The Mechanism of Transfer Factor

Balancing T-Helper Cell Activity

Question: How can Transfer Factor change a predominantly TH-2 Immune System to a TH-1 predominant System so rapidly?

Answer: In the case of Transfer Factor, clinicians have been well ahead of scientists and immunologists. Dr. Sherwood Lawrence, lead immunologist at New York University, discovered Transfer Factor in 1949 though at the time, his discovery went no further than the library shelf. Now there are an estimated 3,000 references on Transfer Factor in the literature worldwide. There are some on the adjuvants as well.

It has been a puzzle HOW Transfer Factors could have such a rapid action if it depended upon new production T-helper cells from an exhausted immune system. Here is the mechanism: Eomesodermin.

T-Helper Cells develop along two different lines – TH-1 and TH-2.

TH-1 predominance modulates cell-mediated immunity and produces cytokines: IL-2, IFN-gamma and TNF-Alpha. TH-2 cells modulate humoral immunity, or antibody production, and produce IL-4, IL-5, IL-6, IL-10 and IL-13. TH-1 predominance increases the body’s ability to defend itself against viruses, fungi, parasites, cancer and intracellular organisms.

TH-2 dominant states, with decrease cellular immunity and increased humoral immunity tend to manifest as Allergies, Chronic Sinusitis, Atopic eczema and Asthma and in systemic autoimmune conditions such as CFS (now observed in horses), Lupus, (SLE), Mercury-induced autoimmunity, Chronic Giardiasis, Chronic Candidiasis, viral infections, Ulcerative Colitis and Cancer.

Transfer Factor augments cell-mediated immunity and modifies a TH-2 dominate state to TH-1 dominance. If the TH-1 response has resulted in an inadequate attempt by the immune system to fight off and eliminate an infection or neoplasia, then Transfer Factor would augment that process and be effective in many cases. Clinically, one sees this in Chron’s Disease, Multiple Sclerosis and Chronic Lyme Disease. In these cases, Transfer Factors help and accentuate the efforts of an already TH-1 dominant immune system.

From SCIENCE, p. 1041, Vol. 302, Nov. 2003: “The attributes of “Helper” T-cells are governed by two master transcriptional regulators, GATA-3 and T-bet, which coordinate the expression of specific cytokine genes. However, neither appears critical to the CD8+ T-cell function, leading Pearce et al to explore other pathways that might specify the transcriptional program in these cells. The trail ended in the identification of Eomesodermin (Eomes), a T-box transcription factor related to T-bet and already characterized as a key regulator of mesodermal differentiation. Eomes was specifically up-regulated in activated CD8+ cells [one of TF’s actions] and forced cellular expression of the factor conferred CD8+ characteristics on cells that had already differentiated into TH-2 [T-helper type two] cells. [It was found that] Disruption of expression significantly reduced the CD8 cytolytic program and interferon Gamma expression.

Thus, Eomes cooperates with T-bet in regulated distinct aspects of cell-mediated immunity.”

Additional note: This is the mechanism of Transfer Factor in increasing the effectiveness of a TH-1 predominant immune system and influencing change from TH-2 state to a TH-1 state. In the past we have not had an explanation of HOW TF affected the immune capability so rapidly. It is one thing to realize that new production T-helper cells could be configured into the TH-1’s, but with a marked effect in 48 hours and a height of effect in five days by TF, it seemed too fast - it takes ten days to two weeks for the production, maturation and configuration of T-cells. Now we see that the Eomes prompted by Transfer Factor while in circulation can convert TH-2’s to TH-1’s.

This is the point – Eomes was specifically up-regulated in activated CD8+ cells [one of TF’s actions] and forced cellular expression of the factor conferred CD8+ characteristics on cells that already differentiated into TH-2.