The Mysterious, and Potentially Revolutionary, Immunological Properties of Transfer Factor: A Review

Abstract

Transfer factor is the name given to material derived from activated lymphocytes that is probably composed of a complex of a peptide and a short segment of RNA and which has the reported ability to transfer specific T cell immunity to uncommitted lymphocytes. Many independent groups around the world reported isolating transfer factors between 1955 and 1990 and demonstrating their ability to transfer passive immunity from one animal or individual to another, often within 24 hours of inoculation. Such activity is potentially revolutionary both in making T cell vaccines readily manufacturable and also because the existence of transfer factors would undermine the basic assumptions of the clonal selection theory, which currently dominates immunological theory. Unfortunately, lack of the microanalytical and synthetic techniques required to properly identify transfer factors, combined with safety factors associated with it derivation from blood sources susceptible to HIV and prion infections, put an end to transfer factor research after 1990. This paper reviews the evidence supporting transfer factor activity and suggests that this potentially revolutionary concept be resurrected and subjected to renewed scrutiny in light of CRISPR-Cas mechanisms and because of its potential to make possible T cell vaccination and provide a novel basis for understanding immunological function.

T-Cell Receptor Sequences Identify Combined Coxsackievirus–Streptococci Infections as Triggers for Autoimmune Myocarditis and Coxsackievirus–Clostridia Infections for Type 1 Diabetes

“…A variety of groups have, over many decades, suggested that such a mechanism might exist and provided arguments for why such a mechanism might be required in place of the textbook mechanism of random clonal production of every possible TCR or antibody sequence (e.g., [167][168][169][170][171][172][173]. This is not the place to provide a detailed description of how such a mechanism might work or the data and logical arguments that might support such a mechanism (some of which are provided in [174,175]). However, in the spirit of examining all possible hypotheses that can explain TCR mimicry of AD-inducing antigens, antigen templating of the hypervariable region is compatible with the results reported here.…”

“…The first involves initiating T1DM in Lewis rats by infecting them with Kilham rat virus (KRV). KRV increased intestinal Bifidobacterium and Clostridium species [178] in parallel with T1DM development such that antibiotic treatment not only prevented the increase in Bifidobacterium and Clostridium abundance but also prevented the onset of T1DM [175]. Similarly, the susceptibility of NOD mice to the development of T1DM depends on gut Clostridial butyrate biosynthesis species [179].…”