KEVIN MCKERNAN: Cannabinoids have immunomodulatory effects that . . . help rebalance T-cell exhaustion…

I think there are many ways to do this that include cannabinoids/IVM/fenben/meth blue and red light

Ask ChatGPT or other AI platforms.

Here is its response for cannabinoids.

Cannabinoids have immunomodulatory effects that could theoretically help rebalance T cell exhaustion… https://t.co/g1DxBEEX4j

— Kevin McKernan (@Kevin_McKernan) February 21, 2025

I think there are many ways to do this that include cannabinoids/IVM/fenben/meth blue and red light Ask ChatGPT or other AI platforms. Here is its response for cannabinoids. Cannabinoids have immunomodulatory effects that could theoretically help rebalance T-cell exhaustion induced by chronic exposure to spike protein (commonly referred to as spikeopathy). T cell exhaustion is characterized by dysfunctional T cells with upregulated inhibitory receptors (e.g., PD-1, LAG-3, TIM-3) and impaired cytokine production, often seen in chronic infections or persistent antigen exposure. Potential Mechanisms by Which Cannabinoids Could Influence T-Cell Exhaustion in Spikeopathy: 1. Reduction of Chronic Inflammation (Cytokine Modulation)

Cannabinoids, particularly CBD (cannabidiol) and THC (tetrahydrocannabinol), can downregulate TNF-α, IL-6, and IL-1β, which are commonly elevated in chronic inflammatory states, including those triggered by persistent spike protein exposure.

Lowering systemic inflammation could reduce T cell exhaustion by decreasing the chronic antigenic stimulation that drives it.

2. Restoration of T Cell Function

CBD has been shown to increase IL-2 production, which is crucial for T-cell proliferation and survival.

Some studies suggest that cannabinoids may downregulate PD-1 expression, which is a key marker of T cell exhaustion.

3. Enhancement of Autophagy and Cellular Repair

CB2 receptor activation (primarily targeted by CBD and some THC analogs) has been linked to enhanced autophagy, which may help clear damaged mitochondria and improve T cell metabolic function.

Autophagy is often impaired in spikeopathy, contributing to persistent immune dysfunction.

4. Regulation of Th1/Th2/Th17 Balance

Persistent spike exposure has been linked to Th2 skewing and excessive Th17 activation, both of which contribute to autoimmune-like inflammation.

CBD has been shown to suppress Th17 while promoting Treg (regulatory T cells), which could restore immune balance.

5. Protection Against Microglial Activation and Neuroinflammation

Since spikeopathy can cause neuroinflammation and microglial activation, cannabinoids’ ability to cross the blood-brain barrier and reduce neuroinflammatory cytokines could provide neuroimmune benefits.

CB1 activation (via THC) may help regulate neuroimmune signaling, which indirectly supports T cell homeostasis.

Considerations & Caveats

While cannabinoids have anti-inflammatory and immune-restorative properties, their effects are context-dependent. High doses of THC can be immunosuppressive, potentially worsening T cell exhaustion if not carefully dosed.

CBD-dominant formulations may be preferable for immune homeostasis without excessive immunosuppression.

Combination therapies (e.g., cannabinoids + flavonoids like luteolin, or metabolic enhancers like NAD+ boosters) might further enhance T-cell recovery.

CONCLUSION There is a strong mechanistic basis for cannabinoids mitigating T cell exhaustion in spikeopathy, particularly through CBD-mediated reduction of inflammation, PD-1 downregulation, and metabolic restoration. However, clinical validation in the context of post-spike syndrome is still lacking. Future research should explore cannabinoid formulations, dosages, and combination therapies that optimize immune restoration without excessive suppression.