CD4+ Cancer Research Results

CD4+, CD4+ T Cells: Click to Expand ⟱
Source:
Type:
CD4+ T cells are T lymphocytes that express T cell receptors (TCRs).
Majority of cancer immunotherapies focus on harnessing the anti-tumour CD8+ cytotoxic T cell response, the potential role of CD4+ ‘helper’ T cells has largely remained in the background. multifaceted role of CD4+ T cells in the anti-tumour immune response.
CD4+ T cells play a critical role in developing and sustaining effective anti-tumour immunity, even in cancer immunotherapies specifically designed to activate a CD8+ CTL response.
Scientific Papers found: Click to Expand⟱
561- ART/DHA,    Antitumor and immunomodulatory properties of artemether and its ability to reduce CD4+ CD25+ FoxP3+ T reg cells in vivo
- in-vivo, NA, NA
TumCG↓,
CD4+↓,
CD25+↓,
FoxP3+↓,
IL4↑,

560- ART/DHA,    Dihydroartemisinin shift the immune response towards Th1, inhibit the tumor growth in vitro and in vivo
- in-vivo, NA, NA
IL4↓,
CD4+↓,
CD25+↓,
FoxP3+↓, Foxp3+
Treg lymp↓,

562- ART/DHA,    Artesunate exerts an anti-immunosuppressive effect on cervical cancer by inhibiting PGE2 production and Foxp3 expression
- in-vivo, NA, HeLa
CD4+↓,
CD25+↓,
FoxP3+↓,
Treg lymp↓,
PGE2↓,
FOXP3↓,
COX2↓,

2674- BBR,    Berberine: A novel therapeutic strategy for cancer
- Review, Var, NA - Review, IBD, NA
Inflam↓, anti-inflammatory, antidiabetic, antibacterial, antiparasitic, antidiarrheal, antihypertensive, hypolipidemic, and fungicide.
AntiCan↑, elaborated on the anticancer effects of BBR through the regulation of different molecular pathways such as: inducing apoptosis, autophagy, arresting cell cycle, and inhibiting metastasis and invasion.
Apoptosis↑,
TumAuto↑,
TumCCA↑,
TumMeta↓,
TumCI↓,
eff↑, BBR is shown to have beneficial effects on cancer immunotherapy.
eff↑, BBR inhibited the release of Interleukin 1 beta (IL-1β), Interferon gamma (IFN-γ), Interleukin 6 (IL-6), and Tumor Necrosis Factor-alpha (TNF-α) from LPS stimulated lymphocytes by acting as a dopamine receptor antagonist
CD4+↓, BBR inhibited the proliferation of CD4+ T cells and down-regulated TNF-α and IL-1 and thus, improved autoimmune neuropathy.
TNF-α↓,
IL1↓,
BioAv↓, On the other hand, P-Glycoprotein (P-gp), a secretive pump located in the epithelial cell membrane, restricts the oral bioavailability of a variety of medications, such as BBR. The use of P-gp inhibitors is a common and effective way to prevent this
BioAv↓, Regardless of its low bioavailability, BBR has shown great therapeutic efficacy in the treatment of a number of diseases.
other↓, BBR has been also used as an effective therapeutic agent for Inflammatory Bowel Disease (IBD) for several years
AMPK↑, inhibitory effects on inflammation by regulating different mechanisms such as 5′ Adenosine Monophosphate-Activated Protein Kinase (AMPK. Increase of AMPK
MAPK↓, Mitogen-Activated Protein Kinase (MAPK), and NF-κB signaling pathways
NF-kB↓,
IL6↓, inhibiting the expression of proinflammatory genes such as IL-1, IL-6, Monocyte Chemoattractant Protein 1 (MCP1), TNF-α, Prostaglandin E2 (PGE2), and Cyclooxygenase-2 (COX-2)
MCP1↓,
PGE2↓,
COX2↓,
*ROS↓, BBR protected PC-12 cells (normal) from oxidative damage by suppressing ROS through PI3K/AKT/mTOR signaling pathways
*antiOx↑, BBR therapy improved the antioxidant function of mice intestinal tissue by enhancing the levels of glutathione peroxidase and catalase enzymes.
*GPx↑,
*Catalase↑,
AntiTum↑, Besides, BBR leaves great antitumor effects on multiple types of cancer such as breast cancer,69 bladder cancer,70 hepatocarcinoma,71 and colon cancer.72
TumCP↓, BBR exerts its antitumor activity by inhibiting proliferation, inducing apoptosis and autophagy, and suppressing angiogenesis and metastasis
angioG↓,
Fas↑, by increasing the amounts of Fas receptor (death receptor)/FasL (Fas ligand), ROS, ATM, p53, Retinoblastoma protein (Rb), caspase-9,8,3, TNF-α, Bcl2-associated X protein (Bax), BID
FasL↑,
ROS↑,
ATM↑,
P53↑,
RB1↑,
Casp9↑,
Casp8↑,
Casp3↓,
BAX↑,
Bcl-2↓, and declining Bcl2, Bcl-X, c-IAP1 (inhibitor of apoptosis protein), X-linked inhibitor of apoptosis protein (XIAP), and Survivin levels
Bcl-xL↓,
IAP1↓,
XIAP↓,
survivin↓,
MMP2↓, Furthermore, BBR suppressed Matrix Metalloproteinase-2 (MMP-2), and MMP-9 expression.
MMP9↓,
CycB/CCNB1↓, Inhibition of cyclin B1, cdc2, cdc25c
CDC25↓,
CDC25↓,
Cyt‑c↑, BBR inhibited tumor cell proliferation and migration and induced mitochondria-mediated apoptosis pathway in Triple Negative Breast Cancer (TNBC) by: stimulating cytochrome c release from mitochondria to cytosol
MMP↓, decreased the mitochondrial membrane potential, and enabled cytochrome c release from mitochondria to cytosol
RenoP↑, BBR significantly reduced the destructive effects of cisplatin on the kidney by inhibiting autophagy, and exerted nephroprotective effects.
mTOR↓, U87 cell, Inhibition of m-TOR signaling
MDM2↓, Downregulation of MDM2
LC3II↑, Increase of LC3-II and beclin-1
ERK↓, BBR stimulated AMPK signaling, resulting in reduced extracellular signal–regulated kinase (ERK) activity and COX-2 expression in B16F-10 lung melanoma cells
COX2↓,
MMP3↓, reducing MMP-3 in SGC7901 GC and AGS cells
TGF-β↓, BBR suppressed the invasion and migration of prostate cancer PC-3 cells by inhibiting TGF-β-related signaling molecules which induced Epithelial-Mesenchymal Transition (EMT) such as Bone morphogenetic protein 7 (BMP7),
EMT↑,
ROCK1↓, inhibiting metastasis-associated proteins such as ROCK1, FAK, Ras Homolog Family Member A (RhoA), NF-κB and u-PA, leading to in vitro inhibition of MMP-1 and MMP-13.
FAK↓,
RAS↓,
Rho↓,
NF-kB↓,
uPA↓,
MMP1↓,
MMP13↓,
ChemoSen↑, recent studies have indicated that it can be used in combination with chemotherapy agents

451- CUR,    The effect of Curcumin on multi-level immune checkpoint blockade and T cell dysfunction in head and neck cancer
- vitro+vivo, HNSCC, SCC15 - vitro+vivo, HNSCC, SNU1076 - vitro+vivo, HNSCC, SNU1041
TumCMig↓,
TumCG↓,
PD-L1↓,
PD-L2↓,
Galectin-9↓,
EMT↓,
T-Cell↑,
TILs↑,
PD-1↓,
TIM-3↓,
CD4+↓,
CD25+↓,
FoxP3+↓,
E-cadherin↑,
CD8+↑,
IFN-γ↑,

193- MFrot,  MF,    Rotating Magnetic Field Mitigates Ankylosing Spondylitis Targeting Osteocytes and Chondrocytes via Ameliorating Immune Dysfunctions
- in-vivo, Arthritis, NA
BMD↑, loss reduced
Cartilage↑, more intact cartilage surfaces and denser proteoglycan
IL17↓,
IL22↓,
IL23↓,
IL28↓,
CD4+↓, tremendously attenuated
CD8+↓, In this investigation, data showed that RMF treatment decreased CD3-expressing proliferative cells via immunostaining and reduced CD4+/CD8+ T-cells via flow cytometry in AS mice
LAMB3↑,
COL4↓,
THBS2↓,
ITGA11↓,
PPARγ↑, mice have decreased expression of peroxisome proliferator-activated receptor γ (PPAR-γ), a ligand-activated transcription factor belonging to the nuclear hormone receptor superfamily, which RMF reverses.
ACAA1↓,
PLIN1↓,
FABP4↓,
PCK1↓,
UCP1↓,
TNF-α↓,

4936- PEITC,    PEITC treatment suppresses myeloid derived tumor suppressor cells to inhibit breast tumor growth
- in-vivo, BC, MDA-MB-231
TumCG↓, oral administration of 12 μmol PEITC attenuated tumor growth by 76%.
CD34↓, significant reduction in the levels of MDSCs bearing the surface markers CD33, CD34 and CD11b in PEITC treated mice
CD11b↓,
CSCs↓,
ALC∅, Surprisingly, PEITC treatment had no effect on the lymphocyte population
CD4+↓, Our results revealed that PEITC treatment caused a small reduction in CD4+ lymphocytes
NF-kB↓, PEITC acts as a strong antitumor agent by inhibiting survival pathways, such as, nuclear factor kB (NFkB), signal transducer and activator of transcription 3 (STAT3) and hypoxia inducible factor 1α (HIF1α)
STAT3↓, Previous studies have shown that inhibition of these pathways suppresses MDSC activity and inhibits cancer progression
Hif1a↓,

1282- RES,    Resveratrol Inhibits CD4+ T Cell Activation by Enhancing the Expression and Activity of Sirt1
- vitro+vivo, NA, NA
T-Cell↓, inhibits the activation and cytokine production of T cells
SIRT1↑,
CD4+↓,


Showing Research Papers: 1 to 8 of 8

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 8

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

CDC25↓, 2,   MMP↓, 1,   UCP1↓, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

ACAA1↓, 1,   AMPK↑, 1,   FABP4↓, 1,   PCK1↓, 1,   PLIN1↓, 1,   PPARγ↑, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   Bcl-xL↓, 1,   Casp3↓, 1,   Casp8↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   Fas↑, 1,   FasL↑, 1,   IAP1↓, 1,   MAPK↓, 1,   MDM2↓, 1,   survivin↓, 1,  

Transcription & Epigenetics ⓘ

other↓, 1,  

Autophagy & Lysosomes ⓘ

LC3II↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

ATM↑, 1,   P53↑, 1,  

Cell Cycle & Senescence ⓘ

CycB/CCNB1↓, 1,   RB1↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CD34↓, 1,   CSCs↓, 1,   EMT↓, 1,   EMT↑, 1,   ERK↓, 1,   mTOR↓, 1,   RAS↓, 1,   STAT3↓, 1,   TumCG↓, 3,  

Migration ⓘ

Cartilage↑, 1,   CD11b↓, 1,   COL4↓, 1,   E-cadherin↑, 1,   FAK↓, 1,   Galectin-9↓, 1,   ITGA11↓, 1,   LAMB3↑, 1,   MMP1↓, 1,   MMP13↓, 1,   MMP2↓, 1,   MMP3↓, 1,   MMP9↓, 1,   Rho↓, 1,   ROCK1↓, 1,   TGF-β↓, 1,   THBS2↓, 1,   Treg lymp↓, 2,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,   TumMeta↓, 1,   uPA↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   Hif1a↓, 1,  

Immune & Inflammatory Signaling ⓘ

CD25+↓, 4,   CD4+↓, 8,   COX2↓, 3,   FOXP3↓, 1,   FoxP3+↓, 4,   IFN-γ↑, 1,   IL1↓, 1,   IL17↓, 1,   IL22↓, 1,   IL23↓, 1,   IL28↓, 1,   IL4↓, 1,   IL4↑, 1,   IL6↓, 1,   Inflam↓, 1,   MCP1↓, 1,   NF-kB↓, 3,   PD-1↓, 1,   PD-L1↓, 1,   PD-L2↓, 1,   PGE2↓, 2,   T-Cell↓, 1,   T-Cell↑, 1,   TILs↑, 1,   TNF-α↓, 2,  

Cellular Microenvironment ⓘ

TIM-3↓, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   ChemoSen↑, 1,   eff↑, 2,  

Clinical Biomarkers ⓘ

ALC∅, 1,   BMD↑, 1,   IL6↓, 1,   PD-L1↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 1,   AntiTum↑, 1,   RenoP↑, 1,  

Infection & Microbiome ⓘ

CD8+↓, 1,   CD8+↑, 1,  
Total Targets: 106

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   ROS↓, 1,  
Total Targets: 4

Scientific Paper Hit Count for: CD4+, CD4+ T Cells
3 Artemisinin
1 Berberine
1 Curcumin
1 Magnetic Field Rotating
1 Magnetic Fields
1 Phenethyl isothiocyanate
1 Resveratrol
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

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