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|a pubmed24n0386.xml
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|a (DE-627)NLM11577923X
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|a (NLM)11683572
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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1 |
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|a Rao, S
|e verfasserin
|4 aut
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|a Targeted delivery of anti-CTLA-4 antibody downregulates T cell function in vitro and in vivo
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|c 2001
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|a Text
|b txt
|2 rdacontent
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|a ohne Hilfsmittel zu benutzen
|b n
|2 rdamedia
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|a Band
|b nc
|2 rdacarrier
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|a Date Completed 07.12.2001
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|a Date Revised 19.11.2015
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|a published: Print
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|a Citation Status MEDLINE
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|a Copyright 2001 Academic Press.
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|a CTLA-4 is a T cell surface molecule that binds to the costimulatory molecules CD80 and CD86 on antigen-presenting cells and downregulates T cell function. Therefore, we wanted to test whether antigen-specific activated T cells could be inhibited through directed CTLA-4 signaling using a bispecific antibody (BiAb) capable of simultaneously binding to CTLA-4 and a tissue-specific antigen. The BiAb was prepared by linking two separate monoclonal antibodies against CTLA-4 and the thyroid-stimulating hormone receptor (TSHR). The mouse B cell lymphoma line M12 (H2(d)) was used to induce alloreactive T cells in CBA/J mice (H2(k)); M12 cells stably transfected with the cDNA encoding murine TSHR (mM12) were used to restimulate the alloresponse in vitro. Results of assays for in vitro T cell proliferation, IL-2 production, and cytotoxicity in the presence of BiAb demonstrated that the BiAb could inhibit the T cell alloresponse when stimulated with mM12 cells but not with M12 cells. This effect was dependent on binding of TSHR-bound BiAb to CTLA-4, since the addition of soluble CTLA-4-Ig blocked the inhibitory effect. Injection of mM12 cells, along with the BiAb, not with antibodies against TSHR or CTLA-4 either separately or together, into CBA/J mice (H2(k)) downregulated alloreactive T cell responses. Our study demonstrated that the presence of CTLA-4 signaling molecules on the surface of target cells can protect those cells from immune attack by antigen-specific T cells and suggested that a similar approach could have potential therapeutic value in transplant rejection and tissue-specific autoimmune diseases
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a Research Support, U.S. Gov't, P.H.S.
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|a Antibodies, Bispecific
|2 NLM
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|a Antibodies, Monoclonal
|2 NLM
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|a Antigens, CD
|2 NLM
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|a Antigens, Differentiation
|2 NLM
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|a CTLA-4 Antigen
|2 NLM
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|a Ctla4 protein, mouse
|2 NLM
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|a Immunoconjugates
|2 NLM
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|a Immunosuppressive Agents
|2 NLM
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|a Interleukin-2
|2 NLM
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|a Receptors, Thyrotropin
|2 NLM
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|a Abatacept
|2 NLM
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|a 7D0YB67S97
|2 NLM
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700 |
1 |
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|a Vasu, C
|e verfasserin
|4 aut
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700 |
1 |
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|a Martinez, O
|e verfasserin
|4 aut
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700 |
1 |
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|a Kaithamana, S
|e verfasserin
|4 aut
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700 |
1 |
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|a Prabhakar, B S
|e verfasserin
|4 aut
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700 |
1 |
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|a Holterman, M J
|e verfasserin
|4 aut
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773 |
0 |
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 101(2001), 2 vom: 01. Nov., Seite 136-45
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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773 |
1 |
8 |
|g volume:101
|g year:2001
|g number:2
|g day:01
|g month:11
|g pages:136-45
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|a GBV_USEFLAG_A
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|a SYSFLAG_A
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|a GBV_NLM
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|a GBV_ILN_11
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|a GBV_ILN_24
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|a GBV_ILN_350
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|a AR
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|d 101
|j 2001
|e 2
|b 01
|c 11
|h 136-45
|