Lionel G. Filion, University of Ottawa
Associate Professor
Biochemistry, Microbiology, and Immunology
Ottawa, Ontario
lionel.filion@uottawa.ca
Office:
(613) 562-5800 ext. 8308
Bio/Research
My laboratory is involved in understanding the regulation of immune responses by studying the interactions of adhesion and accessory models in several models. These models include an Multiple Sclerosis model, HIV model and a radiation model. The dysfunction that occurs can be partly attributed to...
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Bio/Research
My laboratory is involved in understanding the regulation of immune responses by studying the interactions of adhesion and accessory models in several models. These models include an Multiple Sclerosis model, HIV model and a radiation model. The dysfunction that occurs can be partly attributed to the suppression of the immune response either directly by antigen (ie HIV) or by modifying the local environment so that the immune system becomes immune suppressed. The first model is the study of HIV. The effects of HIV on accessory function of monocytes are being characterized. These functions are depressed 24 hours after infection even though production infection does not occur for 48 hours. It seems that HIV interferes with the network of accessory cell functions in accessory cells that preventing the immune response to respond adequately to the infection. HIV may perform this action by altering the expression of molecules of the surface of T cells and Accessory cells that are necessary in the development of the immune response specifically a Th1 response.
The second model involves the study of the immune response of Multiple Sclerosis patients. There immune response is poorly characterized but it is believed that the response is mainly a Th1 response. It is believed that if the response can be modified to switch from a Th1 to a Th2 the patients would benefit. Our studies is determine how we shift the Th1 response of MS patients to a Th2 phenotype and to devise appropriate measures to predict a beneficial outcome.
The third model of immune suppression that we have developed deals with the effect of radiation in the induction of immune suppression. We are trying to determine the mechanism by which radiation induces suppression. We have shown that radiation itself does not induce immune suppression but makes the host more susceptible to immune suppression. We have also observed that radiation can alter immune functions of cells without necessary eliminating these from the host. Apoptosis is induced even a extremely low levels of radiation.
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The second model involves the study of the immune response of Multiple Sclerosis patients. There immune response is poorly characterized but it is believed that the response is mainly a Th1 response. It is believed that if the response can be modified to switch from a Th1 to a Th2 the patients would benefit. Our studies is determine how we shift the Th1 response of MS patients to a Th2 phenotype and to devise appropriate measures to predict a beneficial outcome.
The third model of immune suppression that we have developed deals with the effect of radiation in the induction of immune suppression. We are trying to determine the mechanism by which radiation induces suppression. We have shown that radiation itself does not induce immune suppression but makes the host more susceptible to immune suppression. We have also observed that radiation can alter immune functions of cells without necessary eliminating these from the host. Apoptosis is induced even a extremely low levels of radiation.
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