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John H. Weis

Professor of Pathology

B.S. Oregon State University

Ph.D. University of Minnesota Medical School

Research

References

john.weis@path.utah.edu

John Weis' Lab Page

John Weis' PubMed Literature Search

Research

Our laboratory studies the interfaces between the innate and acquired immune responses. We take a genetics approach, using the mouse as a model system, to decipher molecular and cellular interactions.

One current focus in the lab includes the maturation and differentiation of B cells with the intent to identify key transcription control proteins that regulate this process. Mouse B cells enter the spleen from the bone marrow requiring a number of maturation steps to insure they are competent to respond to antigen following an infection. These immature B cells must negotiate through a series of differentiation checkpoints, requiring transcriptional induction and suppression of key target genes. We have identified a number of transcriptional control proteins that are up regulated and down regulated during this stage of B cell development. To define their roles in B cell function, we have created and are analyzing lines of mice that lack these gene products in maturing B cells, or inappropriately maintain their expression during B cell maturation.

Another project in the lab has been to study the structure, expression and function of a set of mouse proteins known as the complement receptors. These proteins are critical for controlling complement activation during immune reactions and serve to assist in the production of the full range of B cell products. Inappropriate expression of such proteins (such as engineered mouse anomalies or human deficiencies) can give rise to a range of symptoms including autoimmunity, susceptibility to natural infections and a degraded antibody response. We have created strains of mice either deficient in such proteins (deficiency of the two major CD21 gene products) or with engineered germ line mutations that result in either mutant protein production or inappropriate expression. We have also created mice that only make one or the other of the two major isoforms of the CD21 proteins. We are currently analyzing such mice and are defining previously unknown feedback pathways that are regulated by this set of proteins.

Another project in the lab focuses upon defining the maturation steps T cells take in positive and negative selection within the thymus, focusing upon the role of the Snai3 transcription factor on the generation and function of CD8+ cytotoxic T cells. Snai3 is a transcriptional repressor, blocking expression of key genes within the lineage of these cells. Our goals in this project are to identify the gene targets for this factor and define the pathways of cell activation controlled by Snai3.

References