scholarly journals Pharmacological prion protein silencing accelerates central nervous system autoimmune disease via T cell receptor signalling

Brain ◽  
2010 ◽  
Vol 133 (2) ◽  
pp. 375-388 ◽  
Author(s):  
Wei Hu ◽  
Stefan Nessler ◽  
Bernhard Hemmer ◽  
Todd N. Eagar ◽  
Lawrence P. Kane ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
T Cell ◽  
Autoimmune Disease ◽  
Prion Protein ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
Receptor Signalling

scholarly journals Enterovirus 71 Infection Shapes Host T Cell Receptor Repertoire and Presumably Expands VP1-Specific TCRβ CDR3 Cluster

Pathogens ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 121
Author(s):  
Yu-Wen Liao ◽  
Bing-Ching Ho ◽  
Min-Hsuan Chen ◽  
Sung-Liang Yu
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
T Cell ◽  
T Cell Receptor ◽  
Enterovirus 71 ◽  
Cell Receptor ◽  
Ev71 Infection ◽  
Asia Pacific ◽  
Binding Prediction ◽  
Tcr Repertoire

Enterovirus 71 (EV71) has become an important public health problem in the Asia-Pacific region in the past decades. EV71 infection might cause neurological and psychiatric complications and even death. Although an EV71 vaccine has been currently approved, there is no effective therapy for treating EV71-infected patients. Virus infections have been reported to shape host T cell receptor (TCR) repertoire. Therefore, understanding of host TCR repertoire in EV71 infection could better the knowledge in viral pathogenesis and further benefit the anti-viral therapy development. In this study, we used a mouse-adapted EV71 (mEV71) model to observe changes of host TCR repertoire in an EV71-infected central nervous system. Neonate mice were infected with mEV71 and mouse brainstem TCRβ repertoires were explored. Here, we reported that mEV71 infection impacted host brainstem TCRβ repertoire, where mEV71 infection skewed TCRβ diversity, changed VJ combination usages, and further expanded specific TCRβ CDR3 clones. Using bioinformatics analysis and ligand-binding prediction, we speculated the expanded TCRβ CDR3 clone harboring CASSLGANSDYTF sequence was capable of binding cleaved EV71 VP1 peptides in concert with major histocompatibility complex (MHC) molecules. We observed that mEV71 infection shaped host TCRβ repertoire and presumably expanded VP1-specific TCRβ CDR3 in mEV71-infected mouse brainstem that integrated EV71 pathogenesis in central nervous system.

Primary peripheral—postthymic T-cell lymphoma in the central nervous system: immunological and molecular approaches to diagnosis

1995 ◽  
Vol 82 (1) ◽  
pp. 77-82 ◽  
Author(s):  
Taizo Nitta ◽  
Ken Uda ◽  
Michimasa Ebato ◽  
Kiyonobu Ikezaki ◽  
Masashi Fukui ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
T Cell ◽  
Adhesion Molecules ◽  
T Cell Receptor ◽  
Cell Lymphoma ◽  
Cell Receptor ◽  
Molecular Techniques ◽  
T Cell Lymphoma ◽  
The Central Nervous System

✓ Primary intracranial T-cell lymphoma is a very rare clinical entity, and only limited biological studies of this disease have been undertaken. A tumor specimen from a patient with a primary leptomeningeal and perivascular presentation of a T-cell lymphoma was analyzed using cellular and molecular techniques. Frozen sections of the sample were examined by immunohistochemical techniques using monoclonal antibodies to phenotypic marker antigens expressed on human lymphoid cells. Intercellular adhesion molecules expressed on the tumor were studied, as was expression of messenger ribonucleic acid (mRNA) transcripts of the T-cell receptor variable α and β chain genes. The immunophenotypical analysis of lymphoma revealed that the tumor expressed CD2, CD3, CD4, CD5, CD25 and HLA-DR. In addition, all of the adhesion molecules studied (ICAM-1, LFA-3, VLA-1, CD11a, CD11b, and CD11c) were detected on the cell surface. Polymerase chain reaction amplification of mRNA from the tumor demonstrated 10 Vα and three Vβ T-cell receptor subfamilies, indicating that this tumor was a low-grade well-differentiated helper type of peripheral T-cell lymphoma of the central nervous system. In addition, the tumor was derived from multiple T-cell lineages.

T cell receptor Vb5 and Vb17 clonal diversity in cerebrospinal fluid and peripheral blood lymphocytes of multiple sclerosis patients

1998 ◽  
Vol 4 (3) ◽  
pp. 154-161 ◽  
Author(s):  
P Lozeron ◽  
D Chabas ◽  
B Duprey ◽  
O Lyon-Caen ◽  
R Liblau
Keyword(s):  
Central Nervous System ◽  
T Cells ◽  
Nervous System ◽  
T Cell ◽  
T Cell Receptor ◽  
Peripheral Blood ◽  
Cell Receptor ◽  
Peripheral Blood Lymphocytes ◽  
Blood Lymphocytes ◽  
Multiple Sclerosis Patients

To better characterize the cellular immune response taking place in the MS central nervous system, we investigated the blood and CSF T cell receptor (TCR) Vβ5 and Vb17 repertoire in HLA-typed patients with recently diagnosed MS or other neurological diseases (OND). Using a RT-PCR based technique, we analysed directly ex vivo the CDR3 size of TCR β chains utilizing Vβ5 (eight patients with MS and one with OND) or Vβ17 (eight patients with MS and six with OND) gene segments on paired blood-CSF samples. Globally, the analysis of Vβ5-Jβ and Vβ17-Jβ repertoire showed a less diverse pattern in the CSF samples than in the corresponding peripheral blood lymphocytes both in MS and in OND patients. However, we did not detect any recurrent clonal expansion within the Vb5+ T cells in MS patients, underlining the potential limits of Vβ5- based immunotherapy in MS. We found an expanded T cell population using the same Vβ17-Jβ1.6 combination with identical CDR3 length in the CSF of three MS patients and none of the control patients. These results suggest selective expansion of T cells expressing this segment gene in the MS central nervous system.

scholarly journals Endogenous T Cell Receptor Rearrangement Represses Aggressive Central Nervous System Autoimmunity in a TcR-Transgenic Model on the Non-Obese Diabetic Background

2020 ◽  
Vol 10 ◽  
Author(s):  
Asmita Pradeep Yeola ◽  
Prenitha Mercy Ignatius Arokia Doss ◽  
Joanie Baillargeon ◽  
Irshad Akbar ◽  
Benoit Mailhot ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
T Cell ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
Transgenic Model

scholarly journals T cell receptor V alpha-V beta repertoire and cytokine gene expression in active multiple sclerosis lesions.

1992 ◽  
Vol 175 (4) ◽  
pp. 993-1002 ◽  
Author(s):  
K W Wucherpfennig ◽  
J Newcombe ◽  
H Li ◽  
C Keddy ◽  
M L Cuzner ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Central Nervous System ◽  
T Cells ◽  
Nervous System ◽  
T Cell ◽  
T Cell Receptor ◽  
Subacute Sclerosing Panencephalitis ◽  
Cell Receptor ◽  
Cytokine Gene Expression ◽  
Tcr Repertoire

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system with presumed autoimmune etiology. A recent study has suggested the presence of a restricted T cell receptor (TCR) V alpha repertoire in MS lesions. The presence of such a restricted TCR repertoire at the site of inflammation would have important consequences for the pathogenesis and the ultimate treatment of MS. To further characterize the TCR V alpha and V beta repertoire in MS plaque tissue, we examined a series of 26 histologically well-characterized central nervous system (CNS) tissue specimens from six MS patients as well as samples from five normal postmortem cases and a case of subacute sclerosing panencephalitis. RNA was extracted from frozen sections and cDNAs were amplified by polymerase chain reaction using primers for TCR V alpha (V alpha 1-18) and V beta (V beta 1-19) gene families. This analysis demonstrated a broad TCR V alpha-V beta repertoire in active lesions, while fewer TCR V genes were detected in chronic plaques and control samples. Even though a large number of TCR V alpha and V beta gene segments were present in the majority of active lesions, there were clear differences in the TCR repertoire between plaques from the same case, suggesting that local events influence the TCR repertoire at the level of T cell recruitment or T cell expansion. Examination of cytokine mRNAs demonstrated that IL-1 mRNA was present in the majority of acute and subacute plaques, while IL-2 and IL-4 mRNA were detected in only a few acute lesions. These data demonstrate that the TCR repertoire in MS plaques is polyclonal. However, autoreactive alpha/beta T cells thought to be critical in the initiation of the inflammatory process probably represent a minor fraction of T cells in active MS plaques and may use a limited number of TCR V gene segments for recognition of the autoantigen.

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