scholarly journals Retracted: Scolopendra subspinipes mutilans L. Koch Ameliorates Rheumatic Heart Disease by Affecting Relative Percentages of CD4+CD25+FoxP3 Treg and CD4+IL17 T Cells

2021 ◽  
Vol 2021 ◽  
pp. 1-1
Author(s):  
Evidence-Based Complementary and Alternative Medicine
Keyword(s):  
T Cells ◽  
Heart Disease ◽  
Rheumatic Heart Disease ◽  
Scolopendra Subspinipes Mutilans ◽  
Rheumatic Heart

scholarly journals Scolopendra subspinipes mutilans L. Koch Ameliorates Rheumatic Heart Disease by Affecting Relative Percentages of CD4+CD25+FoxP3 Treg and CD4+IL17 T Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-12
Author(s):  
Tiechao Jiang ◽  
Qini Zhao ◽  
Hongyan Sun ◽  
Lirong Zhang ◽  
Shanshan Song ◽  
...  
Keyword(s):  
T Cells ◽  
Heart Disease ◽  
Rheumatic Heart Disease ◽  
Blood Lactate ◽  
Venous Pressure ◽  
Negative Relationship ◽  
Treg Cells ◽  
Scolopendra Subspinipes Mutilans ◽  
To Receive ◽  
Rheumatic Heart

Scolopendra subspinipes mutilans L. Koch. (SSLK) helps reduce the risk of coronary heart disease (CHD) but its effects on rheumatic heart disease (RHD) patients remain unclear. 80 RHD patients were recruited and randomly assigned into SG (to receive SSLK treatment) and CG (to receive placebo) groups, and the intervention lasted for 3 months. The following cardiac indexes were measured, including mean arterial pressure (MAP), heart rate (HR), central venous pressure (CVP), blood lactate, fatigue, shortness of breath, palpitation, and chest pain. ELISA kits were used to analyze creatine kinase isoenzyme (CK-MB), serum troponin T (cTnT), CRP, IL-1β, IL-6, and TNF-α, malondialdehyde (MDA), and superoxide dismutase (SOD). Relative percentages of CD4+CD25+FoxP3 regulatory (Treg) and CD4+IL-17 T cells were measured using flow cytometry. After 3-month therapy, SSLK intervention improved MAP, HR, CVP, fatigue, palpitation, and shortness breath of CHD patients, reduced the levels of blood lactate, CK-MB, cTnT, CRP, IL-1β, IL-6, TNF-α, MDA, and increased SOD level (p < 0.05). Meanwhile, SSLK treatment increased the percentages of CD4+CD25+FoxP3 Treg cells and reduced relative percentages of CD4+IL-17 T cells in a dose-dependent way (p < 0.05). Relative percentage of CD4+CD25+FoxP3 Treg cells had negative relationship while CD4+IL17 T cells had positive relationship with CK-MB, cTnT, CRP, and TNF-a (p < 0.01). SSLK ameliorated RHD by affecting the balance of CD4+CD25+FoxP3 Treg and CD4+IL17 T cells.

Role of Lymphocyte Subsets in Pathogenesis of Chronic Rheumatic Heart Disease

1998 ◽  
Vol 6 (2) ◽  
pp. 104-107
Author(s):  
Rajendar K Suri ◽  
Neerod K Jha ◽  
Harpreet Vohra ◽  
Ratna S Manjari ◽  
Rajam Venkateshwaran ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
T Cells ◽  
Heart Disease ◽  
Rheumatic Heart Disease ◽  
Left Atrial ◽  
Left Atrial Appendage ◽  
Lymphocyte Subsets ◽  
Cd4 Cells ◽  
Activated T Cells ◽  
Rheumatic Heart

Analyses of lymphocyte subsets using flow cytometry were conducted to determine the significance of these cells in the pathogenesis of chronic rheumatic heart disease. Lymphocytes (B cells, T cells, CD4 cells, CD8 suppressor or cytotoxic T cells, activated T cells, and natural killer cells) were measured in blood and left atrial appendage samples of 30 patients with rheumatic heart disease and 10 patients with acyanotic congenital heart disease. Monoclonal fluorescent-labeled antibodies were used to identify various cells by flow cytometry. There was a significant increase in CD4 cells and activated T cells with a significant decrease in B cells in the left atrial appendage tissue of patients with rheumatic heart disease compared to those in the control group. There was no significant difference between the two groups in the distribution pattern of T lymphocytes in peripheral blood. These changes in rheumatic heart disease reflect an abnormal immunoregulatory mechanism with an ongoing enhanced immunological process continuing into the chronic phase of the disease. In our opinion, this persistent T cell response may lead to fresh damage to the myocardium and deformation of the heart valves.

Restriction in the Usage of Variable β Regions in T-cells Infiltrating Valvular Tissue from Rheumatic Heart Disease Patients

2002 ◽  
Vol 19 (4) ◽  
pp. 233-240 ◽  
Author(s):  
F. Figueroa ◽  
M. González ◽  
F. Carrión ◽  
C. Lobos ◽  
F. Turner ◽  
...  
Keyword(s):  
T Cells ◽  
Heart Disease ◽  
Rheumatic Heart Disease ◽  
Rheumatic Heart

scholarly journals Circulating level of regulatory T cells in rheumatic heart disease: An observational study

2016 ◽  
Vol 68 (3) ◽  
pp. 342-348 ◽  
Author(s):  
Saibal Mukhopadhyay ◽  
Saurabh Varma ◽  
H.N. Mohan Kumar ◽  
Jamal Yusaf ◽  
Mayank Goyal ◽  
...  
Keyword(s):  
T Cells ◽  
Heart Disease ◽  
Regulatory T Cells ◽  
Observational Study ◽  
Rheumatic Heart Disease ◽  
Rheumatic Heart

scholarly journals T-Cell Reactivity against Streptococcal Antigens in the Periphery Mirrors Reactivity of Heart-Infiltrating T Lymphocytes in Rheumatic Heart Disease Patients

2001 ◽  
Vol 69 (9) ◽  
pp. 5345-5351 ◽  
Author(s):  
Luiza Guilherme ◽  
Sandra E. Oshiro ◽  
Kellen C. Faé ◽  
Edécio Cunha-Neto ◽  
Guilherme Renesto ◽  
...  
Keyword(s):  
T Cells ◽  
Heart Disease ◽  
T Cell ◽  
Rheumatic Heart Disease ◽  
Peripheral Blood ◽  
Cell Reactivity ◽  
T Cell Clones ◽  
Cell Clones ◽  
T Cell Reactivity ◽  
Rheumatic Heart

ABSTRACT T-cell molecular mimicry between streptococcal and heart proteins has been proposed as the triggering factor leading to autoimmunity in rheumatic heart disease (RHD). We searched for immunodominant T-cell M5 epitopes among RHD patients with defined clinical outcomes and compared the T-cell reactivities of peripheral blood and intralesional T cells from patients with severe RHD. The role of HLA class II molecules in the presentation of M5 peptides was also evaluated. We studied the T-cell reactivity against M5 peptides and heart proteins on peripheral blood mononuclear cells (PBMC) from 74 RHD patients grouped according to the severity of disease, along with intralesional and peripheral T-cell clones from RHD patients. Peptides encompassing residues 1 to 25, 81 to 103, 125 to 139, and 163 to 177 were more frequently recognized by PBMC from RHD patients than by those from controls. The M5 peptide encompassing residues 81 to 96 [M5(81–96) peptide] was most frequently recognized by PBMC from HLA-DR7+DR53+ patients with severe RHD, and 46.9% (15 of 32) and 43% (3 of 7) of heart-infiltrating and PBMC-derived peptide-reactive T-cell clones, respectively, recognized the M5(81–103) region. Heart proteins were recognized more frequently by PBMC from patients with severe RHD than by those from patients with mild RHD. The similar pattern of T-cell reactivity found with both peripheral blood and heart-infiltrating T cells is consistent with the migration of M-protein-sensitized T cells to the heart tissue. Conversely, the presence of heart-reactive T cells in the PBMC of patients with severe RHD also suggests a spillover of sensitized T cells from the heart lesion.

Selective depletion of Vβ2+CD8+ T cells in peripheral blood from rheumatic heart disease patients

2003 ◽  
Vol 20 (2) ◽  
pp. 183-190 ◽  
Author(s):  
F Carrión ◽  
M Fernandez ◽  
M Iruretagoyena ◽  
L.E Coelho Andrade ◽  
M Odete-Hilário ◽  
...  
Keyword(s):  
T Cells ◽  
Heart Disease ◽  
Rheumatic Heart Disease ◽  
Cd8 T Cells ◽  
Peripheral Blood ◽  
Selective Depletion ◽  
Rheumatic Heart

Molecular pathogenesis of rheumatic fever and rheumatic heart disease

2005 ◽  
Vol 7 (28) ◽  
pp. 1-15 ◽  
Author(s):  
Luiza Guilherme ◽  
Kellen Faé ◽  
Sandra E. Oshiro ◽  
Jorge Kalil
Keyword(s):  
T Cells ◽  
Heart Disease ◽  
Rheumatic Fever ◽  
Rheumatic Heart Disease ◽  
Mononuclear Cells ◽  
Molecular Mimicry ◽  
Interleukin 4 ◽  
T Helper 1 ◽  
Heart Lesions ◽  
Rheumatic Heart

Molecular mimicry between streptococcal and human proteins has been proposed as the triggering factor leading to autoimmunity in rheumatic fever (RF) and rheumatic heart disease (RHD). This article summarises studies on genetic susceptibility markers involved in the development of RF/RHD. It also focuses on the molecular mimicry in RHD mediated by the responses of B and T cells of peripheral blood, and T cells infiltrating heart lesions, against streptococcal antigens and human tissue proteins. The molecular basis of T-cell recognition is assessed through the definition of heart-crossreactive antigens. The production of cytokines from peripheral and heart-infiltrating mononuclear cells suggests that T helper 1 (Th1)-type cytokines are the mediators of RHD heart lesions. An insufficiency of interleukin 4 (IL-4)-producing cells in the valvular tissue might contribute to the maintenance and progression of valve lesions.

PDIA3, HSPA5 and vimentin, proteins identified by 2-DE in the valvular tissue, are the target antigens of peripheral and heart infiltrating T cells from chronic rheumatic heart disease patients

2008 ◽  
Vol 31 (2) ◽  
pp. 136-141 ◽  
Author(s):  
Kellen C. Faé ◽  
Danielle Diefenbach da Silva ◽  
Angelina M.B. Bilate ◽  
Ana C. Tanaka ◽  
Pablo M.A. Pomerantzeff ◽  
...  
Keyword(s):  
T Cells ◽  
Heart Disease ◽  
Rheumatic Heart Disease ◽  
Rheumatic Heart
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