Immunology

Cover image for Vol. 152 Issue 2

Edited By: Danny Altmann

Impact Factor: 3.701

ISI Journal Citation Reports © Ranking: 2016: 53/150 (Immunology)

Online ISSN: 1365-2567

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  • Signals that drive T follicular helper cell formation

    Signals that drive T follicular helper cell formation

    Expression of co-receptors during the three phases of T follicular helper (Tfh) cell differentiation. Schematic depicting the multistage and location-specific nature of Tfh cell differentiation. The expression of co-receptors is shown at each stage with stimulatory receptors coloured green and inhibitory receptors coloured red. During the first phase of differentiation (days 0–3) naive CD4+ T cells are activated by dendritic cells in the T-cell zone where they proliferate and alter expression of co-receptors. This allows the resulting pre-Tfh cell to migrate towards the T–B-cell border where it engages with antigen-specific B cells. Co-receptors expressed by Tfh cells also modulate the signals transduced through the T-cell receptor, allowing their differentiation. In the second phase (days 4–5) antigen is presented by B cells and the co-receptors expressed by pre-Tfh cells are used symbiotically to both induce Tfh cell differentiation and provide co-stimulation to B cells. In the third phase (days 6–10), Tfh cells engage with germinal centre (GC) B cells within the GC. Tfh cells provide a limiting source of help to ensure that appropriate B cells differentiate into antibody-secreting cells and memory B cells. During the resolution phase the Tfh cell can leave the GC and in the absence of further antigenic stimulation resides as a long-lived memory Tfh cell in the periphery.

  • Intestinal dysbiosis and probiotic applications in autoimmune diseases

    Intestinal dysbiosis and probiotic applications in autoimmune diseases

    A schematic representation of the interaction between commensal microbiota and the immune system. Under eubiosis, there are microbiota diversity and immune homeostasis in the gut mucosa. Commensal microorganisms instruct dendritic cells to induce IgA-secreting cell differentiation, and in turn, IgA regulates the composition of the gut microbiota. During dysbiosis, there are decreased diversity in commensal microbiota and deregulated interactions between immune cells and these microorganisms. Some specific bacteria, such as Bacteroides fragilis, induce regulatory T cell differentiation and the secretion of anti-inflammatory cytokines, whereas segmented filamentous bacteria (SFB) promote T helper type 17 (Th17) cell differentiation and the secretion of pro-inflammatory cytokines, which play roles in several autoimmune diseases.

  • The immune response to Prevotella bacteria in chronic inflammatory disease

    The immune response to Prevotella bacteria in chronic inflammatory disease

    Gut inflammation associated Prevotella-rich dysbiosis. Prevotella stimulates release of interleukin-1β (IL-1β), IL-6 and IL-23 by dendritic cells (DC), which in turn mediate IL-17 production by T helper 17 (Th17) cells that activate neutrophils. DCs also produce IL-12, which mediates the activation of Th1 and cytotoxic T (Tc) cells. Epithelial cells may contribute to recruitment of CCR5-positive T cells through the production of CCL5. HIV infection and exposure to Prevotella are risk factors for Prevotella-rich dysbiosis in the gut. Dysbiosis leads to systemic release of inflammation, bacteria, lipopolysaccharides (endotoxaemia) and Toll-like receptor 9 (TLR9) agonists, which in turn mediates systemic disease expression, including liver inflammation, insulin resistance, weight gain and increased blood pressure (BP). Dysbiosis-associated increase in Th17 immune responses may affect new-onset rheumatoid arthritis (NORA). Dysbiosis increases Th1-mediated inflammation in dextran sulphate sodium (DSS)-induced experimental colitis.

  • Ageing adversely affects the migration and function of marginal zone B cells

    Ageing adversely affects the migration and function of marginal zone B cells

    B cells in aged mice have a decreased uptake of trinitrophenyl (TNP) -Ficoll. Young and old mice were immunized with TNP-Ficoll. After 30 min spleens were collected for analysis. (a) Representative immunofluorescence images of TNP localization in the spleens of young and old mice (TNP – red, MAdCAM-1 – green, CD35 – blue). Scale bars = 200 μm. (b) A flow cytometric analysis was performed to determine the percentage of follicular (B220+CD21midCD23hi), marginal zone (B220+CD21hiCD23lo) and CD21/35−CD23− (B220+CD21loCD23lo) B cells that are binding TNP-Ficoll. (c) Expression levels of TNP on the follicular (B220+CD21midCD23hi), marginal zone (B220+CD21hiCD23lo) and CD21/35−CD23− (B220+CD21loCD23lo) B cells in non-immunized, young and old mice as determined via flow cytometry. (d) Median fluorescence intensity levels of TNP on follicular, marginal zone and CD21/35−CD23− B cells. Results are representative of two experiments. Median is shown, n = 4 mice per group, and analysis was via t-test. **P < 0·01, *P < 0·05.

  • From dendritic cells to B cells dysfunctions during HIV-1 infection: T follicular helper cells at the crossroads

    From dendritic cells to B cells dysfunctions during HIV-1 infection: T follicular helper cells at the crossroads

    Follicular helper T (Tfh) cell dysregulations during chronic HIV/SIV infection.

  • Nerve growth factor: a neuroimmune crosstalk mediator for all seasons

    Nerve growth factor: a neuroimmune crosstalk mediator for all seasons

    Scheme showing how nerve growth factor (NGF) might modulate neuro–endocrino–immune interactions. NGF released from tissue mast cells as a consequence of nervous, immune or endocrine system inputs can, in turn, influence the same systems (locally or via the circulation), for example, by the release of blood-borne immune cells to act on mast cells. NGF released from mast cells could also function in an autocrine manner. Possible actions of NGF derived from mast cells are listed in the box.

  • Chronic infections with viruses or parasites: breaking bad to make good

    Chronic infections with viruses or parasites: breaking bad to make good

    The good (light) and bad (dark) side of chronic virus infection. Infection of tissues by viruses and subsequent chronic inflammation can lead to tissue damage, e.g. hepatitis. In chronic hepatitis C virus (HCV) infection, progression to disease is associated with the expression of the natural killer (NK) cell receptor NKp46. Many other viruses directly infect antigen-presenting cells (APCs) or have a number of molecules that can down-regulate MHC class I expression expressed by these cells; this molecule is important for viral recognition by CD8+ T cells but is also important for elimination of tumour cells. The NK cell killing of cells expressing low MHC class I is prevented by the dismantling of NK activating receptors. viral interleukin-10 (vIL-10) can transform B cells and help the virus to establish a chronic infection. This molecule is also reported to reduce autoimmunity, inflammation and tissue rejection. Chronic virus infection can promote anti-inflammatory responses, including the expansion of regulatory T (Treg) cells and, production of transforming growth factor-β (TGF-β) and is associated with a switch from interferon-γ (IFN-γ) to IL-10-producing CD4+ T cells. Viral infection is also able to reduce antigen presentation and activation of APCs, reducing CD4+ T-cell activation and inflammatory responses.

  • 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.

  • Signals that drive T follicular helper cell formation
  • Intestinal dysbiosis and probiotic applications in autoimmune diseases
  • The immune response to Prevotella bacteria in chronic inflammatory disease
  • Ageing adversely affects the migration and function of marginal zone B cells
  • From dendritic cells to B cells dysfunctions during HIV-1 infection: T follicular helper cells at the crossroads
  • Nerve growth factor: a neuroimmune crosstalk mediator for all seasons
  • Chronic infections with viruses or parasites: breaking bad to make good
  • 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

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