Detailed Information on Publication Record
1996
Activation via the antigen receptor is impaired in T cells, but not in B cells from patients with common variable immunodeficiency
FISCHER, MB., HM. WOLF, I. HAUBER, H. EGGENBAUER, Vojtěch THON et. al.Basic information
Original name
Activation via the antigen receptor is impaired in T cells, but not in B cells from patients with common variable immunodeficiency
Name in Czech
Aktivace cestou antigenního receptoru je porušena u T buněk, avšak ne u B buněk pacientů s běžnou variabilní imunodeficiencí
Authors
FISCHER, MB. (40 Austria), HM. WOLF (40 Austria), I. HAUBER (276 Germany), H. EGGENBAUER (40 Austria), Vojtěch THON (203 Czech Republic, guarantor), M. SASGARY (40 Austria) and MM. EIBL (40 Austria)
Edition
EUROPEAN JOURNAL OF IMMUNOLOGY, 1996, 0014-2980
Other information
Language
English
Type of outcome
Článek v odborném periodiku
Field of Study
30102 Immunology
Country of publisher
United States of America
Confidentiality degree
není předmětem státního či obchodního tajemství
RIV identification code
RIV/00216224:14110/96:00035801
Organization unit
Faculty of Medicine
UT WoS
A1996UD13800035
Keywords (in Czech)
TCR; CVID
Keywords in English
T cell activation; common variable immunodeficiency; T cell receptor; inositol phosphates
Tags
International impact, Reviewed
Změněno: 26/6/2009 00:18, prof. MUDr. Vojtěch Thon, Ph.D.
V originále
The patients included in this study belong to a subset of common variable immunodeficiency (CVID) patients whose peripheral blood T cells have a T cell receptor (TCR)-mediated activation defect leading to impaired expression of the interleukin (IL)-2 gene upon stimulation with recall antigens (tetanus toxoid, Escherichia coli) or superantigens (staphy lococcal enterotoxins). In the present report we demonstrate that the patients' peripheral blood T cells failed to generate the second messenger inositol 1,4,5-trisphosphate (Ins(1,4,5)P-3) following stimulation with superantigen or mAb specific for the monomorphic region of the TCR beta-chain. Patients' T cell lines were also impaired in generating Ins(1,4,5)P, when stimulated with tetanus toxoid-pulsed autologous monocytes. Addition of a second or third co-stimulatory signal provided by recombinant IL-2, CD28 or both had no effect on the Ins(1,4)P-3 formation of the patients' antigen-driven T cell lines. The T cell activation defect, however, was not absolute, as Ins(1,4,5)P-3 formation in the patients T cells after phytohemagglutinin or aluminium fluoride stimulation was normal. The impairment in signal transduction via the T cell antigen receptor was limited to the patients' T cells, as no activation defect after ligation of surface immunoglobulin. the antigen receptor on B cells, could be detected.
In Czech
Aktivace cestou antigenního receptoru je porušena u T buněk, avšak ne u B buněk pacientů s běžnou variabilní imunodeficiencí.