|
|
|
|
LEADER |
01000caa a22002652 4500 |
001 |
NLM18857820X |
003 |
DE-627 |
005 |
20250210102707.0 |
007 |
cr uuu---uuuuu |
008 |
231223s2009 xx |||||o 00| ||eng c |
024 |
7 |
|
|a 10.1016/j.clim.2009.04.002
|2 doi
|
028 |
5 |
2 |
|a pubmed25n0629.xml
|
035 |
|
|
|a (DE-627)NLM18857820X
|
035 |
|
|
|a (NLM)19447680
|
040 |
|
|
|a DE-627
|b ger
|c DE-627
|e rakwb
|
041 |
|
|
|a eng
|
100 |
1 |
|
|a MacMillan, Heather F
|e verfasserin
|4 aut
|
245 |
1 |
0 |
|a Intravenous immunoglobulin G-mediated inhibition of T-cell proliferation reflects an endogenous mechanism by which IgG modulates T-cell activation
|
264 |
|
1 |
|c 2009
|
336 |
|
|
|a Text
|b txt
|2 rdacontent
|
337 |
|
|
|a ƒaComputermedien
|b c
|2 rdamedia
|
338 |
|
|
|a ƒa Online-Ressource
|b cr
|2 rdacarrier
|
500 |
|
|
|a Date Completed 17.09.2009
|
500 |
|
|
|a Date Revised 16.11.2017
|
500 |
|
|
|a published: Print-Electronic
|
500 |
|
|
|a Citation Status MEDLINE
|
520 |
|
|
|a Commercial intravenous immunoglobulin G (IVIG) at high doses has therapeutic benefit in autoimmune and inflammatory diseases. It has been shown to inhibit T-cell function but the mechanisms are unclear. Inhibition could result from IVIG processing, donor pooling or intrinsic downregulatory activity of IgG. To address these points, we compared the effects on T-cell activation of IVIG, Fab(2) fragment and IgG isolated from single-donor plasma. We also investigated the role of accessory cells in the IVIG effects using highly purified T cells stimulated through CD3 and CD28 engagement. T-cell proliferation was evaluated by Oregon Green 488 dye dilution and (3)H-thymidine incorporation. IVIG, Fab(2) fragment of IVIG and autologous, single-donor IgG significantly inhibited T-cell proliferation (35-50%), even in the absence of accessory cells. Depletion of IgG from plasma used for culture significantly increased (by 50%) the T-cell proliferation. The addition of physiological concentrations of single-donor, autologous IgG or IVIG to IgG-depleted plasma reduced T-cell proliferation to levels observed in normal plasma. Therefore, donor pooling in IVIG and accessory cells are not required for inhibition of T-cell proliferation by IVIG and the Fab(2) region is sufficient to mediate this inhibition. Suppression of T-cell activation by IVIG likely reflects a physiologic, endogenous mechanism of IgG-mediated regulation of T-cell activation
|
650 |
|
4 |
|a Journal Article
|
650 |
|
4 |
|a Research Support, Non-U.S. Gov't
|
650 |
|
7 |
|a Antibodies, Monoclonal
|2 NLM
|
650 |
|
7 |
|a CD28 Antigens
|2 NLM
|
650 |
|
7 |
|a CD3 Complex
|2 NLM
|
650 |
|
7 |
|a Immunoglobulin Fab Fragments
|2 NLM
|
650 |
|
7 |
|a Immunoglobulin G
|2 NLM
|
650 |
|
7 |
|a Immunoglobulins, Intravenous
|2 NLM
|
650 |
|
7 |
|a Receptors, Antigen, T-Cell
|2 NLM
|
700 |
1 |
|
|a Lee, Tim
|e verfasserin
|4 aut
|
700 |
1 |
|
|a Issekutz, Andrew C
|e verfasserin
|4 aut
|
773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 132(2009), 2 vom: 01. Aug., Seite 222-33
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
|
773 |
1 |
8 |
|g volume:132
|g year:2009
|g number:2
|g day:01
|g month:08
|g pages:222-33
|
856 |
4 |
0 |
|u http://dx.doi.org/10.1016/j.clim.2009.04.002
|3 Volltext
|
912 |
|
|
|a GBV_USEFLAG_A
|
912 |
|
|
|a SYSFLAG_A
|
912 |
|
|
|a GBV_NLM
|
912 |
|
|
|a GBV_ILN_11
|
912 |
|
|
|a GBV_ILN_24
|
912 |
|
|
|a GBV_ILN_350
|
951 |
|
|
|a AR
|
952 |
|
|
|d 132
|j 2009
|e 2
|b 01
|c 08
|h 222-33
|