Viral Immunity & Pathogenesis
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Group Leader |
Research topics
During the last years, our group has been interested to understand how some viruses could modulate immune responses concomitant to infection, and what could be the results of this immunomodulation on diseases not directly related to the infection. Another project involves the analysis of expression of the cellular receptor for mouse hepatitis virus (MHV), in relationship with the pathogenicity of this virus.
1. Immunomodulation triggered by virus infection: The possibility for evoluted organisms to survive viral infections depends on the ability of their immune system to eliminate the infectious agent. Therefore, numerous mechanisms, involving different types of immune cells such as cytolytic lymphocytes, T helper and B lymphocytes and macrophages, the molecules that allow those cells to communicate, namely the lymphokines, and the products of those interactions, including antibodies, have been elaborated. On the other hand, viruses have developed strategies to escape the immune system of their hosts, such as large frequencies of mutations or latency, or even to impair this system, which often leads to diseases such as autoimmunity or immunodeficiencies. Our project is to analyse, in murine models, some aspects of these relations between viruses and the immune system. It is focused on the modulations of the immune microenvironment of the infected host that can lead to modifications in the course of ongoing diseases initially unrelated to the virus.
2. MHV receptor: In collaboration with K.V. Holmes (Denver, USA), expression of CEACAM1, a glycoprotein that serves as receptor for MHV-A59 has been analysed in cells from the immune system (11). This molecule was highly expressed in B lymphocytes, including cells of the B-1a (CD5+) lineage, in NK cell subpopulations and in macrophages, but was not detectable in resting T lymphocytes. We analyse its normal function in the immune system and its role in immune modulations induced by MHV infection.
