Lupus

Larry A. Law

Lupus is a chronic autoimmune disease that causes the body to attack its own tissues and organs, including the joints, skin, kidneys, blood cells, brain, heart, and lungs. According to traditional medicine, there is no cure for lupus. The work of the GRM demonstrates that there is hope through nutritional glycobiology. Current lupus medical treatments often target symptoms or broadly suppress the immune system, leading to side effects. However, Marina Zhang, an outstanding health reporter with The Epoch Times, reported that according to a Nature study published in 2024, science has discovered that patients with lupus have an imbalance in a crucial chemical pathway in their bodies. Researchers found that this imbalance produces more disease-causing cells that promote lupus. If this chemical imbalance can be corrected, they believe lupus can be reversed. 

Aryl Hydrocarbon Receptor (AHR)

Scientists believe targeting the specific chemical imbalance identified could more effectively treat lupus without systemic immunosuppression interventions. Nutrition is a key component for restoring chemical imbalance. Below is what Marina Zhang discovered in the latest medical research.

Marina Zhang reported, "The chemical that researchers identified is the aryl hydrocarbon receptor (AHR). AHR is a key protein involved in the imbalance of immune cells in lupus patients. It regulates the body’s response to environmental pollutants, bacteria, and metabolites. While AHR is present in all cells, it is not always active. Researchers found that lupus patients have reduced AHR activity. This reduction leads to an increase in follicular and peripheral T helper cells, which are involved in inflammation and autoimmunity. However, when AHR activity increases, these T-cells are reprogrammed to be T-cells that promote wound healing and barrier protection."

AHR is a protein in the family of transcription factors and is 848 amino acids long. It is normally inactive and bound to co-chaperones in the cytoplasm, but when it binds to a ligand (any molecule fitting this receptor), it moves to the nucleus and stimulates transcription of target genes. 

The Molecular Switch

Dr. Jaehyuk Choi, associate professor of dermatology at Northwestern University Feinberg School of Medicine, and the study’s senior author, explained that AHR can be compared to “a molecular switch” that determines the fate of immune cells. By developing therapeutics that target AHR in rogue T-cells, researchers believe they may be able to reverse lupus.
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Dr. Choi and Dr. Deepak Rao, an assistant professor of medicine at Harvard Medical School, expressed their surprise at discovering that AHR could be vital in reversing autoimmunity, given that the receptor had no known connection to it. Dr. Rao, who is also a senior author of the study, added that it was initially surprising to find that a T-cell involved in wound healing would be the opposite of an autoimmune T-cell. “Those two T-cell populations with those two functions are not obviously connected or related,” he said. He added that he could not have predicted that when wound-healing T-cells increased, autoimmune T-cells would decrease, and vice versa.

T-Cells

Follicular and peripheral T helper cells have long been known to play a major role in driving lupus, Dr. Rao explained in the The Epoch Times article. In lupus, the patient’s body produces autoantibodies, antibodies that attack self-tissues. B-cells generate these autoantibodies under the control of rogue autoimmune T-cells. Therefore, by converting these autoimmune T-cells into cells involved in wound healing, the production of autoantibodies is reduced, thereby decreasing autoimmunity.
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“It is almost like a cell streamline, where if you can block one part, then the downstream is blocked,” Dr. Choi explained. He highlighted the study’s findings demonstrating that adding AHR to rogue T-cells in cell culture transforms them into wound-healing cells. These reprogrammed cells can no longer help B-cells make autoantibodies.

Dr. Rao added that these rogue T-cells are also present in other autoimmune conditions, like rheumatoid arthritis, raising the possibility that other drug targets for these cells may apply to such conditions.

Treatment Without Immune System Suppression

Current lupus treatments elicit broad immunosuppressive effects by reducing B- and T-cell activity. However, when rogue T-cells are targeted explicitly with AHR, patients can experience Lupus symptoms reversal without compromising their overall immunity. Additionally, the increase in cells involved in wound and barrier repair helps alleviate gastrointestinal problems. The only drawback is that since AHR is present in all cells, broad administration of AHR-targeted treatments could cause systemic adverse effects, so further study is merited. But the good news is that the incorporation of sugar nutrients that coat these proteins and cell receptors can make incredible differences in cellular performance and chemical imbalances. So there is real hope. For more information, see my book.