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Bruton's Tyrosine Kinase Is Required For Lipopolysaccharide-induced Tumor Necrosis Factor α Production

Nicole J. Horwood,Tara Mahon,John P. McDaid,Jamie Campbell,Hiroyuki Mano,Fionula M. Brennan,David Webster,Brian M.J. Foxwell
View Articletitled, Bruton's Tyrosine Kinase Is Required For Lipopolysaccharide-induced Tumor Necrosis Factor α Production

Differential Requirement for Rel/Nuclear Factor κB Family Members in Natural Killer T Cell Development

Vallabhapurapu Sivakumar,Kirsten J.L. Hammond,Norma Howells,Klaus Pfeffer,Falk Weih
View Articletitled, Differential Requirement for Rel/Nuclear Factor κB Family Members in Natural Killer T Cell Development

NIK-dependent RelB Activation Defines a Unique Signaling Pathway for the Development of Vα14i NKT Cells

Dirk Elewaut,Raziya B. Shaikh,Kirsten J. L. Hammond,Hilde De Winter,Andrew J. Leishman,Stephane Sidobre,Olga Turovskaya,Theodore I. Prigozy,Lisa Ma,Theresa A. Banks,David Lo,Carl F. Ware,Hilde Cheroutre,Mitchell Kronenberg
View Articletitled, NIK-dependent RelB Activation Defines a Unique Signaling Pathway for the Development of Vα14<em>i</em> NKT Cells

Normal Incidence of Diabetes in NOD Mice Tolerant to Glutamic Acid Decarboxylase

Elmar Jaeckel,Ludger Klein,Natalia Martin-Orozco,Harald von Boehmer
View Articletitled, Normal Incidence of Diabetes in NOD Mice Tolerant to Glutamic Acid Decarboxylase

Memory CD8+ T Cells Are Required for Protection from Persistent Hepatitis C Virus Infection

In Special Collection: 2020 Nobel Prize Collection
Naglaa H. Shoukry,Arash Grakoui,Michael Houghton,David Y. Chien,John Ghrayeb,Keith A. Reimann,Christopher M. Walker
View Articletitled, Memory CD8<strong><sup>+</sup></strong> T Cells Are Required for Protection from Persistent Hepatitis C Virus Infection

CD36 Mediates the Innate Host Response to β-Amyloid

Joseph B. El Khoury,Kathryn J. Moore,Terry K. Means,Josephine Leung,Kinya Terada,Michelle Toft,Mason W. Freeman,Andrew D. Luster
View Articletitled, CD36 Mediates the Innate Host Response to β-Amyloid

A Reversible Defect in Natural Killer T Cell Function Characterizes the Progression of Premalignant to Malignant Multiple Myeloma

Madhav V. Dhodapkar,Matthew D. Geller,David H. Chang,Kanako Shimizu,Shin-Ichiro Fujii,Kavita M. Dhodapkar,Joseph Krasovsky
View Articletitled, A Reversible Defect in Natural Killer T Cell Function Characterizes the Progression of Premalignant to Malignant Multiple Myeloma

Visualization of the Genesis and Fate of Isotype-switched B Cells during a Primary Immune Response

Kathryn A. Pape,Valerie Kouskoff,David Nemazee,H. Lucy Tang,Jason G. Cyster,Lina E. Tze,Keli L. Hippen,Timothy W. Behrens,Marc K. Jenkins
View Articletitled, Visualization of the Genesis and Fate of Isotype-switched B Cells during a Primary Immune Response

Transforming Growth Factor β Blocks Tec Kinase Phosphorylation, Ca2+ Influx, and NFATc Translocation Causing Inhibition of T Cell Differentiation

Chang-Hung Chen,Carole Seguin-Devaux,Nancy A. Burke,Timothy B. Oriss,Simon C. Watkins,Neil Clipstone,Anuradha Ray
View Articletitled, Transforming Growth Factor β Blocks Tec Kinase Phosphorylation, Ca<sup>2+</sup> Influx, and NFATc Translocation Causing Inhibition of T Cell Differentiation

Fractalkine Preferentially Mediates Arrest and Migration of CD16+ Monocytes

Petronela Ancuta,Ravi Rao,Ashlee Moses,Andrew Mehle,Sunil K. Shaw,F. William Luscinskas,Dana Gabuzda
View Articletitled, Fractalkine Preferentially Mediates Arrest and Migration of CD16<sup>+</sup> Monocytes

Unraveling a Revealing Paradox : Why Major Histocompatibility Complex I–signaled Thymocytes “Paradoxically” Appear as CD4+8lo Transitional Cells During Positive Selection of CD8+ T Cells

Remy Bosselut,Terry I. Guinter,Susan O. Sharrow,Alfred Singer
View Articletitled, Unraveling a Revealing Paradox <span class="subtitle-colon">: </span><span class="subtitle">Why Major Histocompatibility Complex I–signaled Thymocytes “Paradoxically” Appear as CD4<sup>+</sup>8<sup>lo</sup> Transitional Cells During Positive Selection of CD8<sup>+</sup> T Cells </span>

B7DC/PDL2 Promotes Tumor Immunity by a PD-1–independent Mechanism

Xingluo Liu,Jian Xin Gao,Jing Wen,Lijie Yin,Ou Li,Tao Zuo,Thomas F. Gajewski,Yang-Xin Fu,Pan Zheng,Yang Liu
View Articletitled, B7DC/PDL2 Promotes Tumor Immunity by a PD-1–independent Mechanism

Tumors Acquire Inhibitor of Apoptosis Protein (IAP)-mediated Apoptosis Resistance through Altered Specificity of Cytosolic Proteolysis

Xu Hong,Lu Lei,Rickard Glas
View Articletitled, Tumors Acquire Inhibitor of Apoptosis Protein (IAP)-mediated Apoptosis Resistance through Altered Specificity of Cytosolic Proteolysis

Stimulus-dependent Deacylation of Bacterial Lipopolysaccharide by Dendritic Cells

Mingfang Lu,Mei Zhang,Richard L. Kitchens,Susan Fosmire,Akira Takashima,Robert S. Munford
View Articletitled, Stimulus-dependent Deacylation of Bacterial Lipopolysaccharide by Dendritic Cells

Multistep Nature of Microvascular Recruitment of Ex Vivo–expanded Embryonic Endothelial Progenitor Cells during Tumor Angiogenesis

Peter Vajkoczy,Sabine Blum,Mathias Lamparter,Reinhard Mailhammer,Ralph Erber,Britta Engelhardt,Dietmar Vestweber,Antonis K. Hatzopoulos
View Articletitled, Multistep Nature of Microvascular Recruitment of Ex Vivo–expanded Embryonic Endothelial Progenitor Cells during Tumor Angiogenesis

H2AX Is Required for Recombination Between Immunoglobulin Switch Regions but Not for Intra-Switch Region Recombination or Somatic Hypermutation

Bernardo Reina-San-Martin,Simone Difilippantonio,Leif Hanitsch,Revati F. Masilamani,André Nussenzweig,Michel C. Nussenzweig
View Articletitled, H2AX Is Required for Recombination Between Immunoglobulin Switch Regions but Not for Intra-Switch Region Recombination or Somatic Hypermutation

Brief Definitive Report

Unmutated Immunoglobulin M Can Protect Mice from Death by Influenza Virus Infection

Yuichi Harada,Masamichi Muramatsu,Toshikatsu Shibata,Tasuku Honjo,Kazumichi Kuroda
View Articletitled, Unmutated Immunoglobulin M Can Protect Mice from Death by Influenza Virus Infection

Monocytes Heterozygous for the Asp299Gly and Thr399Ile Mutations in the Toll-like Receptor 4 Gene Show No Deficit in Lipopolysaccharide Signalling

Clett Erridge,John Stewart,Ian R. Poxton
View Articletitled, Monocytes Heterozygous for the Asp299Gly and Thr399Ile Mutations in the Toll-like Receptor 4 Gene Show No Deficit in Lipopolysaccharide Signalling