Inhibition Of Tnf Alpha And Tgf Beta1 In Mt-4 Cells Treated With Transfer
Factor
Authors: Fernández-Ortega, C. (1); Ojeda-Ojeda, M. (1) Alcocer,
J.M. (2) Javier, F. (2); Rodriguez-Padilla, C. (2); Tamez Guerra, R. (2)
And Araña Rosainz, M. (1)
Institution: (1) Center Of Genetic Engineering And Biotechnology, La Habana
Cuba. (2) Laboratory Of Immunology And Viorlogy, School Of Biological Sciences,
Uanl, Monterrey, Mexico
Abstract:
In 1954 Lawerence used the term Transfer Factor (TF) for a dialyzable extract
of sensitized leukocytes, which transfers reactivity from skin test-positive
donors to skin test-negative recipients. The immune system is regulated
by a complex network of pleiotropic and redundant cytokines, which are
continually secreted to a greater or lesser degree even then the system
is apparently quiescent. Human Immunodeficiency Virus (HIV) directly infects
cells of the immune system and triggers a robust immune response, which
is an important and persistent source of immune activation. This activation
is intimately linked to cytokine secretion. Numerous cytokines induce HIV
expression, others suppress sit whereas others induce or suppress HIV expression,
depending on the culture system used. Previously, our group reported that
HIV production in MT-4 cells is inhibited after several days treatment
with TF. In this study we evaluate gene expression of different cytokines
on this cell line treated with TF. We showed that Transfer Factor inhibit
the TNF alpha and TGF beta1 gene expression. IL-2 and IL-10 gene expression
could not be observed in these culture conditions. It has been reported
that TNFalpha induces HIV expression whereas TGFbeta 1 increases or reduces
it depending on the cell system used, Our results indicate that the inhibition
of HIV production in MT4 cells by Transfer Factor could be in relation
with the inhibition of the TNFalpha and TGFbeta1 gene expression by Transfer
Factor in MT4 cells. These results could not have relevance for the treatment
of diseases where TNF and/or TGF plays a pathogenic role.