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The chaperone protein BiP forms complexes with Ire1 and Perk that dissociate when unfolded proteins bind to BiP to activate the unfolded protein response in the ER.

Self-reactive B cells downregulate the IgM but not the IgD B cell receptor, and this serves as a critical tolerance mechanism because IgD is less sensitive to bona fide endogenous antigens than IgM.

Plasmodium-specific atypical memory B cells generated to naturally (mosquito) transmitted rodent malaria infection are short-lived activated B cells, and do not prevent resolution of infection or generation of long-lived memory.

HLA class I-disease associations have been studied for decades; a new approach for investigating the underlying mechanism can overcome past problems with interpretation and help to understand the etiology of human diseases.

Structure, dynamics, and mutation of a gamete fusion protein and comparisons to viral homologues suggest that after trimerization the domain bearing the membrane-inserting fusion loops can pivot with respect to the trimer 3-fold axis.

Human CRACR2A insufficiency underlies progressive loss of immune competence by uncoupling TCR activation from Ca2+ and MAPK signaling and should be included within the group of combined immunodeficiency disorders in the IEI classification.

The scaffold protein Kidins220 regulates the development of λLC B cells by supporting B cell precursor survival and optimizing pre‑BCR and BCR signaling.

Microbial-sensing TLRs drive responses to the microbiota, while nucleic-acid sensing TLRs control responses to endogenous ligands, revealing novel regulation of B-1a responses through integrated BCR/TLR mediated activation.

Biophysical differential adhesion principles drive non-canonical, zippering mechanisms in vivo, regulating precise neurite placement, and synaptic specificity within Caenorhabditis elegans brain bundles.

A single-nucleotide I232T polymorphic change in FcγRIIB's transmembrane domain bends FcγRIIB's ectodomains toward cell membrane to allosterically hinder FcγRIIB's ligand association, providing novel molecular mechanism for functional loss of FcγRIIB-I232T.