Holistic Health & Wellness Clinic

11/20/2025

The truth on molds and mycotoxins based on medical evidence and science, not anecdotes.“Mold is the gun, mycotoxin is the bullet”— Andrew W. Campbell, M.D.SPECIALTIESIt’s about helping peopleAs a life long humanist and expert in the fields of integrative health and traditional medicine, Dr. ...

11/20/2025

Dr. Andrew W. Campbell is a Professor of Immunology and Toxicology and the world-leading expert in mold- and mycotoxin-related illness. With over 35 years of...

11/20/2025

overview of Gal-3 effect on the immune system👇

✅Central Role of Galectin-3 Oligomer

The image illustrates the central immunomodulatory role of Galectin-3 oligomers, which interact with multiple immune cell types to regulate inflammation, immunity, and tissue remodeling. Galectin-3 acts as a hub connecting neutrophils, macrophages, monocytes, dendritic cells, mast cells, eosinophils, T cells, and B cells.

✅Effects on Neutrophils

Galectin-3 promotes neutrophil migration and extravasation toward infection sites.
It enhances cell adhesion and modulates the respiratory burst, supporting phagocytosis and the clearance of bacterial and fungal pathogens.

✅Effects on Macrophages

In macrophages, Galectin-3 supports recruitment and activation.
It enhances phagocytosis, contributes to macrophage polarization, and promotes cytokine production and cell survival.

✅Effects on Monocytes and Dendritic Cells

Galectin-3 influences monocyte differentiation into dendritic cells.
In dendritic cells, it promotes migration, cytokine release, T-cell activation, and antigen presentation.

✅Effects on Mast Cells

In mast cells, Galectin-3 regulates mediator release, modulates IgE receptor expression, and affects JNK1 signaling.
It can also promote apoptosis under specific conditions.

✅Effects on Eosinophils

Galectin-3 functions as a cell-surface adhesion molecule on eosinophils and regulates their interaction with VCAM-1 and α4 integrins.
It supports rolling and adhesion and contributes to the regulation of cell morphology.

✅Effects on T Cells

Galectin-3 down-regulates T-cell receptor (TCR) activation, leading to reduced cytokine responses.
It can promote apoptosis while simultaneously supporting cell survival depending on context.

✅Effects on B Cells

Galectin-3 inhibits B-cell differentiation into plasma cells and modulates B-cell development in lymphoid organs.

✅Interaction With Toll-Like Receptors

The diagram shows Galectin-3 interacting with Toll-like receptors (TLRs), indicating its role in innate immune sensing and inflammatory signaling pathways.

✅Related Diseases

🔴Dysregulation of Galectin-3 is associated with several diseases, including:

🔴Autoimmune diseases (RA, SLE, Sjögren’s syndrome)

🔴Atherosclerosis

🔴Infectious diseases (viral, bacterial, fungal regulation)

🔴Inflammatory diseases (IBD)

🔴Fibrotic diseases (IPF, chronic kidney disease, NASH, heart failure)

💡Morello, M.; Titolo, G.; D’Elia, S.; Caiazza, S.; Luisi, E.; Solimene, A.; Serpico, C.; Morello, A.; Natale, F.; Golino, P.; et al. Galectin-3: A Multitasking Protein Linking Cardiovascular Diseases, Immune Disorders and Beyond. Targets 2025, 3, 34. https://doi.org/10.3390/targets3040034

11/19/2025

Interaction of Immune Checkpoints and Their Corresponding Ligands👇

✅Immune checkpoints are regulatory pathways that maintain immune homeostasis and prevent excessive immune activation. In cancer, tumor cells often exploit these pathways by expressing checkpoint ligands that suppress anti-tumor immune responses. Below is a summary of key immune checkpoints and their major ligands.

✅PD-1 / PD-L1 and PD-L2
Programmed cell death protein-1 (PD-1), expressed on activated T cells, B cells, and NK cells, engages with its ligands PD-L1 and PD-L2. PD-L1 is broadly expressed on tumor cells and antigen-presenting cells, whereas PD-L2 is more restricted. Their interaction inhibits T-cell proliferation, cytokine production, and cytotoxic activity, enabling immune evasion.

✅CTLA-4 / CD80 and CD86
CTLA-4, expressed on activated T cells and regulatory T cells, competes with CD28 for binding to CD80 and CD86 on antigen-presenting cells. When engaged, CTLA-4 inhibits early T-cell activation, reduces IL-2 production, and promotes immune tolerance, limiting anti-tumor responses.

✅LAG-3 / MHC Class II
Lymphocyte activation gene-3 (LAG-3) binds to MHC class II molecules with higher affinity than CD4. This interaction suppresses T-cell activation and contributes to T-cell exhaustion in chronic inflammation and cancer.

✅TIM-3 / Galectin-9, CEACAM1, and Others
TIM-3 interacts with several ligands, including galectin-9 and CEACAM1. These interactions trigger T-cell inhibition, promote exhaustion, and impair effective anti-tumor immunity. TIM-3 is commonly upregulated in dysfunctional T-cell populations.

✅TIGIT / CD155 and CD112
TIGIT binds to CD155 and CD112 on tumor cells and antigen-presenting cells. This interaction inhibits NK cell cytotoxicity and suppresses T-cell activity, shaping a highly immunosuppressive microenvironment.

✅Together, these immune checkpoint interactions regulate the balance between immune activation and inhibition. In cancer, tumors exploit these pathways to suppress effective anti-tumor immunity, making immune checkpoint blockade a powerful therapeutic strategy.
💡 Leone, G.M.; Scuderi, G.; Fagone, P.; Mangano, K. Directions of Immunotherapy for Non-Small-Cell Lung Cancer Treatment: Past, Present and Possible Future. Int. J. Mol. Sci. 2025, 26, 11055. https://doi.org/10.3390/ijms262211055

11/17/2025

11/16/2025

"Fighting Cancer Metastasis & Heavy Metal Toxicities with Modified Citrus Pectin" - a presentation by Dr. Isaac Eliaz at Silicon Valley Heath Institute/ Sma...

11/13/2025

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11/13/2025

Want to help your autistic child speak? Learn about the critical test every parent should know when it comes to speech issues and cerebral folate deficiency ...

11/04/2025

Transitions vs Transversions in DNA Mutations👇

✅Point mutations are small changes in the DNA sequence that can have important biological effects. They occur when a single nucleotide base is substituted for another. Among these, transitions and transversions are two main types.

✅Transitions happen when a purine is replaced by another purine (adenine ↔ guanine) or a pyrimidine is replaced by another pyrimidine (cytosine ↔ thymine). Because the bases involved have similar structures, transitions are more frequent and less disruptive to the DNA molecule.

✅Transversions, on the other hand, involve a purine being exchanged for a pyrimidine or vice versa. Examples include adenine or guanine changing to cytosine or thymine, and the reverse. These mutations are less common but can cause more significant alterations in the genetic code.

✅Understanding the difference between transitions and transversions is essential for studying mutation mechanisms and their impact on genetic diseases and evolution.

11/03/2025

Cell Plasticity: The Hidden Power of Cells 👇
🔹 What is Cell Plasticity?
Cell plasticity is the remarkable ability of cells to change their identity, function, or state in response to internal signals or environmental changes.
🔹 Why is it Important?
- Development: It allows cells during embryogenesis to differentiate into various specialized types.
- Regeneration: Plays a role in wound healing and tissue repair.
- Disease: Cancer cells exploit plasticity to survive, resist treatment, and metastasize.
🔹 Key Mechanisms of Plasticity
- Epithelial–Mesenchymal Transition (EMT): Cells shift from an epithelial state (organized, attached) to a mesenchymal one (migratory, invasive).
- Transdifferentiating: A mature cell type directly converts into another type.
- Stemness acquisition: Differentiated cells regain stem cell-like properties.
🔹 Applications & Research
- Cancer biology: Understanding how tumor cells adapt.
- Regenerative medicine: Harnessing plasticity for tissue engineering.
- Therapeutics: Targeting plasticity to overcome drug resistance.