Jing W. Zhu

TL;DR: Analysis of CD148 loss-of-function mice showed that CD148 has a positive regulatory function in B cells and macrophages, similar to the role of CD45 as a positive regulator of Src family kinases (SFKs), and suggests a level of redundancy not previously appreciated.

TL;DR: CD148 is highlighted as a global regulator of platelet activation and a novel antithrombotic drug target after basal SFK activity was found to be markedly reduced in CD148-deficient platelets, resulting in a global hyporesponsiveness to agonists that signal through SFKs, including collagen and fibrinogen.

TL;DR: The need for host cell participation in the initial step of the infection and its implications in the L. pneumophila lifestyle are discussed and real-time analysis of effector translocation suggests that effector export is rate-limited by phagocytosis.

TL;DR: Two RPTPs, CD45 and CD148, previously shown to share redundant roles in positively regulating Src family kinases (SFKs) in immunoreceptor signaling pathways in B cells and macrophages, are critical in the neutrophil response to S. aureus infection and, surprisingly, in chemoattractant-mediated chemotaxis.

TL;DR: Interestingly, CD148 levels are elevated on freshly isolated T cells from MRL lpr/lpr and CTLA-4-deficient mice, two murine models of autoimmunity, suggesting that CD148 may play an important regulatory role to control an immune response.