Annotated Bibliography of Research in the Teaching of English

Since 2003, RTE has published the annual “Annotated Bibliography of Research in the Teaching of English,” and we are proud to share these curated and annotated citations once again. The goal of the annual bibliography is to offer a synthesis of the research published in the area of English language arts within the past year that may be of interest to RTE readers. Abstracted citations and those featured in the “Other Related Research” sections were published, either in print or online, between June 2019 and June 2020. The bibliography is divided into nine subject area sections. A three-person team of scholars with diverse research interests and background experiences in preK–16 educational settings reviewed and selected the manuscripts for each section using library databases and leading empirical journals. Each team abstracted significant contributions to the body of peer-reviewed studies that addressed the current research questions and concerns in their topic area

Major histocompatibility complex class I molecules protect motor neurons from astrocyte-induced toxicity in amyotrophic lateral sclerosis

Astrocytes isolated from individuals with amyotrophic lateral sclerosis (ALS) are toxic to motor neurons (MNs) and play a non–cell autonomous role in disease pathogenesis. The mechanisms underlying the susceptibility of MNs to cell death remain unclear. Here we report that astrocytes derived from either mice bearing mutations in genes associated with ALS or human subjects with ALS reduce the expression of major histocompatibility complex class I (MHCI) molecules on MNs; reduced MHCI expression makes these MNs susceptible to astrocyte-induced cell death. Increasing MHCI expression on MNs increases survival and motor performance in a mouse model of ALS and protects MNs against astrocyte toxicity. Overexpression of a single MHCI molecule, HLA-F, protects human MNs from ALS astrocyte–mediated toxicity, whereas knockdown of its receptor, the killer cell immunoglobulin-like receptor KIR3DL2, on human astrocytes results in enhanced MN death. Thus, our data indicate that, in ALS, loss of MHCI expression on MNs renders them more vulnerable to astrocyte-mediated toxicity