Th1 response Cancer Research Results

Th1 response, T helper response: Click to Expand ⟱
Source: HalifaxProj(promote)
Type:
The Th1 (T helper 1) response is a crucial component of the immune system, particularly in the context of cell-mediated immunity. Th1 cells are a subset of CD4+ T cells that primarily produce cytokines such as interferon-gamma (IFN-γ), which activate macrophages and enhance the ability of the immune system to combat intracellular pathogens, including viruses and certain types of cancer cells.

Increased infiltration of Th1 cells and a strong Th1 cytokine profile within tumors are often associated with better clinical outcomes in various cancers (including melanoma, colorectal, and ovarian cancers).

A robust Th1 response is a critical component of effective antitumor immunity. Th1 cells and their signature cytokines (such as IFN-γ and IL-2) enhance the activation and proliferation of cytotoxic T cells, macrophages, and natural killer cells, thereby promoting immune-mediated tumor cell destruction. High infiltration of Th1 cells and a strong Th1 cytokine profile within the tumor microenvironment are generally associated with favorable prognostic outcomes and improved responses to immunotherapies.


Scientific Papers found: Click to Expand⟱
552- Anamu,    A critical review of the therapeutic potential of dibenzyl trisulphide isolated from Petiveria alliacea L (guinea hen weed, anamu)
- Review, NA, NA
p‑MAPK↑, hyper-phosphorylation of growth factor induced MAPKinases (erk 1 and erk 2) phosphorylation,
Th1 response↓,
Th2↑,

2690- BBR,    Berberine Differentially Modulates the Activities of ERK, p38 MAPK, and JNK to Suppress Th17 and Th1 T Cell Differentiation in Type 1 Diabetic Mice
- in-vivo, Diabetic, NA
*Inflam↓, Recent studies suggested that berberine has many beneficial biological effects, including anti-inflammation.
*Th17↓, Here we reported that 2 weeks of oral administration of berberine prevented the progression of type 1 diabetes in half of the NOD mice and decreased Th17 and Th1 cytokine secretion.
*Th1 response↓,
*ERK↑, berberine inhibited Th17 differentiation by activating ERK1/2 and inhibited Th1 differentiation by inhibiting p38 MAPK and JNK activation.
*p38↓,
*JNK↓,
*STAT1↓, Berberine down-regulated the activity of STAT1 and STAT4 through the suppression of p38 MAPK and JNK activation,
*STAT4↓,
*MAPK↓,

2776- Bos,    Anti-inflammatory and anti-cancer activities of frankincense: Targets, treatments and toxicities
- Review, Var, NA
*5LO↓, Arthritis Human primary chondrocytes: 5-LOX↓, TNF-α↓, MMP3↓
*TNF-α↓,
*MMP3↓,
*COX1↓, COX-1↓, Leukotriene synthesis by 5-LOX↓
*COX2↓, Arthritis Human blood in vitro: COX-2↓, PGE2↓, TH1 cytokines↓, TH2 cytokines↑
*PGE2↓,
*Th2↑,
*Catalase↑, Ethanol-induced gastric ulcer: CAT↑, SOD↑, NO↑, PGE-2↑
*SOD↑,
*NO↑,
*PGE2↑,
*IL1β↓, inflammation Human PBMC, murine RAW264.7 macrophages: TNFα↓ IL-1β↓, IL-6↓, Th1 cytokines (IFNγ, IL-12)↓, Th2 cytokines (IL-4, IL-10)↑; iNOS↓, NO↓, phosphorylation of JNK and p38↓
*IL6↓,
*Th1 response↓,
*Th2↑,
*iNOS↓,
*NO↓,
*p‑JNK↓,
*p38↓,
GutMicro↑, colon carcinogenesis: gut microbiota; pAKT↓, GSK3β↓, cyclin D1↓
p‑Akt↓,
GSK‐3β↓,
cycD1/CCND1↓,
Akt↓, Prostate Ca: AKT and STAT3↓, stemness markers↓, androgen receptor↓, Sp1 promoter binding↓, p21(WAF1/CIP1)↑, cyclin D1↓, cyclin D2↓, DR5↑,CHOP↑, caspases-3/-8↑, PARP cleavage, NFκB↓, IKK↓, Bcl-2↓, Bcl-xL↓, caspase 3↑, DNA
STAT3↓,
CSCs↓,
AR↓,
P21↑,
DR5↑,
CHOP↑,
Casp3↑,
Casp8↑,
cl‑PARP↑,
DNAdam↑,
p‑RB1↓, Glioblastoma: pRB↓, FOXM1↓, PLK1↓, Aurora B/TOP2A pathway↓,CDC25C↓, pCDK1↓, cyclinB1↓, Aurora B↓, TOP2A↓, pERK-1/-2↓
FOXM1↓,
TOP2↓,
CDC25↓,
p‑CDK1↓,
p‑ERK↓,
MMP9↓, Pancreas Ca: Ki-67↓, CD31↓, COX-2↓, MMP-9↓, CXCR4↓, VEGF↓
VEGF↓,
angioG↓, Apoptosis↑, G2/M arrest, angiogenesis↓
ROS↑, ROS↑,
Cyt‑c↑, Leukemia : cytochrome c↑, AIF↑, SMAC/DIABLO↑, survivin↓, ICAD↓
AIF↑,
Diablo↑,
survivin↓,
ICAD↓,
ChemoSen↑, Breast Ca: enhancement in combination with doxorubicin
SOX9↓, SOX9↓
ER Stress↑, Cervix Ca : ER-stress protein GRP78↑, CHOP↑, calpain↑
GRP78/BiP↑,
cal2↓,
AMPK↓, Breast Ca: AMPK/mTOR signaling↓
mTOR↓,
ROS↓, Boswellia extracts and its phytochemicals reduced oxidative stress (in terms of inhibition of ROS and RNS generation)


Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress

ROS↓, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics

AIF↑, 1,   CDC25↓, 1,  

Core Metabolism/Glycolysis

AMPK↓, 1,  

Cell Death

Akt↓, 1,   p‑Akt↓, 1,   Casp3↑, 1,   Casp8↑, 1,   Cyt‑c↑, 1,   Diablo↑, 1,   DR5↑, 1,   ICAD↓, 1,   p‑MAPK↑, 1,   survivin↓, 1,  

Kinase & Signal Transduction

SOX9↓, 1,  

Protein Folding & ER Stress

CHOP↑, 1,   ER Stress↑, 1,   GRP78/BiP↑, 1,  

DNA Damage & Repair

DNAdam↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence

p‑CDK1↓, 1,   cycD1/CCND1↓, 1,   P21↑, 1,   p‑RB1↓, 1,  

Proliferation, Differentiation & Cell State

CSCs↓, 1,   p‑ERK↓, 1,   FOXM1↓, 1,   GSK‐3β↓, 1,   mTOR↓, 1,   STAT3↓, 1,   TOP2↓, 1,  

Migration

cal2↓, 1,   MMP9↓, 1,  

Angiogenesis & Vasculature

angioG↓, 1,   VEGF↓, 1,  

Immune & Inflammatory Signaling

Th1 response↓, 1,   Th2↑, 1,  

Hormonal & Nuclear Receptors

AR↓, 1,  

Drug Metabolism & Resistance

ChemoSen↑, 1,  

Clinical Biomarkers

AR↓, 1,   FOXM1↓, 1,   GutMicro↑, 1,  
Total Targets: 43

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress

Catalase↑, 1,   SOD↑, 1,  

Cell Death

iNOS↓, 1,   JNK↓, 1,   p‑JNK↓, 1,   MAPK↓, 1,   p38↓, 2,  

Proliferation, Differentiation & Cell State

ERK↑, 1,   STAT1↓, 1,   STAT4↓, 1,  

Migration

5LO↓, 1,   MMP3↓, 1,  

Angiogenesis & Vasculature

NO↓, 1,   NO↑, 1,  

Immune & Inflammatory Signaling

COX1↓, 1,   COX2↓, 1,   IL1β↓, 1,   IL6↓, 1,   Inflam↓, 1,   PGE2↓, 1,   PGE2↑, 1,   Th1 response↓, 2,   Th17↓, 1,   Th2↑, 2,   TNF-α↓, 1,  

Clinical Biomarkers

IL6↓, 1,  
Total Targets: 26

Scientific Paper Hit Count for: Th1 response, T helper response
1 dibenzyl trisulphide(DTS) from Anamu
1 Berberine
1 Boswellia (frankincense)
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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