This Commentary discusses an article by Lossius et al. [Eur. J. Immunol. 2014. 44: 3439-52], in which the authors dissect the TCR repertoire in multiple sclerosis (MS). The authors show that the TCR repertoire in CSF is distinct from that of blood and enriched in EBV-reactive CD8⁺ T cells.

The inositol phosphatase SHIP limits antigen-mediated B cell activation to prevent autoimmune phenomena. SHIP action is believed to require BCR coreceptors such as FcγRIIb. Manno et al. now show that the BCR can engage SHIP directly by virtue of Igα/Igβ ITAMs and the Dok3/Grb2 protein adaptor module. The BCR-autonomous feed-back inhibition can balance B cell activation independently of additional signal input.

A single instillation of papain rapidly induces IL-1α and IL-1β secretion by epithelial cells. This signal induces inflammation characterized by neutrophils and eosinophils recruitment in lung via IL-1R/MyD88 signaling pathway in DC, macrophages, T cells and epithelial cells. In a second time, IL-33 is secreted and take part in lung inflammation via ST2/MyD88 pathway though ILC2.

Factors in the inflammatory milieu of rheumatoid arthritis (RA) induce polymorphonuclear cells to undergo neutrophil extracellular trap formation. RA neutrophil extracellular traps serve as a source of neoantigens complexed with DNA to promote the activation and cytokine release by DCs, leading in the production of IFN-γ by T cells. This cascade contributes in the RA autoimmune responses.

Using cDNA libraries from wild-type pre-BI-cells genes were screened that cooperate with c-myc in pre-BI-cells transformation. Only one transforming gene (Exosc1) was detected in vitro, while fivefold more genes were detected in in vivo. Our data indicates that the microenvironment provided by the host contributes to cell transformation in vivo.

CD40L is absolutely essential for an effective pathogen clearance, but CD40L expressed by pathogen-specific CD8⁺ T cells does not regulate immune responses and CD8⁺ T-cell memory formation in acute viral and bacterial infections.2

Recognition of Mycobacterium tuberculosis via TLR-2 drives activation of the mammalian target of rapamycin (mTOR)/AKT signaling cascade. This contributes to the upregulation of glycolysis and the metabolic changes needed to fuel energy demands and drive transcriptional changes that account for functional outputs like cytokine production.

During the peak of chronic intestinal Trichuris muris infection in mice, we show enhanced, IFN-γ-driven proliferation/differentiation of hematopoietic stem cells (HSC) and concurrent accumulation of IFN-γ+ T cells in the bone marrow. These results provide insight into the systemic effects of intestinally-restricted helminth infections on the bone marrow.

In asymptomatic posttransplant renal transplant recipients, persistent, and active CMV expands a population of FcRγ^–LIR-1⁺NKG2C^– NK cells, which on cross-linking with CMV antibody displays increased antibody dependent cell cytotoxicity, i.e. increased expression of CD107a and TNF-α.

Mutations in skin barrier function genes and increased neonatal Th2 responses are risk factors for the development of atopic dermatitis (AD). Using a mouse model of AD, we demonstrate that genetic lesions in these two pathways cooperate in generating a more severe and earlier onset allergic skin inflammation.

House dust mite triggers an Irf3-dependent antiviral-like transcriptional program in lung resident type 2 conventional dendritic cells. This program promotes Th2 responses by increasing CD86 gene expression and hence CD86 costimulation. .

The initial immunization with Collagen II (CII) and CFA induces Tenascin-C release and TLR4 activation. TLR4 activation on macrophages and osteoclasts promotes joint inflammation and bone erosion. Joint inflammation and damage increase the production of numerous endogenous TLR4 ligands (immune complexes containing citrullinated fibrinogen (cFb-IC), Tenascin-C, S100A8/A9, and HMGB1). Endogenous TLR4 ligands promote joint damage, sustaining disease progression.

IFN-λ mediated signal transduction is functionally retained in TYK2 deficient human cell lines. This, together with functional NK cell responses in vitro, might account for the absence of severe viral infections in patients with TYK2 deficiency despite the lack of IFN-α mediated signal transduction.

ABC are non follicular, non marginal zone B cells that accumulate with aging that exhibit a memory phenotype (CD80hi/CD73hi). These cells exhibit enhanced T-cell priming and impair immune modulation to allografts. .

pDCs internalize and process exogenous antigens but they cannot directly interact with cognate CD4⁺ T cells. Instead they transfer the antigen to LN-resident conventional DCs. Such antigen transfer in steady-state conditions cause abortive proliferation of cognate CD4⁺ T cells that results in immune tolerance.

OPN, generally known to promote tumor growth, can also inhibit tumor growth based on TRAMP prostate tumor models. NK cells are effectors that show enhanced migration by OPN. However, the protective role of OPN is not exerted to B16 tumor due to low chemokine expression by B16 cells.