Frailein muṭer : roman

Ernsṭ Georgi.

Dirnfurṭer prifilegirṭe tzaiṭung

Nebent.: Dyhernfurter privilegierthe Zeitung

Shalom ʿAlekhem : zayne ṿikhṭigsṭe ṿerḳ, zayn humor un zayn orṭ in der idisher liṭeraṭur

Sh. Niger

In milḥome-tzaiṭen : (bleṭer fun a ṭage-buch)

fun Šmarje Lewin

Ms. hebr. oct. 53 - Sefer Beʼer Yitsḥaḳ

Vorbesitzer: Lyon Benedek Gaudechaux; Michel Godchaux; Abraham Merzbacher

Fun der uralṭer tzaiṭ biz'n goles Bovl

H. Gretz [[Elektronische Ressource]] : Bd. 1

Noṭitsn fun Ṿarsheṿer geṭo

ʿEmanuʾel Ringelblum

Geshikhṭe fun alṭerṭum : lernbukh farn 5-ṭn un 6-ṭn ḳlas fun der miṭlshul

unṭer der red. funem ... A. Ṿ. Mishulin. Yidish M. Iṭḳoviṭsh

Moris Shṿarts un der Idisher ḳunsṭ ṭeaṭer

A. H. Bialin

Fun Poyln biz Ṭerḳay : reporṭazshn

L. Malʾakh

Mutation of the ER retention receptor KDELR1 leads to cell-intrinsic lymphopenia and a failure to control chronic viral infection

Endoplasmic reticulum (ER)-resident proteins are continually retrieved from the Golgi and returned to the ER by Lys-Asp-Glu-Leu (KDEL) receptors, which bind to an eponymous tetrapeptide motif at their substrate's C terminus. Mice and humans possess three paralogous KDEL receptors, but little is known about their functional redundancy, or if their mutation can be physiologically tolerated. Here, we present a recessive mouse missense allele of the prototypical mammalian KDEL receptor, KDEL ER protein retention receptor 1 (KDELR1). Kdelr1 homozygous mutants were mildly lymphopenic, as were mice with a CRISPR/Cas9-engineered frameshift allele. Lymphopenia was cell intrinsic and, in the case of T cells, was associated with reduced expression of the T-cell receptor (TCR) and increased expression of CD44, and could be partially corrected by an MHC class I-restricted TCR transgene. Antiviral immunity was also compromised, with Kdelr1 mutant mice unable to clear an otherwise self-limiting viral infection. These data reveal a nonredundant cellular function for KDELR1, upon which lymphocytes distinctly depend.