In 1960 H.S. Lawrence showen that the final effect of TF results from the action of many effector substances included in the leukocyte dialysate, and introduced a term dialysable leukocyte extract (DLE). DLE contains at least 200 components, the most abundant is thymosin (G.B. Wilson, et al., 1983), and there is a wide spectrum of other biologically active substances, all of molecular weight from 1,000 Da to 20,000 Da, such as oligopeptides, nucleotides, serotonin, bradykinine, nicotine amide, prostaglandins, ascorbate, etc. One of them – with a molecular weight of only 3,000 Da – is an antigen specific transfer factor (H.H. Fudenberg, 1987).
Because of the small molecule the transfer factor cannot be damaged by enzymes of the digestive tract so that there is no loss of transfer factor activity when taken orally. Dialyzable leukocyte extract causes the immune system of the recipient to respond to a new antigen as if the immune system would have had a memory of previous encounters with that antigen, i.e. primary immune response: patient’s ‘virgin’ T-lymphocytes would have been already activated, clonal selection would have taken place, even before the first exposure to this new antigen. So when the actual contact with the new antigen is made, a massive proliferation of memory and effector T-cells, as in a typical ‘secondary reaction’, promptly develops.
Importantly, the molecule of dialyzable leukocyte extract is small, its molecular weight is low, so that DLE is non-antigenic, and thus does not cause any(!) immune reaction in a recipient at all.
Even though the induction of cell-mediated immunity (i.e. antigen recognition) is strictly dependent upon the identification of MHC of the individual, dialysable leukocyte extract acts as xenogeneic, it means that it ignores any species barriers in its effect (i.e. it is ‘species non-specific’). In other words, there are no species barriers for transfer factor therapy. Even primitive species have cells from which one can prepare transfer factor.
Cell-mediated type of immunity invovles various type of T lymphocytes or T cells, named because they developed inside the thymus gland. Once a T cell recognizes the antigen, it multiplies rapidly and its offspring differentiate into several types. Helper T cells activate both B cells to help antibody-mediated immunity and macrophages to engulf the microbes and debris. Killer T cells attack micro-organisms as well as any body cells infected with them, using powerful proteins called lymphokines. Suppressor T cells inhibit the response of other cells to the invading microbes.
The term ‘transfer factor’ has been defined as the leukocyte dialysate capable of transferring the antigen-specific T-lymphocyte response (G.B. Wilson and H.H. Fudenberg, 1983). In other words, ‘transfer factors’ are molecules that “educate” recipients to express cell-mediated immunity, and this effect is antigen-specific (C.H. Kirkpatrick, 1993).
So ‘transfer factor’ transfers the ability to express cell mediated immunity (or delayed type hypersensitivity) from immune donors to non-immune recipients, i.e. they are immune messengers with normalizing effect on aberrant immune response.
As such it does not act in the same way as an antibiotic or a chemotherapeutic agent but rather, it may up regulate or down regulate immune responsiveness through its helper/suppressor activities to achieve normalcy. Transfer factors do not act as drugs for specific disease conditions but endow the recipient with de novo immune capacity to resist and repel infections. In other words, TF transfers immune power to a recipient who will thereby gain specific immunity.
