M
Matthew G. Booty
Researcher at University of Massachusetts Medical School
Publications - 21
Citations - 3584
Matthew G. Booty is an academic researcher from University of Massachusetts Medical School. The author has contributed to research in topics: T cell & Cytotoxic T cell. The author has an hindex of 15, co-authored 19 publications receiving 3187 citations. Previous affiliations of Matthew G. Booty include National Institutes of Health & Brigham and Women's Hospital.
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Journal ArticleDOI
STAT4 and the Risk of Rheumatoid Arthritis and Systemic Lupus Erythematosus
Elaine F. Remmers,Robert M. Plenge,Annette Lee,Robert R. Graham,Robert R. Graham,Geoffrey Hom,Timothy W. Behrens,Paul I.W. de Bakker,Julie M. Le,Hye Soon Lee,Hye Soon Lee,Franak Batliwalla,Wentian Li,Seth L. Masters,Matthew G. Booty,John P. Carulli,Leonid Padyukov,Lars Alfredsson,Lars Klareskog,Wei V. Chen,Christopher I. Amos,Lindsey A. Criswell,Michael F. Seldin,Daniel L. Kastner,Peter K. Gregersen +24 more
TL;DR: A haplotype of STAT4 is associated with increased risk for both rheumatoid arthritis and systemic lupus erythematosus, suggesting a shared pathway for these illnesses.
Journal ArticleDOI
An autoinflammatory disease with deficiency of the interleukin-1-receptor antagonist
Ivona Aksentijevich,Seth L. Masters,Polly J. Ferguson,Paul Dancey,Joost Frenkel,Annet van Royen-Kerkhoff,R. M. Laxer,Ulf Tedgård,Edward W. Cowen,Tuyet-Hang Pham,Matthew G. Booty,Jacob D. Estes,Netanya G. Sandler,Nicole Plass,Deborah L. Stone,Maria L. Turner,Suvimol Hill,John A. Butman,Rayfel Schneider,Paul Babyn,Hatem El-Shanti,Elena Pope,Karyl S. Barron,Xinyu Bing,Arian Laurence,Chyi-Chia Richard Lee,Dawn Chapelle,Gillian I. Clarke,Kamal Ohson,Marc Nicholson,Massimo Gadina,Barbara Yang,Benjamin D. Korman,Peter K. Gregersen,P. Martin van Hagen,A. Elisabeth Hak,Marjan Huizing,Proton Rahman,Daniel C. Douek,Elaine F. Remmers,Daniel L. Kastner,Raphaela Goldbach-Mansky +41 more
TL;DR: The term deficiency of the interleukin-1-receptor antagonist, or DIRA, is proposed to denote this autosomal recessive autoinflammatory disease caused by mutations affecting IL1RN, resulting in life-threatening systemic inflammation with skin and bone involvement.
Journal ArticleDOI
Apoptosis is an innate defense function of macrophages against Mycobacterium tuberculosis
Samuel M. Behar,Martin Cj,Matthew G. Booty,Tomoyasu Nishimura,Xiaomin Zhao,Huixian Gan,Maziar Divangahi,Maziar Divangahi,Heinz G. Remold +8 more
TL;DR: It is demonstrated that during mycobacterial infection, cell death is regulated by the eicosanoids, prostaglandin E2 (proapoptotic) and lipoxin (LX)A4 (pronecrotic) and, although PGE2 protects against necrosis, virulent Mtb induces LXA4 and inhibits P GE2 production.
Journal ArticleDOI
In search of a new paradigm for protective immunity to TB
Cláudio Nunes-Alves,Matthew G. Booty,Stephen M. Carpenter,Pushpa Jayaraman,Alissa C. Rothchild,Samuel M. Behar +5 more
TL;DR: Recent advances in the understanding of the immune control of M. tuberculosis are discussed and how this knowledge could be used for vaccine design and evaluation is discussed.
Journal ArticleDOI
Efferocytosis Is an Innate Antibacterial Mechanism
Constance J. Martin,Matthew G. Booty,Matthew G. Booty,Tracy R. Rosebrock,Cláudio Nunes-Alves,Cláudio Nunes-Alves,Danielle Desjardins,Iris Keren,Sarah M. Fortune,Heinz G. Remold,Samuel M. Behar,Samuel M. Behar +11 more
TL;DR: In this article, the authors show that after apoptosis, M. tuberculosis is killed only after efferocytosis, indicating that apoptosis itself is not intrinsically bactericidal but requires subsequent phagocytic uptake and lysosomal fusion of the apoptotic body harboring the bacterium.