Wayne M. Yokoyama

Washington University in St. Louis

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Liping Yang

Henan Normal University

Sytse J. Piersma

Washington University in St. Louis

Jennifer Poursine‐Laurent

Washington University in St. Louis

Marco Colonna

Washington University in St. Louis

Robert D. Schreiber

Washington University in St. Louis

Anthony R. French

Washington University in St. Louis

Anthony A. Scalzo

Saint Louis University

Sung‐Jin Kim

Korea University

Béatrice Plougastel-Douglas

Washington University in St. Louis

Bijal A. Parikh

Washington University in St. Louis

Cooperative Institutions

Washington University in St. Louis

391

Howard Hughes Medical Institute

123

National Institutes of Health

Harvard University

RELX Group (United States)

Triangle

John Wiley & Sons (United States)

Indianapolis Zoo

National Center on Birth Defects and Developmental Disabilities

University of Washington

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Deficiency of the adaptor protein SLy1 results in a natural killer cell ribosomopathy affecting tumor clearance

OncoImmunology (2016)

Saeed Arefanian Daniel Schäll Stephanie H. Chang Reza Ghasemi Ryuji Higashikubo

Individuals with robust natural killer (NK) cell function incur lower rates of malignancies. To expand our understanding of genetic factors contributing to this phenomenon, we analyzed NK cells from cancer resistant and susceptible strains of mice. We identified a correlation between NK levels of the X-chromosome-located adaptor protein SLy1 and immunologic susceptibility to cancer. Unlike the case for T or B lymphocytes, where SLy1 shuttles between the cytoplasm and nucleus to facilitate signal transduction, in NK cells SLy1 functions as a ribosomal protein and is located solely in the cytoplasm. In its absence, ribosomal instability results in p53-mediated NK cell senescence and decreased clearance of malignancies. NK defects are reversible under inflammatory conditions and viral clearance is not impacted by SLy1 deficiency. Our work defines a previously unappreciated X-linked ribosomopathy that results in a specific and subtle NK cell dysfunction leading to immunologic susceptibility to cancer.

10.1080/2162402x.2016.1238543

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Citations (9)

Corrigendum: Intraocular human cytomegaloviruses of ocular diseases are distinct from those of viremia and are capable of escaping from innate and adaptive immunity by exploiting HLA-E-mediated peripheral and central tolerance

Frontiers in Immunology (2023)

Mariko Shirane Nobuyo Yawata Daisuke Motooka Kensuke Shibata Seik‐Soon Khor

[This corrects the article DOI: 10.3389/fimmu.2022.1008220.].

Viremia

10.3389/fimmu.2022.1124440

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Murine Roseolovirus Induces Autoimmune Gastritis and Disrupts Thymic Antigen Presenting Cells.

The Journal of Immunology (2021)

Tarin M. Bigley Liping Yang Liang‐I Kang José B. Sáenz Jason C. Mills

Abstract Murine roseolovirus (MRV) is a beta-herpesvirus that is a natural murine pathogen and is genetically highly related to the human roseoloviruses, HHV6 and HHV7. The human roseoloviruses have been associated with autoimmune disease but demonstrating causality has been difficult due to the ubiquitous and chronic nature of roseolovirus infections. Neonatal MRV infection resulted in transient thymic and peripheral CD4+ T cell depletion, including CD4+Foxp3+ regulatory T cells (Tregs). We found that neonatal MRV infection induced autoimmune gastritis in adult mice. Our studies showed that autoimmune gastritis occurs in the absence of detectable virus in gastric mucosa. Ganciclovir (GCV) inhibited MRV replication as well as MRV-mediated CD4+ T cell depletion and development of autoimmune gastritis. This suggests that MRV replication is necessary for altering immunologic tolerance early in life. Interestingly, neonatal MRV infection resulted in the production of a wide array of autoantibodies in adult mice. The inflammatory infiltrate into the gastric mucosa was characterized by an increase in T cells, neutrophils and eosinophils. Furthermore, the CD4+ T cells in the gastric mucosa exhibited Th2 and Th17 differentiation. The development of autoimmune gastritis was CD4+ T cell and IL-17 dependent, while B cells were only necessary early in life. Neonatal MRV infection resulted in a transient decrease in medullary thymic epithelial and thymic dendritic cells numbers, as well as reduced expression of AIRE and tissue restricted self-antigens in the thymus. These findings strongly suggest that infection with a roseolovirus early in life results in disruption of central tolerance and development of autoimmune disease.

Autoimmune Gastritis

10.4049/jimmunol.206.supp.20.09

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222: NEONATAL MURINE ROSEOLOVIRUS INFECTION DISRUPTS IMMUNE TOLERANCE AND INDUCES AUTOIMMUNE GASTRITIS

Gastroenterology (2022)

Tarin M. Bigley Liping Yang Liang‐I Kang J.R. Sáenz Francisco Victorino

Autoimmune Gastritis

10.1016/s0016-5085(22)60102-1

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S 2.3 ‐ Lymphocyte Signalling

European Journal of Immunology (2009)

Noam Stern‐Ginossar Daphna Nachmani Ofer Mandelboim James P. Di Santo Naoko Satoh‐Takayama

Abstract No Abtract

Signalling

10.1002/eji.200990110

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Diagnosis and Treatment of Mycoplasma‐Contaminated Cell Cultures

Current Protocols in Immunology (1997)

Frank W. Fitch Thomas F. Gajewski Wayne M. Yokoyama

Abstract Mycoplasma contamination is a serious and frequent problem in the culture laboratory. Although mycoplasma contamination may be suspected by the failure of cells to thrive, the formal diagnosis rests on the detection of adenosine phosphorylase secretion by infected cell lines. This appendix describes how to test for mycoplasma contamination, and also presents methods for antibiotic treatment of infected cultures.

10.1002/0471142735.ima03es21

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Citations (4)

Primary naïve and interleukin-2-activated natural killer cells do not support efficient ectromelia virus replication

Journal of General Virology (2008)

April Keim Parker Wayne M. Yokoyama John A. Corbett Nanhai G. Chen R. Mark L. Buller

Natural killer (NK) cells are known for their ability to lyse tumour cell targets. Studies of infections by a number of viruses, including poxviruses and herpesviruses, have demonstrated that NK cells are vital for recovery from these infections. Little is known of the ability of viruses to infect and complete a productive replication cycle within NK cells. Even less is known concerning the effect of infection on NK cell biology. This study investigated the ability of ectromelia virus (ECTV) to infect NK cells in vitro and in vivo. Following ECTV infection, NK cell gamma interferon (IFN-gamma) production was diminished and infected cells ceased proliferating and lost viability. ECTV infection of NK cells led to early and late virus gene expression and visualization of immature and mature virus particles, but no detectable increase in viable progeny virus. It was not unexpected that early gene expression occurred in infected NK cells, as the complete early transcription system is packaged within the virions. The detection of the secreted early virus-encoded immunomodulatory proteins IFN-gamma-binding protein and ectromelia inhibitor of complement enzymes (EMICE) in NK cell culture supernatants suggests that even semi-permissive infection may permit immunomodulation of the local environment.

Ectromelia virus

Ectromelia

NK-92

10.1099/vir.0.83205-0

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Citations (7)

Localization on a Physical Map of the NKC-Linked Cmv1 Locus Between Ly49b and the Prp Gene Cluster on Mouse Chromosome 6

The Journal of Immunology (1999)

Michael G. Brown Jun Zhang Ying Du Janis Stoll Wayne M. Yokoyama

The Cmv1 locus controls NK cell-mediated resistance to infection with murine CMV. Our recent genetic analysis of backcross mice demonstrated that the NK gene complex (NKC)-linked Cmv1 locus should reside between the Ly49 and Prp gene clusters on distal mouse chromosome 6. We have aligned yeast artificial chromosome (YAC) inserts in a contig spanning the interval between the Ly49 and Prp gene clusters. This YAC contig includes 13 overlapping YAC inserts that span more than 2 megabases (Mb) in C57BL/6 (B6) mice. Since we have identified genomic clones that span the Ly49-Prp gene region, we hypothesize that at least one should contain the Cmv1 locus. To narrow the Cmv1 critical region, we developed novel NKC genetic markers and used these to genotype informative backcross and intra-NKC recombinant congenic mouse DNA samples. These data suggest that Cmv1 resides on a single YAC insert within an interval that corresponds to a physical distance of approximately 390 kb. This high resolution, integrated physical and genetic NKC map will facilitate identification of Cmv1 and other NKC-linked loci that regulate NK cell-mediated immunity.

Yeast artificial chromosome

Congenic

Gene cluster

10.4049/jimmunol.163.4.1991

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Citations (32)

Diseases of Skeletal Muscle

Medicine & Science in Sports & Exercise (2000)

Wayne M. Yokoyama

Diseases of Skeletal MuscleEditor: WORTMANN, Robert L., MD (Univ of Oklahoma) Bibliographic Data: (ISBN: 0-7817-1614-4, Lippincott Williams & Wilkins, 2000, $99.00) 380 pages, hard cover Audiences: Muscle Researchers, Rheumatologists Subjects: Rheumatology, Physical Medicine and Rehabilitation Other Info: The book contains predominantly black-and-white illustrations, with some color illustrations. DESCRIPTION: This book is a review of skeletal muscle disorders from the rheumatologist’s perspective. PURPOSE: The purpose is to provide a broader review with greater depth than is available in standard textbooks. This is a worthy objective and the editor and contributors have achieved this goal. AUDIENCE: The editor does not clearly state the target audience but the book appears best suited for rheumatologists who deal with inflammatory myopathies and fibromyalgia. The editor and panel are experts in this field. ASSESSMENT: This is a welcome addition to the rheumatologist’s library. Written by a rheumatologist and from the perspective of a rheumatologist’s practice, the in-depth and scholarly chapters provide a useful reference for diseases of skeletal muscle. SCORE: Weighted Numerical Score: 88 - ***

10.1097/00005768-200004000-00027

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Citations (25)

Ligands for murine NKG2D display heterogeneous binding behavior

European Journal of Immunology (2002)

Leonidas N. Carayannopoulos Olga V. Naidenko Jeremy M. Kinder Emily Ho Daved H. Fremont

NKG2D transmits stimulatory signals to natural killer cells and other hematopoietic cells, leading to enhanced proliferation, cytokine secretion and target killing. Murine and human NKG2D eachrecognize five known class I-related molecules with distinct primary structures. Here, we used surface plasmon resonance to examine the binding of murine NKG2D to its cognate ligands: RAE-1B6 (a newly described C57BL/6J variant of RAE-1), RAE-1δ (common to BALB and C57BL6/J), and H60 (expressed in BALB, but not C57BL/6J). While RAE-1B6 and H60 display relatively high affinities for NKG2D with KD in the 20-30 nM range and koff in the 0.03 s–1 to 0.06 s–1 range (t1/2 approximately 10–20 s); the RAE-1δ variant binds with a lower affinity: KD of approximately 750 nM. Furthermore, RAE-1δ displays biphasic kinetics with dominant koff of approximately 0.2 s–1 (t1/2 approximately 3 s), partially explaining the lower affinity. Thus, H60 and RAE-1B6 bind NKG2D with almost identical kinetics while sharing only 20% amino acid sequence identity; whereas other RAE-1 molecules demonstrate faster dissociationand lower affinities than RAE-1B6 despite sharing 90% sequence identity. C57BL/6J mice, although not expressing the H60 gene product, retain a high-affinity ligand for NKG2D in the form of RAE-1B6.

NKG2D

10.1002/1521-4141(200203)32:3<597::aid-immu597>3.0.co;2-e

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Citations (32)