scholarly journals Role of the MHC restriction during maturation of antigen-specific human T cells in the thymus

2015 ◽  
Vol 46 (3) ◽  
pp. 560-569 ◽  
Author(s):  
Leslie Hesnard ◽  
François Legoux ◽  
Laetitia Gautreau ◽  
Melinda Moyon ◽  
Olivier Baron ◽  
...  
Keyword(s):  
T Cells ◽  
Mhc Restriction ◽  
Human T Cells

Role of three isoforms of phospholipase A2 in capacitative calcium influx in human T-cells

2002 ◽  
Vol 269 (22) ◽  
pp. 5557-5563 ◽  
Author(s):  
Aziz Hichami ◽  
Beenu Joshi ◽  
Anne Marie Simonin ◽  
Naim Akhtar Khan
Keyword(s):  
T Cells ◽  
Phospholipase A2 ◽  
Calcium Influx ◽  
Human T Cells

scholarly journals Splicing factor SRSF1 limits IFN-γ production via RhoH and ameliorates experimental nephritis

Rheumatology ◽  
2020 ◽  
Vol 60 (1) ◽  
pp. 420-429
Author(s):  
Takayuki Katsuyama ◽  
Hao Li ◽  
Suzanne M Krishfield ◽  
Vasileios C Kyttaris ◽  
Vaishali R Moulton
Keyword(s):  
T Cells ◽  
T Cell ◽  
Molecular Mechanisms ◽  
Elevated Serum ◽  
Splicing Factor ◽  
Type I ◽  
Human T Cells ◽  
Experimental Nephritis ◽  
Ifn Γ

Abstract Objective CD4 T helper 1 (Th1) cells producing IFN-γ contribute to inflammatory responses in the pathogenesis of SLE and lupus nephritis. Moreover, elevated serum type II IFN levels precede the appearance of type I IFNs and autoantibodies in patient years before clinical diagnosis. However, the molecules and mechanisms that control this inflammatory response in SLE remain unclear. Serine/arginine-rich splicing factor 1 (SRSF1) is decreased in T cells from SLE patients, and restrains T cell hyperactivity and systemic autoimmunity. Our objective here was to evaluate the role of SRSF1 in IFN-γ production, Th1 differentiation and experimental nephritis. Methods T cell-conditional Srsf1-knockout mice were used to study nephrotoxic serum-induced nephritis and evaluate IFN-γ production and Th1 differentiation by flow cytometry. RNA sequencing was used to assess transcriptomics profiles. RhoH was silenced by siRNA transfections in human T cells by electroporation. RhoH and SRSF1 protein levels were assessed by immunoblots. Results Deletion of Srsf1 in T cells led to increased Th1 differentiation and exacerbated nephrotoxic serum nephritis. The expression levels of RhoH are decreased in Srsf1-deficient T cells, and silencing RhoH in human T cells leads to increased production of IFN-γ. Furthermore, RhoH expression was decreased and directly correlated with SRSF1 in T cells from SLE patients. Conclusion Our study uncovers a previously unrecognized role of SRSF1 in restraining IFN-γ production and Th1 differentiation through the control of RhoH. Reduced expression of SRSF1 may contribute to pathogenesis of autoimmune-related nephritis through these molecular mechanisms.

scholarly journals Role of Cell Surface Glycosaminoglycans of Human T Cells in Human Immunodeficiency Virus Type-1 (HIV-1) Infection

1996 ◽  
Vol 40 (11) ◽  
pp. 827-835 ◽  
Author(s):  
Yukako Ohshiro ◽  
Tsutomu Murakami ◽  
Kazuhiro Matsuda ◽  
Kiyoshi Nishioka ◽  
Keiichi Yoshida ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
T Cells ◽  
Cell Surface ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Human T Cells ◽  
Immunodeficiency Virus ◽  
Hiv 1

The role of T3 in the activation of human T cells

1984 ◽  
Vol 4 (3) ◽  
pp. 165-173 ◽  
Author(s):  
Arthur Weiss ◽  
John Imboden ◽  
Robert Wiskocil ◽  
John Stobo
Keyword(s):  
T Cells ◽  
Human T Cells

Constitutive Activation of Toll like Receptor Signaling in Adult T-Cell Leukemia Cells.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 2291-2291
Author(s):  
Takamitsu Mizobe ◽  
Junichi Tsukada ◽  
Takehiro Higashi ◽  
Fumihiko Mouri ◽  
Ai Matsuura ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cells ◽  
T Cell ◽  
Adaptor Protein ◽  
T Cell Leukemia ◽  
Cell Leukemia ◽  
Constitutive Activation ◽  
Adult T Cell Leukemia ◽  
Human T Cells

Abstract Human T-cell leukemia virus type I (HTLV-I) is etiologically associated with the development of an aggressive and fatal malignancy of CD4+ T lymphocytes called adult T-cell leukemia (ATL). Constitutive activation of nuclear factor-κB (NF-κB) is a common feature of ATL. Although the mechanism by which NF-κB is spontaneously activated in ATL cells still remains unclear, inhibition of NF-κB activity induces apoptosis, suggesting a central role of NF-κB in their proliferation. Toll like receptors (TLRs) are involved in innate cell activation by conserved structures expressed by microorganisms. Engagement of IL-1R or TLR with their cognate ligands causes an adaptor protein MyD88 to be recruited to the receptor complex, which in turn promotes its association with the IL-1R-associated kinase (IRAK) via an interaction between the respective death domains of each molecule. Several recent reports have indicated unique expression profiles of TLRs on different subsets of human T cells, and that some TLR ligands modulate the function of human T cells. We examined expression of the TLR mRNAs in primary ATL cells and ATL cell lines, MT2, MT4 and HUT102 by RT-PCR. Expression of TLR mRNAs, except of TLR7 and TLR8, was detected in all cell samples examined. We further demonstrated constitutive association of MyD88, an adaptor protein for the TLR signaling, with the IL-1R-associated kinase 1 (IRAK1) in ATL cell lines, MT2, MT4 and HUT102. In MT2 cells, constitutive activation of NF-κB and NF-IL6, but not Stat3 was significantly inhibited by expression of a dominant negative form of MyD88 protein (MyD88dn). Spontaneous transcriptional activation of IL-1α, IFN-γ and TNF-α gene promoters in MT2 cells was also suppressed by MyD88dn expression. MyD88dn inhibited cell proliferation and induced apoptosis of MT2 cells. In addition, overexpression of wild-type MyD88 and HTLV-I Tax induces synergistically transcriptional activity of NF-κB in 293T cells, showing interaction of Tax with MyD88. Thus, our results show a critical role of MyD88 in dysregulated gene activation and cell proliferation in HTLV-I-transformed T-cells, and further suggest the involvement of MyD88 in Tax-mediated intracellular signal transduction in HTLV-I-infected cells. Considering the fact that blocking NF-κB is a potential strategy to treat ATL, our argument raises a possibility that we may be able to find new treatment targets against ATL.

scholarly journals Somatic mutagenesis studies of NF-κB signaling in human T cells: evidence for an essential role of IKKγ in NF-κB activation by T-cell costimulatory signals and HTLV-I Tax protein

Oncogene ◽  
2000 ◽  
Vol 19 (11) ◽  
pp. 1448-1456 ◽  
Author(s):  
Edward W Harhaj ◽  
LiFeng Good ◽  
Gutian Xiao ◽  
Mark Uhlik ◽  
Mary Ellen Cvijic ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Essential Role ◽  
Tax Protein ◽  
Human T Cells ◽  
Costimulatory Signals ◽  
Somatic Mutagenesis
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