Principles of cellular and molecular immunology

AUSTYN, Jonathan M; Kathryn, J. WOOD

doi:10.1590/s0036-46651994000300017

Cited by 8 publications

(10 citation statements)

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“…Activation can occur via two pathways, the classical (mediated by immune complexes) and alternative (mediated by yeast or bacterial cells) pathways, and can result in lysis of certain bacteria and viruses, opsonization, and inflammation (33). The importance of complement in the opsonisation and phagocytosis of many fungi, including C. albicans (414), Aspergillus (232), and Cryptococcus (107), has been demonstrated.…”

Section: Activation Of the Complement Cascadementioning

confidence: 99%

“…Opsonized and live Malassezia yeast cells were more stimulatory than were nonopsonised or heat-killed Malassezia yeast cells. The effects of IL-1␣ include the activation of lymphocytes, chemotaxis and activation of neutrophils and induction of inflammation (33). IL-8 also induces chemotaxis and activation of neutrophils and T cells.…”

Section: Phagocytosis Of Malasseziamentioning

confidence: 99%

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Immunology of Diseases Associated withMalasseziaSpecies

2002

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SUMMARY Malassezia species are members of the human cutaneous commensal flora, in addition to causing a wide range of cutaneous and systemic diseases in suitably predisposed individuals. Studies examining cellular and humoral immune responses specific to Malassezia species in patients with Malassezia-associated diseases and healthy controls have generally been unable to define significant differences in their immune response. The use of varied antigenic preparations and strains from different Malassezia classifications may partly be responsible for this, although these problems can now be overcome by using techniques based on recent work defining some important antigens and also a new taxonomy for the genus. The finding that the genus Malassezia is immunomodulatory is important in understanding its ability to cause disease. Stimulation of the reticuloendothelial system and activation of the complement cascade contrasts with its ability to suppress cytokine release and downregulate phagocytic uptake and killing. The lipid-rich layer around the yeast appears to be pivotal in this alteration of phenotype. Defining the nonspecific immune response to Malassezia species and the way in which the organisms modulate it may well be the key to understanding how Malassezia species can exist as both commensals and pathogens.

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Section: Activation Of the Complement Cascadementioning

confidence: 99%

Section: Phagocytosis Of Malasseziamentioning

confidence: 99%

Immunology of Diseases Associated withMalasseziaSpecies

2002

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“…The fact that dying astrocytes appeared to be swollen suggested that CRP deficiencies had allowed membrane insertion of the cytotoxic membrane attack complex (MAC). The MAC is a multimeric 100 Å pore composed of the CЈ factors C5b, C6, C7, C8, and multiple copies of C9, which allows ions and water free passage across the membrane of an attacked cell, causing cell swelling and lysis (Austyn and Wood, 1993). The CRP CD59 prevents MAC formation by preventing incorporation of C9 into the developing MAC (Morgan and Meri, 1994).…”

Section: Cellular Specificity Of C Regulatory Protein Expressionmentioning

confidence: 99%

GluR3 Autoantibodies Destroy Neural Cells in a Complement-Dependent Manner Modulated by Complement Regulatory Proteins

Whitney¹,

McNamara

2000

J. Neurosci.

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GluR3 autoantibodies have been implicated in the development of Rasmussen's encephalitis, a rare neurodegenerative disease of humans characterized by epilepsy and degeneration of a single cerebral hemisphere. GluR3 autoantibodies are found in some Rasmussen's encephalitis patients, and GluR3 antibodies raised in rabbits destroy cultured cortical cells in a complementdependent manner. In this study, the cellular targets of antiGluR3 antisera-mediated cytotoxicity were examined in mixed primary neuronal-glial cultures of rat cortex. Unexpectedly, astrocytes were the principal target of the cytotoxic effects as assessed by immunohistochemistry and lactate dehydrogenase activity; neurons were destroyed to a lesser extent. Astrocyte vulnerability was rescued by transfection with complement regulatory proteins, and neuronal resistance was defeated by impairing complement regulatory protein function. Astrocyte death may occur in Rasmussen's encephalitis, and destruction of this cell type may play a critical role in the progression of this disorder. The present findings suggest complement regulatory protein expression may in part determine the nature and severity of Rasmussen's encephalitis and other complement-dependent nervous system diseases and thus underscore the need for a systematic investigation of the expression of all known complement regulatory proteins in healthy and diseased nervous system tissues.

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“…They were first isolated from mouse lymphoid tissues, in particular the spleen [53][54][55], in the course of studies on the function of immune accessory cells in culture. The cell surface phenotypic markers of lymphoid DC [51,70] indicate that they are not some kind of aberrant macrophage, but indeed belong to a unique lineage. As do all leukocytes, they express CD45 (leukocyte common antigen) but unlike macrophages, they express low levels of Fc and complement receptors.…”

Section: The Dendritic Cell: Classical and Changing Perceptionsmentioning

confidence: 99%

“…This may involve antigen-independent, intercellular adhesion systems that operate before antigen recognition via the TCR, but which facilitate delivery of as yet unidentified DC-derived cytokines. Unlike macrophages, DC cannot produce (or produce only low levels of) interleukin 1 (IL-l) [70]. There is evidence that, like activated macrophages, mature DC produce IL-12 [71] that directs nai ve T cells towards a Thl pattern of cytokine production.…”

Section: How Do DC Stimulate T Cells?mentioning

confidence: 99%

Microchimerism, dendritic cell progenitors and transplantation tolerance

et al. 1995

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Abstract. The recent discovery of multilineage donor leukocyte microchimerism in allograft recipients up to three decades after organ transplantation implies the migration and survival of donor stem cells within the host. It has been postulated that in chimeric graft recipients, reciprocal modulation of immune responsiveness between donor and recipient leukocytes may lead, eventually, to the induction of mutual immunologic nonreactivity (tolerance). A prominent donor leukocyte, both in human organ transplant recipients and in animals, has invariably been the bone marrowderived dendritic cell (DC). These cells have been classically perceived as the most potent antigenpresenting cells but evidence also exists for their tolerogenicity. The liver, despite its comparatively heavy leukocyte content, is the whole organ that is most capable of inducing tolerance. We have observed that DC progenitors propagated from normal mouse liver in response to GM-CSF express only low levels of major histocompatibility complex (MHC) class II antigen and little or no cell surface B7 family T cell costimulatory molecules. They fail to activate resting naive allogeneic T cells. When injected into normal allogeneic recipients, these DC progenitors migrate to T -dependent areas of host lymphoid tissue, where some at least up regulate cell surface MHC class II. These donor-derived cells persist indefinitely, recapitulating the behavior pattern of donor leukocytes after the successful transplantation of all whole organs, but most dramatically after the orthotopic (replacement) engraftment of the liver.Correspondence: Dr.

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Principles of cellular and molecular immunology

Cited by 8 publications

References 0 publications

Immunology of Diseases Associated withMalasseziaSpecies

Immunology of Diseases Associated withMalasseziaSpecies

GluR3 Autoantibodies Destroy Neural Cells in a Complement-Dependent Manner Modulated by Complement Regulatory Proteins

Microchimerism, dendritic cell progenitors and transplantation tolerance

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