0254-9670

IS - 2

ER -

ID: 8545434