Dr. Thomas E. Lane
Ph.D., University of California, Los Angeles,1993
Work in my laboratory at the University
of California, Irvine has focused on understanding the molecular and cellular
mechanisms involved in regulating inflammation following microbial infection.
Specifically, we are interested in evaluating the functional contributions of
chemokines (chemotactic chemokines) and their receptors in the initiation and
maintenance of inflammation following infection. Current work is divided into
three major research areas: i) utilize a mouse model of viral-induced encephalomyelitis
and immune-mediated demyelination to study the functional contributions of chemokine
and chemokine receptor expression in regulating neuroinflammation, host defense,
and disease development ii) evaluate the mechanisms by which chemokine and chemokine
receptors participate in linking innate and adaptive immune responses following
viral infection, iii) utilize a model of remyelination developed in my laboratory
to identify unique gene(s) involved in this complex process.
One major area of ongoing work in the laboratory is to study how chemokines and chemokine receptors contribute to defense and disease following mouse hepatitis virus (MHV) infection of the central nervous system (CNS). Persistent MHV infection of the CNS results in an immune-mediated demyelinating disease that is similar clinically and histologically to the human demyelinating disease Multiple Sclerosis (MS). As such, the MHV system offers a relevant model to study the underlying molecular and cellular mechanisms contributing to MS. Importantly, chemokines and their receptors have been shown to be expressed within demyelinating lesions present in MS patients and have been proposed to be important in contributing to demyelination by attracting inflammatory cells into the CNS. Over the past four years, we have systematically determined that expression of chemokine and chemokine receptor genes is regulated within the CNS following MHV infection. Specifically, studies have determined that expression of CXCL10/IP-10 (interferon inducible protein 10 kDa) is important in host defense during acute disease by attracting T lymphocytes into the CNS that participate in host defense. Conversely, chronic expression of CXCL10/IP-10 is important in amplifying demyelination by attracting T lymphocytes into the CNS of persistently infected mice. Other chemokines such as CCL5/RANTES are also important in disease by attracting both T lymphocytes and macrophages into the CNS of MHV-infected mice. In addition, our laboratory has also determined that chemokine receptors including CCR2 and CCR5 also enhance leukocyte accumulation within the CNS following MHV infection. Collectively, these studies highlight the importance of chemokines and their receptors in enhancing inflammation within the CNS of virally-infected mice and indicate these molecules may be relevant targets for treatment of MS as well as other neuroinflammatory diseases.
Additional efforts are now focused on understanding how chemokines/chemokine receptors regulate innate immunity within the CNS following viral infection as well as how chemokine signaling contributes to the generation of anti-viral effector T cells
Dr. Lane is part of the UCI Graduate Track in Virology within the UCI graduate Program in Molecular Biology, Genetics, and Biochemistry. Applications requests or additional information about the graduate program may be obtained by electronic mail at firstname.lastname@example.org or by phone at (949) 824-8145. On-line applications may also be submitted through the Office of Research and Graduate Studies.
1) Molecular Biology, Genetics, and Biochemistry
2) Email: email@example.com or call (949) 824-8145
3) Graduate Studies Home Page, with
links to On-line applications and the Office of Research and Graduate Studies
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