Ian Parker

University of California, Irvine

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Co-Authors

Michael D. Cahalan

University of California, Irvine

Ricardo Miledi

University of California, Irvine

Angelo Demuro

University of California, Irvine

Ian F. Smith

University of California, Irvine

Melanie P. Matheu

University of California, San Francisco

Shivashankar Othy

University of California, Irvine

Milton L. Greenberg

University of California, Irvine

Jeffrey T. Lock

University of California, Irvine

Ghanim Ullah

University of South Florida

Nick Callamaras

Tempus Labs (United States)

Cooperative Institutions

Laboratoire Lorrain de Recherche en Informatique et ses Applications

267

University of California, Irvine

153

University of Liverpool

Duke Medical Center

Liverpool Heart and Chest Hospital

Inserm

University of Pennsylvania

University College London

University of California, San Diego

Harvard University

Author Statistics

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Research Field

Calcium conductance of acetylcholine-induced endplate channels

Nature (1979)

Pìotr Bregestovski Ricardo Miledi Ian Parker

10.1038/279638a0

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Citations (103)

TLR4-activated B cells out-compete TLR9-activated B cells to establish peripheral tolerance (50.16)

The Journal of Immunology (2011)

Melanie P. Matheu Yan Su Milton L. Greenberg Ian Parker David A. Scott

Abstract Antigen presentation by B cells can generate either long-lived antigen-specific CD4+ T cell tolerance or activate T cells for additional B cell help during the humoral response. In our model, both naïve and LPS-activated B cells mOVA B cells expressing ovalbumin induced long-lived peripheral T cell tolerance, suppressing OTII T cell proliferation and T-cell-dependent antibody production in vivo. In contrast, CpG-activated mOVA B cells did not induce tolerance to OVA. Using two-photon microscopy we compared T-B cell interactions in the lymph node during tolerance induction or priming of OTII T cells mOVA B cells. Naïve, LPS- or CpG-activated mOVA B cells were individually capable of establishing long-lived interactions with OTII-T cells. Disruption of CTLA-4 / B7 interactions prevented establishment of long-lived T-B cognates and inhibited tolerance induced by LPS-treated B cells in vivo. In competition experiments with co-transferred LPS- and CpG-activated B cells, LPS- activated B cells dominated cell-cell interactions and were capable of establishing tolerance. In addition, tolerogenic LPS-activated B cells were capable of physically disrupting pre-established CpG-activated mOVA T-B pairs, exhibiting directional motility towards pre-established CpG-OTII pairs prior to disruption. Our findings demonstrate that LPS-activated B cells can act early in an immune response to establish tolerogenic dominance in the presence of priming CpG-activated B cells.

Priming (agriculture)

Naive B cell

Peripheral tolerance

TLR9

10.4049/jimmunol.186.supp.50.16

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Citations (0)

Speculating on transverse grooves in African elephant tusks

Pachyderm (2023)

Ian Parker Erwan Theleste Gerhard Steenkamp

10.69649/pachyderm.v64i.528

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Citations (0)

Confronting Death: Co-infection with HIV/AIDS and Hepatitis C

Ian Parker

Hepatitis C

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Two-photon imaging of remyelination of spinal cord axons by engrafted neural precursor cells in a viral model of multiple sclerosis

Proceedings of the National Academy of Sciences (2014)

Milton L. Greenberg Jason G. Weinger Melanie P. Matheu Kevin Carbajal Ian Parker

Significance Stem cell transplantation has emerged as a promising cell-based therapy for the treatment of demyelinating diseases such as multiple sclerosis (MS). This study provides the first real-time imaging of transplanted stem cell-mediated remyelination in a mouse model of MS. Whereas current treatments solely delay disease progression, transplanted stem cells actively reverse clinical disease in animal models. Using two-photon microscopy and viral-induced demyelination, we describe a technique to visualize cellular migration and remyelination in the mouse spinal cord. Transplanted neural precursor cells physically wrap damaged axons with newly formed myelin, preserving axonal health.

Remyelination

Yellow fluorescent protein

10.1073/pnas.1406658111

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Citations (31)

Public Montessori as a Reform Model: Questions and Considerations for School Districts (Poster 16)

Aera (2022)

Ian Parker

10.3102/ip.22.1891587

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Citations (0)

Ca2+ Signals in CD4+ T Cells during Early Contacts with Antigen-Bearing Dendritic Cells in Lymph Node

The Journal of Immunology (2007)

Sindy H. Wei Olga Safrina Ying Yu Kym R. Garrod Michael D. Cahalan

Abstract T cell activation by APC requires cytosolic Ca2+ ([Ca2+]i) elevation. Using two-photon microscopy, we visualized Ca2+ signaling and motility of murine CD4+ T cells within lymph node (LN) explants under control, inflammatory, and immunizing conditions. Without Ag under basal noninflammatory conditions, T cells showed infrequent Ca2+ spikes associated with sustained slowing. Inflammation reduced velocities and Ca2+ spiking in the absence of specific Ag. During early Ag encounter, most T cells engaged Ag-presenting dendritic cells in clusters, and showed increased Ca2+ spike frequency and elevated basal [Ca2+]i. These Ca2+ signals persisted for hours, irrespective of whether T cells were in contact with visualized dendritic cells. We propose that sustained increases in basal [Ca2+]i and spiking frequency constitute a Ca2+ signaling modality that, integrated over hours, distinguishes immunogenic from basal state in the native lymphoid environment.

Basal (medicine)

10.4049/jimmunol.179.3.1586

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Citations (88)

Class IA Phosphoinositide 3-Kinase Modulates Basal Lymphocyte Motility in the Lymph Node

The Journal of Immunology (2007)

Melanie P. Matheu Jonathan A. Deane Ian Parker David A. Fruman Michael D. Cahalan

Abstract Recruitment of PI3K to the cell membrane is an indispensable step in normal lymphocyte proliferation and activation. In this study we identify PI3K as an important signaling molecule for maintaining basal T and B lymphocyte motility and homing in the intact lymph node. Pharmacological inhibition of PI3K catalytic isoforms exerted broad effects on basal lymphocyte motility, including changes in homing kinetics, localization of B cells within the lymph node, and reduced cell velocities. Lymphocytes deficient in either or both of the class IA PI3K regulatory subunits p85α and p85β also exhibited reduced velocities, with the magnitude of reduction depending upon both cell type and isoform specificity. B cells deficient in p85α exhibited gross morphological abnormalities that were not evident in cells treated with a PI3K inhibitor. Our results show, for the first time, that class IA PI3Ks play an important role in regulating basal lymphocyte motility and that p85α regulatory subunit expression is required to maintain B cell morphology in a manner independent of PI3K catalytic function. Moreover, we demonstrate distinct roles for catalytic domain function and class IA PI3K regulatory domain activity in lymphocyte motility, homing, and homeostatic localization of mature resting B cells.

Phosphoinositide 3-kinase

Homing (biology)

Lymphocyte homing receptor

10.4049/jimmunol.179.4.2261

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Citations (39)

The raw ivory trade 1979-1987 : a consultant report for Parties to the Convention on Trade in Endangered Species of Wild Fauna and Flora through the Secretary General

Ian Parker

CITES

Flora

Source

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