scispace - formally typeset
W

William J. Murphy

Researcher at Texas A&M University

Publications -  320
Citations -  27304

William J. Murphy is an academic researcher from Texas A&M University. The author has contributed to research in topics: Genome & Immune system. The author has an hindex of 80, co-authored 293 publications receiving 25360 citations. Previous affiliations of William J. Murphy include Pontifícia Universidade Católica do Rio Grande do Sul & Texas College.

Papers
More filters
Journal ArticleDOI

The immunobiology of natural killer cells and bone marrow allograft rejection.

TL;DR: The current issues in bone marrow transplantation and the potential clinical role of NK cell alloreactivity in the efficacy of this procedure for immunotherapy of cancer and infectious states are discussed.
Journal ArticleDOI

Nuclear gene sequences confirm an ancient link between New Zealand’s short-tailed bat and South American noctilionoid bats

TL;DR: Maximum likelihood, minimum evolution, maximum parsimony, and Bayesian posterior probabilities all provide robust support for the association of Mystacina with the South American noctilionoids.
Journal ArticleDOI

Antibodies to CD40 prevent Epstein-Barr virus-mediated human B-cell lymphomagenesis in severe combined immune deficient mice given human peripheral blood lymphocytes

TL;DR: Stimulation of CD40 by antibodies or its physiologic ligand may be of significant clinical use in the prevention ofEBV-induced B lymphomas that may arise when EBV-seropositive individuals receive immunosuppressive regimens after transplantation or in immune deficiency states, such as acquired immune deficiency syndrome.
Journal ArticleDOI

Altered T-cell receptor + CD28-mediated signaling and blocked cell cycle progression in interleukin 10 and transforming growth factor-β–treated alloreactive T cells that do not induce graft-versus-host disease

TL;DR: It is determined that IL-10 + TGF-beta-tolerant CD4(+) T cells exhibit an altered pattern of T-cell receptor (TCR) + CD28-mediated signaling and are incapable of progressing out of the G(1) phase of the cell cycle during stimulation with HLA class II disparate antigen-presenting cells.