Epigallocatechin gallate (EGCG), the primary catechin in green tea, has been investigated for its potential immunomodulatory and anti-inflammatory properties in the context of autoimmune disorders. Preclinical studies, primarily in animal models and in vitro experiments, have demonstrated that EGCG can modulate immune cell function, suppress the production of pro-inflammatory cytokines (such as TNF-α, IL-6, and IL-17), and inhibit the proliferation of autoreactive T cells. These effects suggest a possible benefit in conditions characterized by immune dysregulation, such as rheumatoid arthritis, multiple sclerosis, and inflammatory bowel disease.

For example, in mouse models of multiple sclerosis (experimental autoimmune encephalomyelitis), EGCG administration has been shown to reduce disease severity and neuroinflammation. Similarly, some studies have documented reduced joint inflammation in animal models of rheumatoid arthritis with EGCG supplementation. However, robust clinical evidence in humans is limited. A few small pilot studies and case reports exist, but large, well-controlled clinical trials are lacking, and no major medical guidelines currently recommend EGCG as a treatment for autoimmune diseases.

In summary, while there is promising preclinical evidence and a plausible biological rationale for EGCG's use in autoimmune disorders, current human data are insufficient to justify routine clinical use. The evidence rating reflects the promising preclinical research but limited clinical validation.