Immunology

Cover image for Vol. 150 Issue 3

Edited By: Danny Altmann

Impact Factor: 4.078

ISI Journal Citation Reports © Ranking: 2015: 44/151 (Immunology)

Online ISSN: 1365-2567

Featured

  • CD4+ and CD8+ T-cell immunity to Dengue – lessons for the study of Zika virus

    CD4+ and CD8+ T‐cell immunity to Dengue – lessons for the study of Zika virus

    Schematic representation of T-cell priming during dengue virus (DENV) and Zika virus (ZIKV) infection and acquisition of tissue-homing receptors by virus-specific T cells. (a) DENV enters the host through the bite of an infected Aedes mosquito, infects local antigen-presenting cells, which then migrate to skin-draining lymph nodes (LN) and prime virus-specific T cells. Dengue-infected, skin-derived antigen-presenting cells imprint expression of the skin-homing receptor cutaneous lymphocyte-associated antigen (CLA) on the activated T cells, such that CLA+ T cells preferentially return to the skin tissue (through the blood). During a secondary DENV infection virus-specific T cells that may already be present in the skin can mount an immediate effector response. From the skin-draining lymph nodes virus-infected cells spread systemically to other lymph nodes, where they can activate more virus-specific T cells, and through the bloodstream where the virus gains access to other tissues capable of sustaining its replication. Primed T cells expressing tissue-specific homing receptors may also gain access to the corresponding infected tissue where they mediate viral clearance by targeting virus-infected cells but may also contribute to tissue damage. For example, DENV was shown to infect cells in the liver and DENV-specific T cells expressing the putative liver-homing chemokine receptor CXCR6 have been identified in the blood of patients with acute dengue. (b) We speculate that during a ZIKV infection virus-specific T cells are similarly primed in skin-draining lymph nodes, up-regulate CLA and subsequently migrate back to the skin. ZIKV spreads systemically through the bloodstream and may infect cells in other tissues, for example the virus displays tropism for neuronal cells of adults or neuronal progenitor cells in the brain of a developing fetus.

  • Antigen processing and immune regulation in the response to tumours

    Antigen processing and immune regulation in the response to tumours

    Altered antigen presentation in tumour immune escape. In the early stages of tumour growth, cells display pMHC I complexes at the cell surface, often presenting tumour associated antigens to CD8+ CTL. This recognition allows immune mediated elimination and control of the tumour to occur and is supported by anti-tumourigenic properties of the surrounding stroma. Over time, however, the components of the antigen presentation pathway are altered, resulting in a loss of pMHC I displayed on tumour cells. In addition, the surrounding stroma and other immune cells display pro-tumourigenic properties, supporting tumour immune escape and resulting in growth and invasion of the tumour.

  • Dendritic cells and adipose tissue

    Dendritic cells and adipose tissue

    Schematic depicting adipose tissue homeostasis and its response in obesity. Under normal/lean conditions, immune cells and adipocytes work in cooperation to develop a tolerogenic milieu to maintain tissue homeostasis. In response to obesity-induced chronic inflammation, immune cells including dendritic cells (DC) and macrophages are recruited to adipose tissue, promoting a pro-inflammatory response. Dotted black arrows indicate possible transcriptional and systemic regulation of DC, which may result in anti- or pro-inflammatory responses. HIF-1α, hypoxia-inducible factor-1α; KLF4, Kruppel-like factor 4; IL-4, interleukin-4; PPARγ, peroxisome proliferator-activated receptor γ; TGF-β, transforming growth factor-β; TNF-α, tumour necrosis factor-α.

  • Increased expression of TACI on NOD B cells results in germinal centre reaction anomalies, enhanced plasma cell differentiation and immunoglobulin production

    Increased expression of TACI on NOD B cells results in germinal centre reaction anomalies, enhanced plasma cell differentiation and immunoglobulin production

    B-cell activating factor (BAFF) is present in non-obese diabetic (NOD) germinal centres (GCs). Representative images from immunofluorescence staining of follicles and GCs as indicated in the figure. Spleen sections from unimmunized and immunized NOD and B6 mice were stained for GCs and BAFF (n = 4 mice per group).

  • Innate lymphoid cell regulation of adaptive immunity

    Innate lymphoid cell regulation of adaptive immunity

    Innate lymphoid cells from groups 2 (ILC2) and 3 (ILC3) reside at key sites of lymphocyte traffic in secondary lymphoid tissue. Cartoon showing the location of ILC2 and ILC3 populations in lymph nodes where both populations reside in the interfollicular spaces and at the interface of the B-cell and T-cell zones. This location facilitates potential interactions with (1) subscapular sinus macrophages located in the immediate vicinity; (2) activated dendritic cells (DCs) entering through the afferent lymph; (3) activated lymphocytes migrating to this region; (4) memory cells recirculating through the tissue.

  • Modulation of antigen processing by haem-oxygenase 1. Implications on inflammation and tolerance

    Modulation of antigen processing by haem‐oxygenase 1. Implications on inflammation and tolerance

    Carbon monoxide (CO) impairs the endosome-to-lysosome pathway to soluble antigens in myeloid cells. (a) After the extracellular antigen is captured, it fuses with Rab5+ early endosomes. After that, these vesicles can fuse with proteasome/MHC-I/TAP-containing endosomes, which drive cross-presentation. In parallel, antigen-containing Rab5+ vesicles can fuse with Rab7+ endosomes to form late endosomes and then, sequentially, they can fuse with lysosomes (Lamp1+). These lysosomes harbour a full repertoire of MHC molecules that receive and present the small peptides obtained after the antigen is processed by lysosomal proteases. Once haem oxygenase 1 (HO-1) is over-expressed and CO is produced, there is an interference in the fusion between antigen-containing late endosomes and lysosomes so compromising the correct antigen processing and antigen presentation to T cells. No effect of CO over cross-presentation has been observed. (b) (i) Under local presence of pathogen-associated molecular pattern (PAMPs); either by soluble molecules or presence of pathogens, dendritic cells (DCs) become activated. After binding the Toll like receptor 4/ myeloid differentiation factor 2 (TLR4/MD2) complex, LPS induces DC maturation by up-regulation of co-stimulatory molecules and secretion of cytokines. In addition, PAMPs cause local tissue damage and release of self- and non-self-antigens. (ii) Resident DCs capture soluble antigens presenting them to local T cells (something also observed in autoimmunity and graft rejection). Antigen-containing mature DCs can travel to secondary lymphoid organs and activate antigen-specific naive T cells. (iii) After PAMPs exposure [or treatment with cobalt protoporphyrin IX (CoPP), for example], DCs over-express HO-1, degrade haem-group and produce CO. This process will modulate the immunogenicity of DCs recovering their initial homeostasis. (iv) CO-producing mature DCs will lose their capacity to process antigens through the endosome-to-lysosome pathway. In addition, DCs reduce their secretion of cytokines. (v) Finally, mature DC-dependent innate and adaptive immune inflammation is suppressed. Tissue homeostasis is recovered and pathologies caused by PAMPs and either foreign or self-antigens are restricted.

  • Distinct expression of interferon-induced protein with tetratricopeptide repeats (IFIT) 1/2/3 and other antiviral genes between subsets of dendritic cells induced by dengue virus 2 infection

    Distinct expression of interferon‐induced protein with tetratricopeptide repeats (IFIT) 1/2/3 and other antiviral genes between subsets of dendritic cells induced by dengue virus 2 infection

    Immunofluorescence assay of IFN-induced protein with tetratricopeptide repeats (IFIT) proteins in primary human monocyte-derived dendritic cells (IMMoDC) and immature MUTZ-3-derived DC (IMDC) cultures 48 hr after dengue virus 2 (DENV2) infection. After DENV2 infection, DENV antigen E protein was detectable in a small proportion of the IMMoDC culture (a,c,e) and IMDC culture (g,i,k). IFIT1, IFIT2 and IFIT3 proteins had low basal expression levels in the mock IMMoDC culture (b,d,f). Upon DENV2 infection, intensive expression of IFIT proteins was detected in the neighbouring uninfected IMMoDCs but not in infected IMMoDCs (a,c,e). Naive IMDCs had stronger expression of IFIT1, IFIT2 and IFIT3 proteins (h,j,l) compared with naive IMMoDCs (b,d,f). The infected IMDCs had higher expression levels of IFIT1, IFIT2 and IFIT3 proteins (g,i,k) compared with bystander IMDCs in the same culture (h,j,l). Blue: DAPI; green: anti-DENV E-FITC; red: anti-IFIT1/anti-IFIT2/anti-IFIT3-Texas Red; white arrowheads: DENV2-infected cells; yellow arrowheads: bystander cells.

  • 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

  • CD4+ and CD8+ T‐cell immunity to Dengue – lessons for the study of Zika virus
  • Antigen processing and immune regulation in the response to tumours
  • Dendritic cells and adipose tissue
  • Increased expression of TACI on NOD B cells results in germinal centre reaction anomalies, enhanced plasma cell differentiation and immunoglobulin production
  • Innate lymphoid cell regulation of adaptive immunity
  • Modulation of antigen processing by haem‐oxygenase 1. Implications on inflammation and tolerance
  • Distinct expression of interferon‐induced protein with tetratricopeptide repeats (IFIT) 1/2/3 and other antiviral genes between subsets of dendritic cells induced by dengue virus 2 infection
  • 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

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