AI and immunology.

AI is rapidly becoming part of many aspects of daily life, with an impact that reaches all fields of research. We asked investigators to share their thoughts on how AI is changing immunology research, what is necessary to move forward, the potential and the pitfalls, and what will remain unchanged as the field journeys into a new era.

Mini-review: CREATE-ive use of primary literature in the science classroom.

CREATE (Consider, Read, Elucidate hypotheses, Analyze and interpret data, Think of the next Experiment) is a pedagogical approach for teaching and learning science through the rigorous analysis of primary scientific literature. This mini-review focuses on the tools, assignments, and in-class activities by which this strategy immerses students in the process of science and further challenges students to embody the intellectual activities of actual scientists. We highlight the innovative ways in which CREATE pedagogy encourages students to think deeply about science.

A Strategy for the Renovation of a Clinical Pathways Program.

Introduction: Clinical pathways (CPs) translate best available evidence to the local care context and intend to inform clinical decision-making, optimize care, and decrease variation. This article describes a CPs program improvement process at a free-standing academic children's hospital. Aims: (1) improve the pathway development process; (2) identify and address gaps; (3) strengthen measurement; (4) increase efficiency in cycle time to build a pathway; (5) increase multidisciplinary participation; (6) integrate into the electronic health record ; and (7) and increase pathway utilization.

MHC class II structural requirements for the association with Igalpha/beta, and signaling of calcium mobilization and cell death.

Emerging evidence indicates that in addition to their well-characterized role in antigen presentation, MHC II molecules transmit signals that induce death of APCs. Appropriately timed APC death is important for prevention of autoimmunity. Though the exact mechanism of MHC II-mediated cell death signaling is unknown, the response appears independent of caspase activation and does not involve Fas-FasL interaction.

Nkx2.2 regulates cell fate choice in the enteroendocrine cell lineages of the intestine.

Nkx2.2 is a homeodomain-containing transcription factor essential for pancreatic islet cell specification. In this study we investigate the role of Nkx2.

A new population of cells lacking expression of CD27 represents a notable component of the B cell memory compartment in systemic lupus erythematosus.

Human memory B cells comprise isotype-switched and nonswitched cells with both subsets displaying somatic hypermutation. In addition to somatic hypermutation, CD27 expression has also been considered a universal memory B cell marker. We describe a new population of memory B cells containing isotype-switched (IgG and IgA) and IgM-only cells and lacking expression of CD27 and IgD.

B cell receptor signaling in human systemic lupus erythematosus.

Purpose Of Review: The purpose of this review is to inform the scientific community of the most recent findings surrounding B cell receptor signaling function in human systemic lupus erythematosus and how altered B cell signaling may explain the characteristic hyperactivity of B cells in active disease and contribute to its pathogenesis.

Recent Findings: B cell receptor signaling is abnormal in patients with active systemic lupus erythematosus as demonstrated by increased calcium flux and global B cell hyperactivity. Altered signaling has been explained by a variety of factors such as defective FcgammaRIIB signaling, decreased expression of the protein tyrosine kinase Lyn, and increased serum levels of B lymphocyte stimulator.

Germinal center exclusion of autoreactive B cells is defective in human systemic lupus erythematosus.

Breach of B cell tolerance is central to the pathogenesis of systemic lupus erythematosus (SLE). However, how B cell tolerance is subverted in human SLE is poorly understood due to difficulties in identifying relevant autoreactive B cells and in obtaining lymphoid tissue. We have circumvented these limitations by using tonsil biopsies to study autoreactive B cells (9G4 B cells), whose regulation is abnormal in SLE.

Rituximab improves peripheral B cell abnormalities in human systemic lupus erythematosus.

Objective: B lymphocyte depletion has recently emerged as a promising approach to the treatment of systemic lupus erythematosus (SLE). As part of a phase I/II dose-ranging trial of rituximab in the treatment of SLE, we evaluated the fate of discrete B cell subsets in the setting of selective depletion by anti-CD20 monoclonal antibody and during the B cell recovery phase.

Methods: B cell depletion and phenotype were examined by flow cytometry of peripheral blood mononuclear cells for CD19, CD20, CD27, IgD, and CD38 expression.

B cell antigen receptor signaling 101.

All cells continually survey their environment and make decisions based on cues encountered. This requires specific receptors that detect such cues, then transduce signals that initiate the appropriate responses. B lymphocytes provide an archetypal model for such 'adaptive' cellular responses, where signals transmitted by the B cell Ag-receptor (BCR) influence not only cellular selection, maturation, and survival, but are imperative in generating the ultimate effector function of B cells, i.

Lupus IgG VH4.34 antibodies bind to a 220-kDa glycoform of CD45/B220 on the surface of human B lymphocytes.

Anti-lymphocyte autoantibodies are a well-recognized component of the autoimmune repertoire in human systemic lupus erythematosus (SLE) and have been postulated to have pathogenic consequences. Early studies indicated that IgM anti-lymphocyte autoantibodies mainly recognized T cells and identified CD45, a protein tyrosine phosphatase of central significance in the modulation of lymphocyte function, as the main antigenic target on T cells. However, more recent work indicates that lupus autoantibodies can also recognize B cells and that CD45 may also represent their antigenic target.

Ghrelin cells replace insulin-producing beta cells in two mouse models of pancreas development.

The pancreatic islet is necessary for maintaining glucose homeostasis. Within the pancreatic islet, the homeodomain protein Nkx2.2 is essential for the differentiation of all insulin-producing beta cells and a subset of glucagon-producing alpha cells (1).