Clinical & Experimental Immunology

Cover image for Vol. 190 Issue 1

Edited By: Leonie Taams

Impact Factor: 3.41

ISI Journal Citation Reports © Ranking: 2016: 60/150 (Immunology)

Online ISSN: 1365-2249

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  • Immune deficiency and autoimmunity in patients with CTLA-4 (CD152) mutations

    Immune deficiency and autoimmunity in patients with CTLA-4 (CD152) mutations

    Schematic view of reported cytotoxic T lymphocyte antigen-4 (CTLA-4) mutations. DNA mutations are shown in the upper half of the diagram and aligned with amino acid changes below. The alignment between exons and protein functional domains is shown. Mutations are colour-coded according to the report in which they are described.

  • T helper type 1-related molecules as well as interleukin-15 are hyperexpressed in the skin lesions of patients with pyoderma gangrenosum

    T helper type 1-related molecules as well as interleukin-15 are hyperexpressed in the skin lesions of patients with pyoderma gangrenosum

    Immunohistochemical staining for the T helper 1-associated markers interleukin (IL)-12, interferon (IFN)-γ and the chemokine receptors C-X-C motif chemokine receptor 3 (CXCR3) and C-C motif chemokine receptor 5 (CCR5) in skin biopsy specimens from patients with pyoderma gangrenosum (PG), Sweet syndrome (SS) and healthy controls (HC). Magnification: ×200.

  • Transplantation tolerance: don't forget about the B cells

    Transplantation tolerance: don't forget about the B cells

    Fate of B cells in rejection and tolerance. The activation and differentiation of naive alloreative B cells during rejection occurs in a T cell- and germinal centre-dependent manner. Under tolerogenic conditions, naive alloreactive B cells encounter antigen, but in the absence of T cell help may be deleted, develop into regulatory B cells (Bregs)/B10 cells that suppress T cell responses, and into anergic or suppressed B cells that fail to develop into antibody-secreting plasma cells.

  • The role of stromal cells in inflammatory bone loss

    The role of stromal cells in inflammatory bone loss

    The role of fibroblast-like synoviocytes (FLS) in inflammatory bone destruction. Under healthy conditions, there is a balance between bone formation and bone destruction to replace old bone tisssue and to repair bone defects. In rheumatoid arthritis (RA), more bone is degraded by osteoclasts than is created by osteoblasts, shifting the balance towards bone destruction. During inflammation, stromal FLS, located in the synovial membrane of the joint space, are able to influence this balance directly or indirectly. FLS release receptor-activator of nuclear factor-kappa B (RANKL) in response to inflammatory cytokines such as tumour necrosis factor (TNF)-α, which subsequently stimulates osteoclastogenesis directly. They also communicate with T cells or release inhibitors of bone formation, such as sclerostin and Dickkopf-1 (DKK1). In contrast to DKK1, sclerostin not only blocks osteoblast differentiation but also inhibits specifically TNF-mediated bone destruction, suggesting a protective effect in TNF-mediated bone loss. Other factors released by FLS, such as myostatin, activates bone destruction directly. Different subsets of FLS, especially gp38+ and FAP+-expressing FLS, are highly migratory and invasive and seem to be important for cartilage and bone destruction.

  • The role of genomics in common variable immunodeficiency disorders

    The role of genomics in common variable immunodeficiency disorders

    There are multiple genetic components involved in common variable immunodeficiency disorder (CVID) pathogenesis. Monogenic causes of CVID has been found in approximately 10% of cases, and primarily modify molecules associated with the B cell receptor complex. In most cases there is a polygenic mode of inheritance, whereby variants in multiple genes can contribute to the same or diverse phenotypes. Further genetic complexity may come from transcriptional and epigenetic disturbances.

  • Production of complement components by cells of the immune system

    Production of complement components by cells of the immune system

    Schematic representation of the complement system. The complement system can be activated via three different pathways: the classical pathway (CP), the lectin pathway (LP) and the alternative pathway (AP). These pathways have their own sequential manner in forming a C3 convertase: C4b2a or C3bBb. These C3 convertases cleave the central component C3 generating two activation fragments, C3a and C3b. The C3a is able to bind its anaphylatoxin receptor the C3aR, whereas C3b can opsonize a target membrane. C3b and its further degradation products, iC3b, C3c and C3d/C3dg are able to bind various complement receptors (CRs). Additionally, C3b can bind to the former C3 convertase which then results in formation of the C5 convertase: C4bC2aC3b or C3bBbC3b. The C5 convertase cleaves C5 in two activation fragments C5a and C5b. C5a can bind to its anaphylatoxin receptors C5aR1 and C5aR2, whereas C5b marks the start of the formation of the membrane attack complex (MAC). In a sequential manner C5b, C6, C7, C8 and up to 16 molecules of C9 bind together to form a MAC. Various inhibitors of this system are marked in pink boxes. MBL = mannose binding lectin; MASP = MBL-associated serine protease; FB = factor B; FP = factor P; FD = factor D; FH = factor H; C1INH = C1 inhibitor; FI = factor I (FI), C4BP = C4b-binding protein; CR = complement receptor.

  • Tumour-activated liver stromal cells regulate myeloid-derived suppressor cells accumulation in the liver

    Tumour‐activated liver stromal cells regulate myeloid‐derived suppressor cells accumulation in the liver

    Liver stromal cells promote myeloid-derived suppressor cells (MDSCs) accumulation in the liver and at the tumour site. (a) 1,1′-dioctadecyl-3,3,3′,3′-tetramethylindotricarbocyanine iodide (DiR)-labelled MDSCs were transferred intravenously (i.v.) (5 × 106 cells per mouse) to recipient mice as indicated (n = 4) and were imaged 3 h later. (b) Tumour nodules from the two groups of tumour-bearing mice were isolated and imaged 3 h after cell transfer. (c) The fold-changes in liver and tumour photo counts in the two groups of tumour-bearing mice. (d) Tumour volumes from the groups of tumour-bearing mice are shown (n = 6 per group). The experiments were repeated three times. * P < 0·05. Student's t-test.

  • Impaired calcium mobilization in natural killer cells from chronic fatigue syndrome/myalgic encephalomyelitis patients is associated with transient receptor potential melastatin 3 ion channels

    Impaired calcium mobilization in natural killer cells from chronic fatigue syndrome/myalgic encephalomyelitis patients is associated with transient receptor potential melastatin 3 ion channels

    A conceptual natural killer (NK) model for chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) patients. Pregnenolone sulphate (PregS) is a potent steroid that activated transient receptor potential melastatin 3 ion channels (TRPM3) on NK cell subsets. PregS in combination with thapsigargin elevated cytoplasmic calcium and is suggested to phosphorylate extracellular-regulated kinase (ERK) 1/2 and polarization of secretory granules for degranulation in CD56dimCD16+ NK cells, resulting in target K562 cell death, whereas PregS-stimulated CD56brightCD16dim/– NK cells may activate p38 MAPK signalling pathways involved in the nuclear factor kappa B (NF-κβ) inflammatory immune response.

  • Herpes zoster and the search for an effective vaccine

    Herpes zoster and the search for an effective vaccine

    Varicella zoster virus (VZV) immune response during reactivation. When immune responses weaken, VZV reactivates by travelling anterograde towards nerve endings, replicates in keratinocytes and epithelial cells causing the formation of polykaryocytes, leading ultimately to a dermatomal rash. The local immune response in the ganglia is characterized by the infiltration of CD8, CD4, natural killer (NK) cells, macrophages and B cells. The immune response in the skin is characterized by CD4, CD8, NK cells and macrophages along with increased expression of interferon (IFN)-γ, tumour necrosis factor (TNF)-α and interleukin (IL)-6.

  • Expression of type III interferons (IFNλs) and their receptor in Sjögren's syndrome

    Expression of type III interferons (IFNλs) and their receptor in Sjögren's syndrome

    Representative double immunofluorescent staining for the common type III interferon (IFN) signalling receptor [IFN-λR1/interleukin (IL)−28Rα] and markers of inflammatory cells [plasmatocytoid dendritic cells (pDCs): CD303 and CD123, macrophages: CD68, T lymphocytes: CD3 and B lymphocytes: CD20] in a minor salivary gland (MSG) tissue from a Sjögren's syndrome (SS) patient. Co-localization is indicated with yellow arrows. Original magnification ×1000.

  • Porphyromonas gingivalis infection exacerbates the onset of rheumatoid arthritis in SKG mice

    Porphyromonas gingivalis infection exacerbates the onset of rheumatoid arthritis in SKG mice

    Osteoclast differentiation from bone marrow mononuclear cells (BMCs) of SKG mice. (a) After the separation of BMCs from each group of SKG mice using Histopaque 1083®, BMCs (2 × 105 cells/well) were cultured on 96-well plates in the presence of soluble nuclear factor kappa B ligand (sRANKL) (50 ng/ml) and macrophage colony-stimulating factor (M-CSF) (20 ng/ml) for 7 days. The number of osteoclasts with multiple nuclei (> 3) on 96-well plates was counted. The data summarized are the results obtained from three independent experiments (in each group of n = 5 mice). *Significantly higher number of osteoclasts by Student's t-test (*P < 0·05). (b) Representative tartrate-resistant acid phosphatase kit (TRAP)-stained images of multinuclear osteoclasts on 96-well plates on day 7. Original magnification ×100; scale bar, 30 µm.

  • The immunology of the vermiform appendix: a review of the literature

    The immunology of the vermiform appendix: a review of the literature

    Transverse section of a healthy adult appendix. 1, mesoappendix; 2, muscularis externa; 3, submucosa; 4, lymphoid follicle; 5, mucosa and 6, lumen.

  • Immune deficiency and autoimmunity in patients with CTLA-4 (CD152) mutations
  • T helper type 1-related molecules as well as interleukin-15 are hyperexpressed in the skin lesions of patients with pyoderma gangrenosum
  • Transplantation tolerance: don't forget about the B cells
  • The role of stromal cells in inflammatory bone loss
  • The role of genomics in common variable immunodeficiency disorders
  • Production of complement components by cells of the immune system
  • Tumour‐activated liver stromal cells regulate myeloid‐derived suppressor cells accumulation in the liver
  • Impaired calcium mobilization in natural killer cells from chronic fatigue syndrome/myalgic encephalomyelitis patients is associated with transient receptor potential melastatin 3 ion channels
  • Herpes zoster and the search for an effective vaccine
  • Expression of type III interferons (IFNλs) and their receptor in Sjögren's syndrome
  • Porphyromonas gingivalis infection exacerbates the onset of rheumatoid arthritis in SKG mice
  • The immunology of the vermiform appendix: a review of the literature

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About Clinical & Experimental Immunology

Clinical & Experimental Immunology (CEI) is an international, authoritative, timely and impactful resource of clinical and translational research articles, reviews, and opinion pieces that further our understanding of the immunology of human disease. CEI also aims to promote and advance best practice in clinical immunology.

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  • 2016 Impact Factor: 3.410

  • All Clinical & Experimental Immunology review articles are free-to-access from point of publication, and all journal content is free-to-access after a period of 12 months


The British Society for Immunology is delighted to announce Leonie Taams as the new Editor-in-Chief of Clinical & Experimental Immunology. Leonie is Professor of Immune Regulation and Inflammation at King’s College London, and takes over from Mark Peakman. Mark oversaw a period of growth in his two terms as EiC and the BSI would like to express their gratitude to him for his outstanding contribution to the journal.

Leonie Taams

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