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11.
No Abstract.
Received 21 February 2002; received after revision 16 May 2002; accepted 14 June 2002 相似文献
12.
Humoral immune reactions to heat shock proteins (hsp) from microorganisms are one aspect of microbial infections in humans. The production of antibodies which are specific to epitopes present on procaryotic hsp leads also to the appearance of cross-reactive serum antibodies in the host organism that react with human hsp. This article discusses the consequences of such autoreactive antibodies for the host in context with the development of immune tolerance and autoimmune diseases, especially rheumatoid arthritis (RA), and in experimental animal models for arthritis such as adjuvant arthritis in rats. On the basis of epitope cross-reactivity between hsp and other host proteins, a hypothesis is presented for the development of autoimmune disease following the production of hsp-specific antibodies. 相似文献
13.
Autoimmune T cells have been viewed for decades as an outcome of immune system malfunction, and specifically as a failure to distinguish between components of self and non-self. The need for discrimination between self and non-self as a way to avoid autoimmunity has been repeatedly debated over the years. Recent studies suggest that autoimmunity, at least in the nervous system, is the bodys defense mechanism against deviations from the normal. The ability to harness neuroprotective autoimmunity upon need is evidently allowed by naturally occurring CD4+CD25+ regulatory T cells, which are themselves controlled by brain-derived compounds. These findings challenge widely accepted concepts of the need for discrimination between self and non-self, as they suggest that while such discrimination is indeed required, it is needed not as a way to avoid an anti-self response but to ensure its proper regulation. Whereas a response to non-self can be self-limited by a decreased presence of the relevant antigen, the response to self needs a mechanism for strict control, such as that provided by the naturally occurring regulatory T cells.Received 8 June 2004; accepted 6 July 2004 相似文献
14.
Lyme disease is a multisystem illness initiated upon infection with the spirochete Borrelia burgdorferi. Whereas the majority of patients who develop Lyme arthritis may be successfully treated with antibiotic therapy, about 10%
go on to develop arthritis which persists for months to years, despite antibiotic therapy. Development of what we have termed
treatment-resistant Lyme arthritis has previously been associated with both the presence of particular major histocompatibility
complex class II alleles and immunoreactivity to the spriochetal outer surface protein A (OspA). Recently, we showed that
patients with treatment-resistant Lyme arthritis, but not patients with other forms of arthritis, generate synovial fluid
T cell responses to an immunodominant epitope of OspA and a highly homologous region of the human-lymphocyte-function-associated
antigen-1α
L chain. Identification of a bacterial antigen capable of propagating an autoimmune response against a self-antigen provides
a model of molecular mimicry in the pathogenesis of treatment-resistant Lyme arthritis.
Received 21 December 1999; received after revision 10 April 2000; accepted 11 April 2000 相似文献
15.
K. L. Sand E. Knudsen J. Rolin Y. Al-Falahi A. A. Maghazachi 《Cellular and molecular life sciences : CMLS》2009,66(8):1446-1456
Glatiramer acetate (GA or Copaxone) is a drug used to treat experimental autoimmune encephalomyelitis in mice and multiple
sclerosis in human. Here, we describe a new mechanism of action for this drug. GA enhanced the cytolysis of human NK cells
against autologous and allogeneic immature and mature monocyte-derived dendritic cells (DCs). This drug reduced the percentages
of mature DCs expressing CD80, CD83, HLA-DR or HLA-I. In contrast, it did not modulate the percentages of NK cells expressing
NKG2D, NKp30, or NKp44. Nonetheless, anti-NKp30 or anti-CD86 inhibited GA-enhanced human NK cell lysis of immature DCs. Hence,
CD86, and NKp30 are important for NK cell lysis of immature DCs, whereas CD80, CD83, HLA-DR and HLA-I are important for the
lysis of mature DCs when GA is used as a stimulus. Further, GA inhibited the release of IFN-γ 24 h but increased the release
of TNF-α 48 h after incubation with NK cells.
Received 13 November 2008; received after revision 10 February 2009; accepted 18 February 2009 相似文献
16.
17.
It has now been more than ten years since the discovery of the major apoptotic nuclease, DNA fragmentation factor (DFF), also
known as caspaseactivated DNase (CAD). Here we review the recent literature that has uncovered new insight into DFF’s regulation,
and both its positive and negative roles in human disease. Cells from mice deficient in DFF still undergo apoptotic death
without significant cellautonomous DNA degradation. Their corpses’ genomes are subsequently degraded by lysosomal DNase II
after phagocytosis. However,DFF-deficient mice are more susceptible to cancer. Indeed, several different cancers in humans
are associated with defects in DFF expression and it has been proposed that DFF is a p53-independent tumor suppressor. Negative
aspects of DFF expression include contributing to susceptibility to acquire systemic lupus erythematosus, to chromosomal translocations
that result in mixed lineage leukemias, and in the possible spreading of oncogenes and HIV due to horizontal gene transfer.
Received 06 August 2008; received after revision 03 September 2008; accepted 09 September 2008 相似文献
18.
Central role of dendritic cells in the regulation and deregulation of immune responses 总被引:1,自引:0,他引:1
Granucci F Zanoni I Ricciardi-Castagnoli P 《Cellular and molecular life sciences : CMLS》2008,65(11):1683-1697
Dendritic cells (DCs) play a critical role in orchestrating the innate and adaptive components of the immune system so that appropriate, coordinated responses are mounted against infectious agents. Tissue-resident DCs interact with microbes through germline-encoded pattern-recognition receptors (PRRs), which recognize molecular patterns expressed by various microorganisms. Antigens use PRR activation to instruct DCs for the appropriate priming of natural killer (NK) cells, followed by specific T-cell responses. Due to the central role of DCs in regulating the activation and progression of immune responses, minor imbalances in the feedback control of Toll-like receptor (TLR)-activated cells have been associated with autoimmunity in genetically prone individuals. We review here recent findings on the role of DCs in the priming of innate and adaptive immune responses and the possible involvement of DCs in inducing and maintaining autoimmune reactions. 相似文献
19.
J. G. Chambó P. M. Cabeza Meckert R. P. Laguens 《Cellular and molecular life sciences : CMLS》1990,46(9):977-979
Summary The existence of antigens shared in common byT. cruzi and heart muscle cells is suggested by the presence of antibodies binding to the parasite surface in the serum of mice with autoimmune myocarditis induced by immunization with syngeneic heart antigens. 相似文献