Fas-independent apoptosis of activated T cells induced by antibodies to the HLA class I alpha1 domain.
In addition to their major function in antigen presentation and natural killer cell activity regulation, HLA class I molecules may modulate T-cell activation and proliferation. Monoclonal antibodies (MoAbs) that recognize distinct epitopes of HLA class I molecules were reported to interfere with T-c...
| Main Authors: | , , , , , , , , , , , |
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| Format: | Journal article |
| Language: | English |
| Published: |
1997
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| _version_ | 1797103618999975936 |
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| author | Genestier, L Paillot, R Bonnefoy-Berard, N Meffre, G Flacher, M Fèvre, D Liu, Y Le Bouteiller, P Waldmann, H Engelhard, V Banchereau, J Revillard, J |
| author_facet | Genestier, L Paillot, R Bonnefoy-Berard, N Meffre, G Flacher, M Fèvre, D Liu, Y Le Bouteiller, P Waldmann, H Engelhard, V Banchereau, J Revillard, J |
| author_sort | Genestier, L |
| collection | OXFORD |
| description | In addition to their major function in antigen presentation and natural killer cell activity regulation, HLA class I molecules may modulate T-cell activation and proliferation. Monoclonal antibodies (MoAbs) that recognize distinct epitopes of HLA class I molecules were reported to interfere with T-cell proliferation. We show here that two MoAbs (mouse MoAb90 and rat YTH862) that bind to an epitope of the alpha1 domain of HLA class I heavy chain induce apoptotic cell death of activated, but not resting, peripheral T lymphocytes. Other reference anti-HLA class I antibodies specific for distinct epitopes of the alpha1 (B9.12.1), alpha2 (W6/32), or alpha3 (TP25.99) domains of the heavy chain decreased T-cell proliferation but had little or no apoptotic effect. Apoptosis shown by DNA fragmentation, phosphatidylserine externalization, and decrease of mitochondrial transmembrane potential was observed whatever the type of T-cell activator. Apoptosis did not result from Fas/Fas-L interaction and distinct though partly overlapping populations of activated T cells were susceptible to Fas- and HLA class I-mediated apoptosis, respectively. Induction of apoptosis did not require HLA class I cross-linking inasmuch as it could be observed with monovalent Fab' fragments. The data indicate that MoAb90 and YTH862 directed against the alpha1 domain of HLA class I trigger apoptosis of activated T lymphocytes by a pathway which does not involve Fas-ligand. |
| first_indexed | 2024-03-07T06:22:38Z |
| format | Journal article |
| id | oxford-uuid:f331e5aa-f20c-43d9-835e-3dfdd7563809 |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-07T06:22:38Z |
| publishDate | 1997 |
| record_format | dspace |
| spelling | oxford-uuid:f331e5aa-f20c-43d9-835e-3dfdd75638092022-03-27T12:10:11ZFas-independent apoptosis of activated T cells induced by antibodies to the HLA class I alpha1 domain.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:f331e5aa-f20c-43d9-835e-3dfdd7563809EnglishSymplectic Elements at Oxford1997Genestier, LPaillot, RBonnefoy-Berard, NMeffre, GFlacher, MFèvre, DLiu, YLe Bouteiller, PWaldmann, HEngelhard, VBanchereau, JRevillard, JIn addition to their major function in antigen presentation and natural killer cell activity regulation, HLA class I molecules may modulate T-cell activation and proliferation. Monoclonal antibodies (MoAbs) that recognize distinct epitopes of HLA class I molecules were reported to interfere with T-cell proliferation. We show here that two MoAbs (mouse MoAb90 and rat YTH862) that bind to an epitope of the alpha1 domain of HLA class I heavy chain induce apoptotic cell death of activated, but not resting, peripheral T lymphocytes. Other reference anti-HLA class I antibodies specific for distinct epitopes of the alpha1 (B9.12.1), alpha2 (W6/32), or alpha3 (TP25.99) domains of the heavy chain decreased T-cell proliferation but had little or no apoptotic effect. Apoptosis shown by DNA fragmentation, phosphatidylserine externalization, and decrease of mitochondrial transmembrane potential was observed whatever the type of T-cell activator. Apoptosis did not result from Fas/Fas-L interaction and distinct though partly overlapping populations of activated T cells were susceptible to Fas- and HLA class I-mediated apoptosis, respectively. Induction of apoptosis did not require HLA class I cross-linking inasmuch as it could be observed with monovalent Fab' fragments. The data indicate that MoAb90 and YTH862 directed against the alpha1 domain of HLA class I trigger apoptosis of activated T lymphocytes by a pathway which does not involve Fas-ligand. |
| spellingShingle | Genestier, L Paillot, R Bonnefoy-Berard, N Meffre, G Flacher, M Fèvre, D Liu, Y Le Bouteiller, P Waldmann, H Engelhard, V Banchereau, J Revillard, J Fas-independent apoptosis of activated T cells induced by antibodies to the HLA class I alpha1 domain. |
| title | Fas-independent apoptosis of activated T cells induced by antibodies to the HLA class I alpha1 domain. |
| title_full | Fas-independent apoptosis of activated T cells induced by antibodies to the HLA class I alpha1 domain. |
| title_fullStr | Fas-independent apoptosis of activated T cells induced by antibodies to the HLA class I alpha1 domain. |
| title_full_unstemmed | Fas-independent apoptosis of activated T cells induced by antibodies to the HLA class I alpha1 domain. |
| title_short | Fas-independent apoptosis of activated T cells induced by antibodies to the HLA class I alpha1 domain. |
| title_sort | fas independent apoptosis of activated t cells induced by antibodies to the hla class i alpha1 domain |
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