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Richard Malley

Researcher at Boston Children's Hospital

Publications -  162
Citations -  9923

Richard Malley is an academic researcher from Boston Children's Hospital. The author has contributed to research in topics: Streptococcus pneumoniae & Antigen. The author has an hindex of 49, co-authored 147 publications receiving 9131 citations. Previous affiliations of Richard Malley include Brigham and Women's Hospital & University of California, Los Angeles.

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Serotype replacement in disease after pneumococcal vaccination

TL;DR: The magnitude of serotype replacement in disease can be attributed, in part, to a combination of lower invasiveness of the replacing serotypes, biases in the pre-vaccine carriage data (unmasking), and bias in the disease surveillance systems that could underestimate the true amount of replacement.
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Recognition of pneumolysin by Toll-like receptor 4 confers resistance to pneumococcal infection.

TL;DR: The interaction of pneumolysin with TLR4 is critically involved in the innate immune response to pneumococcus and is found to stimulate tumor necrosis factor-α and IL-6 release in wild-type macrophages but not in macrophage from mice with a targeted deletion of the cytoplasmic TLR-adapter molecule myeloid differentiation factor 88, suggesting the involvement of the TLRs in pneumoly sin recognition.
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Interleukin-17A Mediates Acquired Immunity to Pneumococcal Colonization

TL;DR: It is shown that intranasal immunization of mice with pneumococci confers CD4+ T cell–dependent, antibody- and serotype-independent protection against colonization, and that IL-17A mediates pneumococcal immunity in mice and probably in humans; its elicitation in vitro could help in the development of candidate pneumococCal vaccines.
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CD4+ T cells mediate antibody-independent acquired immunity to pneumococcal colonization

TL;DR: It is found that immunity to pneumococcal colonization can be induced in the absence of antibody, independent of the capsular type, and this protection requires the presence of CD4(+) T cells at the time of challenge.