| 1. |
- Bennett, Matthew, et al.
(författare)
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Was it there all the time?
- 2003
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Ingår i: Scandinavian Journal of Immunology. - : Wiley. - 1365-3083 .- 0300-9475. ; 57:6, s. 499-505
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Forskningsöversikt (refereegranskat)abstract
- The complement system is old, yet it may still have something new to teach us. For many years, research has existed which shows that C3d, in addition to its established role as an adjuvant, could have an immunosuppressive activity. Being true, it suggests that a common mechanism may be used both by organisms and by their pathogens to prevent unwanted immune responses.
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| 2. |
- Johansson, Åsa C M, et al.
(författare)
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Genetic heterogeneity of autoimmune disorders in the nonobese diabetic mouse.
- 2003
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Ingår i: Scandinavian Journal of Immunology. - : Wiley. - 1365-3083 .- 0300-9475. ; 57:3, s. 203-213
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Forskningsöversikt (refereegranskat)abstract
- The nonobese diabetic mouse is highly susceptible not only to diabetes but to several autoimmune diseases, and one might suspect that these are controlled by a shared set of genes. However, based on various gene-segregation experiments, it seems that only a few loci are shared and that each disorder is influenced also by a unique set of genes.
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| 3. |
- Persson, Carl, et al.
(författare)
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Contribution of plasma-derived molecules to mucosal immune defence, disease and repair in the airways
- 1998
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Ingår i: Scandinavian Journal of Immunology. - : Wiley. - 1365-3083 .- 0300-9475. ; 47:4, s. 302-313
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Forskningsöversikt (refereegranskat)abstract
- This review discusses recent observations, in health and disease, on the release and distribution of plasma-derived molecules in the airway mucosa. Briefly, the new data on airway mucosal exudation mechanisms suggest that the protein systems of plasma contribute significantly to the mucosal biology, not only in injured airways but also in such mildly inflamed airways that lack oedema and exhibit no sign of epithelial derangement. Plasma as a source of pluripotent growth factor, adhesive, leucocyte-activating, etc., molecules may deserve a prominent position in schemes that claim to illustrate immunological and inflammatory mechanisms of the airway mucosa in vivo.
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| 4. |
- Olofsson, Peter, et al.
(författare)
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Positional cloning of ncf1- a piece in the puzzle of arthritis genetics.
- 2003
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Ingår i: Scandinavian Journal of Immunology. - : Wiley. - 1365-3083 .- 0300-9475. ; 58:2, s. 155-164
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Forskningsöversikt (refereegranskat)abstract
- Positional cloning of susceptibility genes in complex diseases like rheumatoid arthritis in humans is hampered by aspects like genetic heterogeneity and environmental variations, while genetic studies in animal models contain several advantages. With animal models, the environment can be controlled, the genetic complexity of the disease is minimized and the disease onset can be predicted, which simplify diagnosis and characterization. We use pristane-induced arthritis in rats to investigate the inheritance of arthritis. Until now, we have identified 15 loci that significantly predispose rats to the development of arthritis. One of these arthritis loci has been isolated and confirmed to be caused by a polymorphism in the Ncf1 gene. In this review, we outline the methods used to identify Ncf1 as one single susceptibility gene in a complex puzzle of inherited factors that render susceptibility to a complex autoimmune disorder like arthritis.
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| 5. |
- Bokarewa, Maria, 1963, et al.
(författare)
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Pathological survivin expression links viral infections with pathogenesis of erosive rheumatoid arthritis.
- 2007
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Ingår i: Scandinavian journal of immunology. - : Wiley. - 0300-9475 .- 1365-3083. ; 66:2-3, s. 192-8
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Forskningsöversikt (refereegranskat)abstract
- Rheumatoid arthritis (RA) is an inflammatory joint disease leading to cartilage and bone destruction. Insufficient apoptosis in the inflamed RA synovium along with accumulation of highly differentiated B- and T-lymphocytes as well as invasive growth of macrophages and fibroblasts is among the major mechanisms supporting joint destruction. We have recently shown that circulating survivin, an apoptosis inhibitor tightly bound to tumorigenesis, is an independent predictor of development and progression of joint destruction in RA. In this review we discuss the possible connectivity between viral infection, leading to interferon (IFN)-alpha production, survivin expression, and subsequent joint inflammation. The role of IFN-alpha and the involvement of IFN transcription factors and phosphoinositide-3-kinase signalling as essential modulators of arthritogenic process are discussed in the context of survivin.
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| 6. |
- Mårtensson, Inga-Lill, 1957, et al.
(författare)
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The Pre-B Cell Receptor; Selecting for or against Autoreactivity
- 2012
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Ingår i: Scandinavian Journal of Immunology. - : Wiley. - 0300-9475 .- 1365-3083. ; 76:3, s. 256-262
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Forskningsöversikt (refereegranskat)abstract
- Antibodies represent a crucial component of humoral immunity as protection against invading pathogens, to which they bind and thereby trigger mechanisms that lead to the disposal of the pathogen. Antibodies are assembled from Ig heavy chains (HCs) and light chains (LCs) and are found in both a secreted and a membrane-bound form, termed B cell receptors (BCRs), where the latter allows the ‘right’ B cell to respond upon recognition of its cognate antigen. The antibody repertoire is almost unlimited because of a process in which germ line V(D)J gene segments, encoding the variable (antigen-binding) region of the antibody HCs and LCs, are recombined. As this process is random, it is apparent that it results in a vast variety of antibodies, those that recognize foreign but also those that recognize self- (auto-) antigens. Control mechanisms are, therefore, in place to ensure that as few autoreactive B cells as possible are allowed to proceed in development. This counter-selection takes place through various mechanisms and at several stages as the cells develop from pre-B cells to antibody-secreting plasma cells. At the first major checkpoint, at the pre-BI to pre-BII cell transition, antibody HCs assemble with the invariant surrogate LC (SLC) forming a pre-BCR. Herein, we will discuss the role of the pre-BCR in the selection at this stage, how a dysfunctional pre- BCR affects selection and its effects on later stages, and whether the pre-BCR selects for or against autoreactivity.
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| 7. |
- Sun, Jia-Bin, 1948, et al.
(författare)
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Mucosally induced immunological tolerance, regulatory T cells and the adjuvant effect by cholera toxin B subunit.
- 2010
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Ingår i: Scandinavian journal of immunology. - : Wiley. - 1365-3083 .- 0300-9475. ; 71:1, s. 1-11
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Forskningsöversikt (refereegranskat)abstract
- Induction of peripheral immunological tolerance by mucosal administration of selected antigens (Ags) ('oral tolerance') is an attractive, yet medically little developed, approach to prevent or treat selected autoimmune or allergic disorders. A highly effective way to maximize oral tolerance induction for immunotherapeutic purposes is to administer the relevant Ag together with, and preferably linked to the non-toxic B subunit protein of cholera toxin (CTB). Oral, nasal or sublingual administration of such Ag/CTB conjugates or gene fusion proteins have been found to induce tolerance with superior efficiency compared with administration of Ag alone, including the suppression of various autoimmune disorders and allergies in animal models. In a proof-of-concept clinical trial in patients with Behcet's disease, this was extended with highly promising results to prevent relapse of autoimmune uveitis. Tolerization by mucosal Ag/CTB administration results in a strong increase in Ag-specific regulatory CD4(+) T cells, apparently via two separate pathways: one using B cells as APCs and leading to a strong expansion of Foxp3(+) Treg cells which can both suppress and mediate apoptotic depletion of effector T cells, and one being B cell-independent and associated with development of Foxp3(-) regulatory T cells that express membrane latency-associated peptide and transforming growth factor (TGF-beta) and/or IL-10. The ability of CTB to dramatically increase mucosal Ag uptake and presentation by different APCs through binding to GM1 ganglioside (which makes most B cells effective APCs irrespective of their Ag specificity), together with CTB-mediated stimulation of TGF-beta and IL-10 production and inhibition of IL-6 formation may explain the dramatic potentiation of oral tolerance by mucosal Ags presented with CTB.
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| 8. |
- Romero, Ana, 1975, et al.
(författare)
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Post-consolidation immunotherapy with histamine dihydrochloride and interleukin-2 in AML.
- 2009
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Ingår i: Scandinavian journal of immunology. - : Wiley. - 1365-3083 .- 0300-9475. ; 70:3, s. 194-205
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Forskningsöversikt (refereegranskat)abstract
- The initial chemotherapy in acute myeloid leukaemia (AML) comprises a first phase of induction and a second phase of consolidation. In the majority of patients, the induction treatment leads to complete remission (CR), defined as microscopic disappearance of leukaemic disease along with the return of normal haematopoiesis. However, despite the introduction of more efficacious consolidation regimens, a worryingly large proportion of AML patients in CR will subsequently experience relapses with poor prospects of long-term survival. A relapse is assumed to be the result of expansion of residual leukaemic cells that have escaped the initial chemotherapy. The anti-leukaemic functions of T cells and natural killer (NK) cells has formed the background to the use of interleukin-2 (IL-2), a T- and NK cell-activating cytokine, with the aim to eliminate residual leukaemia and hence reduce the relapse rate in AML, but the clinical trials using IL-2 monotherapy have yielded disappointment. A recent phase III study has demonstrated that post-consolidation treatment with the combination of histamine dihydrochloride (HDC) and IL-2 significantly prevents relapse in AML patients. Here we account for the preclinical background to the use of HDC/IL-2 in AML along with a review of clinical results.
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| 9. |
- Alfredsson, Johannes, et al.
(författare)
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Mechanism of fibrosis and stricture formation in Crohn's disease
- 2020
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Ingår i: Scandinavian Journal of Immunology. - : Wiley. - 0300-9475 .- 1365-3083. ; 92:6
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Forskningsöversikt (refereegranskat)abstract
- Crohn's disease (CD) is a chronic inflammatory disease of the gastrointestinal tract that leads to substantial suffering for millions of patients. In some patients, the chronic inflammation leads to remodelling of the extracellular matrix and fibrosis. Fibrosis, in combination with expansion of smooth muscle layers, leaves the bowel segment narrowed and stiff resulting in strictures, which often require urgent medical intervention. Although stricture development is associated with inflammation in the affected segment, anti-inflammatory therapies fall far short of treating strictures. At best, current therapies might allow some patients to avoid surgery in a shorter perspective and no anti-fibrotic therapy is yet available. This likely relates to our poor understanding of the mechanism underlying stricture development. Chronic inflammation is a prerequisite, but progression to strictures involves changes in fibroblasts, myofibroblasts and smooth muscle cells in a poorly understood interplay with immune cells and environmental cues. Much of the experimental evidence available is from animal models, cell lines or non-strictured patient tissue. Accordingly, these limitations create the basis for many previously published reviews covering the topic. Although this information has contributed to the understanding of fibrotic mechanisms in general, in the end, data must be validated in strictured tissue from patients. As stricture formation is a serious complication of CD, we endeavoured to summarize findings exclusively performed using strictured tissue from patients. Here, we give an update of the mechanism driving this serious complication in patients, and how the strictured tissue differs from adjacent unaffected tissue and controls.
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| 10. |
- Amin, Kawa, et al.
(författare)
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Role of Eosinophil Granulocytes in Allergic Airway Inflammation Endotypes
- 2016
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Ingår i: Scandinavian Journal of Immunology. - : Wiley. - 0300-9475 .- 1365-3083. ; 84:2, s. 75-85
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Forskningsöversikt (refereegranskat)abstract
- Eosinophil granulocytes are intriguing members of the innate immunity system that have been considered important defenders during parasitic diseases as well as culprits during allergy-associated inflammatory diseases. Novel studies have, however, found new homoeostasis-maintaining roles for the cell. Recent clinical trials blocking different Th2 cytokines have uncovered that asthma is heterogeneous entity and forms different characteristic endotypes. Although eosinophils are present in allergic asthma with early onset, the cells may not be essential for the pathology. The cells are, however, likely disease causing in asthma with a late onset, which is often associated with chronic rhinosinusitis. Assessment of eosinophilia, fraction exhaled nitric oxide (FeNO) and periostin are markers that have emerged useful in assessing and monitoring asthma severity and endotype. Current scientific knowledge suggests that eosinophils are recruited by the inflammatory environment, activated by the innate interleukin (IL)-33 and prevented from apoptosis by both lymphocytes and innate immune cells such as type two innate immune cells. Eosinophils contain four specific granule proteins that exhibit an array of toxic and immune-modulatory activates. The granule proteins can be released by different mechanisms. Additionally, eosinophils contain a number of inflammatory cytokines and lipid mediators as well as radical oxygen species that might contribute to the disease both by the recruitment of other cells and the direct damage to supporting cells, leading to exacerbations and tissue fibrosis. This review aimed to outline current knowledge how eosinophils are recruited, activated and mediate damage to tissues and therapies used to control the cells.
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