310 Increased number of CD4+ T cells in the peripheral blood in patients with chronic heart failure

2004 ◽  
Vol 3 (1) ◽  
pp. 76
Author(s):  
E JANKOWSKA
Keyword(s):  
Heart Failure ◽  
T Cells ◽  
Chronic Heart Failure ◽  
Peripheral Blood ◽  
Cd4 T Cells

Predictive power of the fractalkine receptor CX3CR1 on CD4 T cells in patients with chronic heart failure

2014 ◽  
Vol 171 (1) ◽  
pp. 96-97 ◽  
Author(s):  
Lorenz Koller ◽  
Steffen Blum ◽  
Magdalena Korpak ◽  
Bernhard Richter ◽  
Georg Goliasch ◽  
...  
Keyword(s):  
Heart Failure ◽  
T Cells ◽  
Chronic Heart Failure ◽  
Cd4 T Cells ◽  
Predictive Power ◽  
Fractalkine Receptor ◽  
Receptor Cx3cr1

Expression of interferon-g and interleukin-4 production in CD4+ T cells in patients with chronic heart failure

2007 ◽  
Vol 22 (3) ◽  
pp. 178-183 ◽  
Author(s):  
Takashi Fukunaga ◽  
Hirofumi Soejima ◽  
Atsushi Irie ◽  
Koichi Sugamura ◽  
Yoko Oe ◽  
...  
Keyword(s):  
Heart Failure ◽  
T Cells ◽  
Chronic Heart Failure ◽  
Cd4 T Cells ◽  
Interleukin 4

Abstract 101: Novel Inhibitors for Temporal Modulation of T-lymphocytes During Chronic Heart Failure

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Shyam S Bansal ◽  
Rachel Rosenzweig ◽  
SARITA NEHRA ◽  
Oscar Bermeo Blanco ◽  
Matthew Stratton ◽  
...  
Keyword(s):  
Heart Failure ◽  
T Cells ◽  
T Cell ◽  
Chronic Heart Failure ◽  
T Cell Activation ◽  
Cd4 T Cells ◽  
Cell Activation ◽  
Left Ventricular ◽  
Male Mice ◽  
Lv Remodeling

CD4+ T-cells mediate wound-healing post-myocardial infarction (MI) but exacerbate left-ventricular (LV) remodeling during chronic heart failure (HF). Mechanisms that lead to this transition are unknown. Therefore, we hypothesized that as opposed to MI, T-cells activate specific pathological signals to promote LV-remodeling during chronic HF. To identify such signals, we conducted limited cell RNA-sequencing of CD4+ T-cells sorted from the failing hearts (8 weeks post-MI) of male mice and, surprisingly, found activation of estrogen receptor (ER)-α signaling. As ERα effects are antagonized by ERβ, we tested a novel ERβ agonist (OSU-ERB-012) to modulate T-cell activity and LV remodeling. In-vitro assays showed that OSU-ERB-012 dose dependently inhibit activation and proliferation of T-cells isolated from male mice (IC 50 3.4 μM). In-vivo assays (60 mg/kg/day; oral) showed no overt toxicity and a significant reduction in circulating T cells without affecting neutrophils, monocytes, or B-cells indicating specificity against T-cells. Furthermore, this effect was specific to TCR-mediated T-cell activation and the drug did not affect T-cells stimulated with PMA/Ionomycin suggesting preferential inhibition of antigenically-activated T-cells. To test therapeutic efficacy, male 10-12 week old mice underwent coronary ligation or sham operation and at 4 weeks post-MI randomized according to their cardiac function to receive either the vehicle or OSU-ERB-012 (60 mg/kg/day, oral) for the next 4 weeks. Consistently, at 8 weeks we observed a significant reduction in T-cells in the circulation and the spleens of drug-treated mice when compared with the vehicle treatment. As expected, vehicle treated HF mice showed progressive LV dilatation with significantly increased end-diastolic and end-systolic volumes (EDV and ESV, respectively) from 4-8 weeks post-MI. Importantly, treatment with OSU-ERB-012 significantly inhibited these changes and blunted LV remodeling from 4-8 weeks post-MI. Significant reduction in tibia-normalized heart weights supported these results. Our studies indicate that OSU-ERB-012 is a novel orally-active drug molecule that selectively inhibits T-cell activation and blunts pathological LV-remodeling during chronic HF.

Increased expression of tumor necrosis factor in peripheral blood memory CD4+ T cells of patients with Crohn's disease

2001 ◽  
Vol 120 (5) ◽  
pp. A317-A317
Author(s):  
J DETENA ◽  
L MANZANO ◽  
J LEAL ◽  
A PRIETO ◽  
E ANTONIO ◽  
...  
Keyword(s):  
T Cells ◽  
Crohn’S Disease ◽  
Tumor Necrosis Factor ◽  
Crohn's Disease ◽  
Peripheral Blood ◽  
Cd4 T Cells ◽  
Tumor Necrosis ◽  
Memory Cd4 T Cells ◽  
Necrosis Factor

Increased frequencies of activated effector CD4+ T cells in the peripheral blood and hepatic tissue of patients with NAFL and NASH

2014 ◽  
Vol 52 (08) ◽  
Author(s):  
M Rau ◽  
AK Schilling ◽  
J Meertens ◽  
I Hering ◽  
T Kudlich ◽  
...  
Keyword(s):  
T Cells ◽  
Peripheral Blood ◽  
Cd4 T Cells ◽  
Hepatic Tissue

Distinctive Pattern of Cytokine Production and Adhesion Molecule Expression in Peripheral Blood Memory CD4+ T Cells from Patients with Active Crohn’s Disease

2006 ◽  
Vol 26 (3) ◽  
pp. 233-242 ◽  
Author(s):  
Jaime García De Tena ◽  
Luis Manzano ◽  
Juan Carlos Leal ◽  
Esther San Antonio ◽  
Verónica Sualdea ◽  
...  
Keyword(s):  
T Cells ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Adhesion Molecule ◽  
Peripheral Blood ◽  
Cd4 T Cells ◽  
Cytokine Production ◽  
Adhesion Molecule Expression ◽  
Distinctive Pattern ◽  
Memory Cd4 T Cells

mTOR pathway regulates the differentiation of peripheral blood Th2/Treg cell subsets in patients with pemphigus vulgaris

2021 ◽  
Author(s):  
Kuan Lai ◽  
Wenjing Zhang ◽  
Songshan Li ◽  
Zhiwen Zhang ◽  
Shuangde Xie ◽  
...  
Keyword(s):  
T Cells ◽  
Peripheral Blood ◽  
Cd4 T Cells ◽  
Pemphigus Vulgaris ◽  
Treg Cells ◽  
Mtor Pathway ◽  
Cd4 T Cell ◽  
Cell Ratio ◽  
Loss Of Balance

Abstract Pemphigus vulgaris (PV) is a chronic and potentially life-threatening autoimmune blistering disease. Aberrant mTOR pathway activity is involved in many autoimmune diseases. This study investigated the correlation of mTOR pathway (PI3K/AKT/mTOR/p70S6K) activity with the loss of balance in T helper 2/regulatory T (Th2/Treg) cells in the peripheral blood of PV patients. CD4+ T cells were isolated from 15 PV patients and 15 healthy controls (HCs), the ratios of Th2/CD4+ T cells and Treg/CD4+ T cells, the activity of the mTOR pathway (PI3K/AKT/mTOR/p70S6K), the transcription factors and cytokines of Th2 and Treg cells were detected. Primary CD4+ T cells from PV patients were cultured under Th2- or Treg-polarizing conditions with or without rapamycin in vitro. We found that PV patients showed significantly elevated serum IL-4 when compared with HCs, and serum IL-4 level was positively correlated with the titer of anti-Dsg1/3 antibody and disease severity, while the serum TGF-β level was negatively correlated with the titer of anti-Dsg3 antibody and disease severity. Meanwhile, PV patients showed increased Th2/CD4+ T cell ratio; decreased Treg/CD4+ T cell ratio; elevated mRNA of PI3K, AKT, mTOR and protein of PI3K (P85), AKT, p-AKT (Ser473), mTOR, p-mTOR (Ser2448), p-p70S6K (Thr389), GATA3; reduced protein of forkhead box protein 3. Rapamycin inhibited Th2 cell differentiation and promoted Treg cell differentiation in vitro. These data suggest a close association between mTOR pathway activation and the loss of balance in Th2/Treg cells in peripheral blood of PV patients. Inhibiting mTORC1 can help restore the Th2/Treg balance.

scholarly journals CD73+ CD127high Long-Term Memory CD4 T Cells Are Highly Proliferative in Response to Recall Antigens and Are Early Targets in HIV-1 Infection

2021 ◽  
Vol 22 (2) ◽  
pp. 912
Author(s):  
Nabila Seddiki ◽  
John Zaunders ◽  
Chan Phetsouphanh ◽  
Vedran Brezar ◽  
Yin Xu ◽  
...  
Keyword(s):  
T Cells ◽  
Peripheral Blood ◽  
Cd4 T Cells ◽  
Significant Proportion ◽  
Long Term Memory ◽  
Ki 67 ◽  
Memory Cd4 T Cells ◽  
Hiv 1

HIV-1 infection rapidly leads to a loss of the proliferative response of memory CD4+ T lymphocytes, when cultured with recall antigens. We report here that CD73 expression defines a subset of resting memory CD4+ T cells in peripheral blood, which highly express the α-chain of the IL-7 receptor (CD127), but not CD38 or Ki-67, yet are highly proliferative in response to mitogen and recall antigens, and to IL-7, in vitro. These cells also preferentially express CCR5 and produce IL-2. We reasoned that CD73+ memory CD4+ T cells decrease very early in HIV-1 infection. Indeed, CD73+ memory CD4+ T cells comprised a median of 7.5% (interquartile range: 4.5–10.4%) of CD4+ T cells in peripheral blood from healthy adults, but were decreased in primary HIV-1 infection to a median of 3.7% (IQR: 2.6–6.4%; p = 0.002); and in chronic HIV-1 infection to 1.9% (IQR: 1.1–3%; p < 0.0001), and were not restored by antiretroviral therapy. Moreover, we found that a significant proportion of CD73+ memory CD4+ T cells were skewed to a gut-homing phenotype, expressing integrins α4 and β7, CXCR3, CCR6, CD161 and CD26. Accordingly, 20% of CD4+ T cells present in gut biopsies were CD73+. In HIV+ subjects, purified CD73+ resting memory CD4+ T cells in PBMC were infected with HIV-1 DNA, determined by real-time PCR, to the same level as for purified CD73-negative CD4+ T cells, both in untreated and treated subjects. Therefore, the proliferative CD73+ subset of memory CD4+ T cells is disproportionately reduced in HIV-1 infection, but, unexpectedly, their IL-7 dependent long-term resting phenotype suggests that residual infected cells in this subset may contribute significantly to the very long-lived HIV proviral DNA reservoir in treated subjects.

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