Immunology

Cover image for Vol. 148 Issue 4

Edited By: Danny Altmann

Impact Factor: 4.078

ISI Journal Citation Reports © Ranking: 2015: 44/150 (Immunology)

Online ISSN: 1365-2567

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  • Emerging role of microRNAs in regulating macrophage activation and polarization in immune response and inflammation

    Emerging role of microRNAs in regulating macrophage activation and polarization in immune response and inflammation

    Role of microRNAs (miRNAs) in the regulation of macrophage activation and polarization. Names in double-strand refer to microRNAs; arrows depicting activation or inhibition between the indicators mean that the upper indicator normally activates or inhibits the one below; solid line implies that the relationship between two indicators is direct, and dotted line implies the relationship between two indicators is indirect in the regulation of macrophage polarization.

  • Immune polarization by hookworms: taking cues from T helper type 2, type 2 innate lymphoid cells and alternatively activated macrophages

    Immune polarization by hookworms: taking cues from T helper type 2, type 2 innate lymphoid cells and alternatively activated macrophages

    Protective cytokines and effector mechanisms in the context of hookworm infections. (a) The site of tissue injury releases an array of cytokines that, in turn promotes release of host protective cytokines (gray box) from innate and adaptive lymphocytes and myeloid populations. (b) Established mechanisms of worm clearance in murine skin (1) and intestine (2,3).

  • Endogenous TWEAK is critical for regulating the function of mouse uterine natural killer cells in an immunological model of pregnancy loss

    Endogenous TWEAK is critical for regulating the function of mouse uterine natural killer cells in an immunological model of pregnancy loss

    Co-localization of tumour necrosis factor-like weak inducer of apoptosis (TWEAK) and fibroblast growth factor-inducible molecule (Fn14) with uterine natural killer (uNK) cells from lipopolysaccharide (LPS) -treated and untreated mice at the indicated gestation days. The percentage of TWEAK-positive (a) and Fn14-positive cells (c) of the Dolichos biflorus agglutinin (DBA) -positive uNK cells from LPS-treated and untreated mice at the indicated gestation days. Representative fluorescence photomicrographs show the co-localization of TWEAK (b) and Fn14 (d) in the uNK cells in the endometrium of a pregnant mouse. Mouse uNK cells in the 4% PFA-fixed, paraffin-embedded tissues were labelled with DBA lectin and rabbit anti-mouse TWEAK or rabbit anti-mouse Fn14 antibodies, and then stained with Cy3-tagged streptavidin for the uNK cells or an FITC-conjugated goat anti-rabbit secondary antibody for TWEAK or Fn14. Nuclei were labelled with DAPI. Scale bars = 200 μm.

  • T-bet as a key regulator of mucosal immunity

    T‐bet as a key regulator of mucosal immunity

    The pathogenic pathways implicated in TRUC colitis model. The first detectable perturbation in TRUC colitis is the increased activation of CD11C+MHCII+CD103− dendritic cells (DCs) that produce increased tumour necrosis factor (TNF) in the absence of T-bet. TNF signaling leads to epithelial cell apoptosis and compromise of epithelial membrane integrity – this initiates colitis and is accompanied by the outgrowth of pathogenic microbiota. Initially, disease is driven solely by TNF, though after several weeks, CD11C+MHCII+CD103−DC produced interleukin-23 (IL-23) and TNF activate type 3 innate lymphoid cells (ILC3s). ILC3s produce inflammatory cytokines, including IL-17, which synergizes with TNF to recruit neutrophils to the colonic lamina propria. Hence, although TNF is key in early stages of pathogenesis, later stages are driven by ILC activation and neutrophil recruitment. Contributing to pathology is the selective outgrowth of the Gram-negative pathogenic microbiota induced by an undefined deficiency in the innate immune system (a, b). This outgrowth of pathogenic microbial species is detected by mucosal DCs, which produce IL-23 and increased levels of TNF in the absence of T-bet (c), leading to epithelial cell apoptosis and increased ILC3 activation (d). Activated ILC3s produce IL-17 and IL-22 leading to further mucosal pathology from neutrophil recruitment and activation.

  • Illuminating vitamin D effects on B cells – the multiple sclerosis perspective

    Illuminating vitamin D effects on B cells – the multiple sclerosis perspective

    Schematic overview of the plasma cell generation in vitro and in vivo, with the hypothesized vitamin D effects explaining the tube-versus-body paradox. (a) In vitro activation of B cells in the presence of vitamin D inhibits plasma cell generation and the subsequent immunoglobulin production. No germinal centres (GCs) and survival niches (SNs) are present. (b) In vivo plasma cell generation outside the central nervous system may occur outside or (in most cases) within lymph secondary lymphoid tissue/GCs. In case GC processes (class switch recombination/somatic hypermutation) are involved, plasma blasts may be generated with a selection advantage for becoming long-lived plasma cells. Those reside in survival niches, enabling ongoing immunoglobulin production (stable immunoglobulin levels). (c) In vivo plasma cell generation within the central nervous system probably takes place in ectopic lymphoid follicless. Here functionally inferior GCs compared with the ones of secondary lymphoid tissue, generate plasma blasts without the selection advantage for becoming long-lived plasma cells. Abbreviations: B, B cell (naive/memory); PB, plasma blast; PC, plasma cell; CNS, central nervous system; SLT, secondary lymphoid tissue; TZ, T-cell zone; GC, germinal centre; Bm, memory B cell; PCsl, short-lived plasma cell; PCll, long-lived plasma cell; SN, survival niche; ELFs, ectopic lymphoid follicles

  • Single-cell technologies to study the immune system

    Single‐cell technologies to study the immune system

    The complexity of the blood cell populations has grown in parallel with the development of always more sophisticated technology. From the discovery of red blood cells in 1658 by the Dutch naturalist, Jan Swammerdam, almost 200 years passed until the identification of leucocytes (1843) by two independent physicians from England and France establishing the beginning of haematology as a new field in medicine. The molecular characterization of the leucocytes required the advent of flow cytometry (1960) and monoclonal antibodies (1975). The latter were a crucial tool for the discrimination of CD4+ and CD8+ T helper cells. In the next decades the scenario of CD4+ T helper cells became more and more complicated with the discovery of distinct subclasses. In 1986 Mosman and Coffman revealed the existence of two functional subsets, termed T helper 1 (Th1) and T helper 2 (Th2). In 1995 Dr Sakaguchi discovered another specific subpopulation of T cells, named regulatory T (Treg) cells, that were specialized for immunosuppression. More recently other subsets have been isolated named Th17 (2005), Th9 (2008) and Th22 (2009). Finally, single-cell RNA-sequencing has revealed the existence of a subpopulation of steroid-producing cells within the Th2 compartment.

  • Microbiota and host immune responses: a love–hate relationship

    Microbiota and host immune responses: a love–hate relationship

    The microbiota affects local and systemic immunity. The intestine (1) contains the greatest number and diversity of microbiota members. Proteobacteria, specifically Sutterella, alter faecal IgA levels, likely through degradation of SIgA. SFB also alter IgA levels by promoting the expansion of germinal centres and inducing IgA-secreting cells in Peyer's patches, isolated lymphoid follicles, and tertiary lymphoid tissue. MHCII-dependent SFB antigen presentation on intestinal DCs induces Th17 cell differentiation, while MHCII-dependent SFB antigen presentation by ILCs constrains Th17 cell differentiation. The intestinal microbiota also influences systemic immunity, including the number and function of circulating neutrophils (2) as well as constraining iNKT levels in the lung (3) and colon (1). DC, dendritic cell; ILCs, innate lymphoid cells; iNKT, invariant natural killer T cell; SFB, segmented filamentous bacteria; SIgA, secretory immunoglobulin A; Th17, T helper 17 lymphocyte; Treg, T regulatory lymphocyte.

  • Emerging role of microRNAs in regulating macrophage activation and polarization in immune response and inflammation
  • Immune polarization by hookworms: taking cues from T helper type 2, type 2 innate lymphoid cells and alternatively activated macrophages
  • Endogenous TWEAK is critical for regulating the function of mouse uterine natural killer cells in an immunological model of pregnancy loss
  • T‐bet as a key regulator of mucosal immunity
  • Illuminating vitamin D effects on B cells – the multiple sclerosis perspective
  • Single‐cell technologies to study the immune system
  • Microbiota and host immune responses: a love–hate relationship

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