Thomas E. Lane

Lack of nitric oxide synthase type 2 (NOS2) results in reduced neuronal apoptosis and mortality following mouse hepatitis virus infection of the central nervous system.

IFN-gamma-inducible protein 10 (IP-10; CXCL10)-deficient mice reveal a role for IP-10 in effector T cell generation and trafficking.

Mouse hepatitis virus infection of the central nervous system: chemokine-mediated regulation of host defense and disease.

Functional expression of chemokine receptor CCR5 on CD4(+) T cells during virus-induced central nervous system disease.

CC chemokine ligand 3 (CCL3) regulates CD8(+)-T-cell effector function and migration following viral infection.

Adenovirus-mediated expression of CXCL10 in the central nervous system results in T-cell recruitment and limited neuropathology.

Functional analysis of the CC chemokine receptor 5 (CCR5) on virus-specific CD8+ T cells following coronavirus infection of the central nervous system.

Effect of anti-CXCL10 monoclonal antibody on herpes simplex virus type 1 keratitis and retinal infection.

Measles virus infection induces chemokine synthesis by neurons.

Reducing inflammation decreases secondary degeneration and functional deficit after spinal cord injury.

CXC chemokine ligand 10 controls viral infection in the central nervous system: evidence for a role in innate immune response through recruitment and activation of natural killer cells.

Distinct roles for IP-10/CXCL10 in three animal models, Theiler's virus infection, EAE, and MHV infection, for multiple sclerosis: implication of differing roles for IP-10.

Antibody targeting of the CC chemokine ligand 5 results in diminished leukocyte infiltration into the central nervous system and reduced neurologic disease in a viral model of multiple sclerosis.

Remyelination, axonal sparing, and locomotor recovery following transplantation of glial-committed progenitor cells into the MHV model of multiple sclerosis.

Enhanced T cell proliferation in mice lacking the p85beta subunit of phosphoinositide 3-kinase.

The CC chemokine ligand 3 regulates CD11c+CD11b+CD8alpha- dendritic cell maturation and activation following viral infection of the central nervous system: implications for a role in T cell activation.

Consequences of CXCL10 and IL-6 induction by the murine IFN-alpha1 transgene in ocular herpes simplex virus type 1 infection.

Differential roles of CCL2 and CCR2 in host defense to coronavirus infection.

Neutralization of chemokines RANTES and MIG increases virus antigen expression and spinal cord pathology during Theiler's virus infection.

Accelerated intestinal epithelial cell turnover: a new mechanism of parasite expulsion.

Transplantation of glial-committed progenitor cells into a viral model of multiple sclerosis induces remyelination in the absence of an attenuated inflammatory response.

The chemokines CXCL9 and CXCL10 promote a protective immune response but do not contribute to cardiac inflammation following infection with Trypanosoma cruzi.

The CC chemokine receptor 5 is important in control of parasite replication and acute cardiac inflammation following infection with Trypanosoma cruzi.

Coronavirus infection of the central nervous system: host-virus stand-off.

Abnormal immune response of CCR5-deficient mice to ocular infection with herpes simplex virus type 1.

Differential roles for CXCR3 in CD4+ and CD8+ T cell trafficking following viral infection of the CNS.

Chemokine CC receptor 2 is important for acute control of cardiac parasitism but does not contribute to cardiac inflammation after infection with Trypanosoma cruzi.

Dengue virus induces expression of CXC chemokine ligand 10/IFN-gamma-inducible protein 10, which competitively inhibits viral binding to cell surface heparan sulfate.

NKG2D signaling and host defense after mouse hepatitis virus infection of the central nervous system.

Sjögren's syndrome-like disease in mice with T cells lacking class 1A phosphoinositide-3-kinase.

T cell antiviral effector function is not dependent on CXCL10 following murine coronavirus infection.

T-cell function is partially maintained in the absence of class IA phosphoinositide 3-kinase signaling.

Anti-viral effector T cell responses and trafficking are not dependent upon DRAK2 signaling following viral infection of the central nervous system.

Expression of CXC chemokine ligand 10 from the mouse hepatitis virus genome results in protection from viral-induced neurological and liver disease.

Therapeutic neutralization of CXCL10 decreases secondary degeneration and functional deficit after spinal cord injury in mice.

DRAK2 regulates memory T cell responses following murine coronavirus infection.

Evidence for differential roles for NKG2D receptor signaling in innate host defense against coronavirus-induced neurological and liver disease.

CCR1 deficiency increases susceptibility to fatal coronavirus infection of the central nervous system.

NKG2D receptor signaling enhances cytolytic activity by virus-specific CD8+ T cells: evidence for a protective role in virus-induced encephalitis.

The Th17-ELR+ CXC chemokine pathway is essential for the development of central nervous system autoimmune disease.

Mouse hepatitis virus infection of the CNS: a model for defense, disease, and repair.

Generation of a protective T-cell response following coronavirus infection of the central nervous system is not dependent on IL-12/23 signaling.

CXCL10/CXCR3-mediated responses promote immunity to respiratory syncytial virus infection by augmenting dendritic cell and CD8(+) T cell efficacy.

Insertion of the CXC chemokine ligand 9 (CXCL9) into the mouse hepatitis virus genome results in protection from viral-induced encephalitis and hepatitis.

IFN-gamma-mediated suppression of coronavirus replication in glial-committed progenitor cells.

Endogenous remyelination is induced by transplant rejection in a viral model of multiple sclerosis.

Cutting edge: the chemokine receptor CXCR3 retains invariant NK T cells in the thymus.

CXCL10 and trafficking of virus-specific T cells during coronavirus-induced demyelination.

A protective role for ELR+ chemokines during acute viral encephalomyelitis.

The Biology of Persistent Infection: Inflammation and Demyelination following Murine Coronavirus Infection of the Central Nervous System.

CXCR2-positive neutrophils are essential for cuprizone-induced demyelination: relevance to multiple sclerosis.

The pathogenesis of murine coronavirus infection of the central nervous system.

Migration of engrafted neural stem cells is mediated by CXCL12 signaling through CXCR4 in a viral model of multiple sclerosis.

CXCR2 signaling protects oligodendrocytes and restricts demyelination in a mouse model of viral-induced demyelination.

Myelin repair is accelerated by inactivating CXCR2 on nonhematopoietic cells.

Cell replacement therapies to promote remyelination in a viral model of demyelination.

Chronic systemic infection exacerbates ischemic brain damage via a CCL5 (regulated on activation, normal T-cell expressed and secreted)-mediated proinflammatory response in mice.

The role of chemokines during viral infection of the CNS.

Impaired immune responses following spinal cord injury lead to reduced ability to control viral infection.

G-CSF-mediated thrombopoietin release triggers neutrophil motility and mobilization from bone marrow via induction of Cxcr2 ligands.

Inflammation induced by infection potentiates tau pathological features in transgenic mice.

CXCR2 signaling protects oligodendrocyte progenitor cells from IFN-γ/CXCL10-mediated apoptosis.

Importance of the CCR5-CCL5 axis for mucosal Trypanosoma cruzi protection and B cell activation.

CXCR4 signaling regulates remyelination by endogenous oligodendrocyte progenitor cells in a viral model of demyelination.

Complementary roles of Fas-associated death domain (FADD) and receptor interacting protein kinase-3 (RIPK3) in T-cell homeostasis and antiviral immunity.