Freund's adjuvant is an
antigen solution emulsified in
mineral oil, used as an
immunopotentiator (booster of the
immune system).
Forms
The so-called
complete form (CFA) is composed of inactivated and dried
mycobacteria, usually
Mycobacterium tuberculosis (the
pathogenic agent of
tuberculosis).
The so-called incomplete form (IFA) is the same adjuvant, but without the mycobacterial components.
Eponym
It is named after
Jules T. Freund (1890-1960),
Hungarian-born
American immunologist.
Regulation
Freund's adjuvant is effective in stimulating
cell-mediated immunity and may lead to the potentiation of the production of certain
immunoglobulins, but this effect depends on the
animal model used. Its use in humans is forbidden, due to its
toxicity. Even for animal research there are currently
guidelines associated with its use, due to its
painful reaction and potential for tissue damage. Injections of CFA should be subcutaneous or intraperitoneal, because intradermal injections may cause skin
ulceration and
necrosis; intramuscular injections may lead to temporary or permanent
muscle lesion, and intravenous injections may produce pulmonary lipid
embolism.
Effects
When administered to mice, in some laboratory experiments Freund's complete adjuvant was said to have prevented
juvenile-onset diabetes and combined with prepared spleen cells was said to have reversed it. In 2006 these claims were challenged by the findings of several other researchers. Although newspapers have described the 2006 findings as confirming the earlier experiments, in substantial ways they conflict with them. A report from
NIH was released on November 23, 2006 in
Science confirming the participation of spleen cells in reversing end-stage diabetes.
It has also been investigated in an animal model of Parkinson's disease.
Mechanism
The adjuvant is known to stimulate production of
tumor necrosis factor, which is thought to kill the
T-cells responsible for the
autoimmune destruction of the pancreatic
Beta cells. Still in question is whether the regrowth of functional
insulin-producing cells occurs due to
differentiation and
proliferation of existing
pancreatic stem cells, or whether the injected spleen cells re-differentiate to an insulin producing form.
Denise Faustman, whose work has been central to developing the protocol, has suggested that both mechanisms may play a role. However, in experiments to verify and examine her work, Suri reported that DNA-based evidence yielded no sign of spleen cell derivatives in
pancreatic islet Beta cells analyzed after treatments.
See also
External links
References