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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
MeSH Review

B-Lymphocytes

 
 
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Disease relevance of B-Lymphocytes

 

Psychiatry related information on B-Lymphocytes

  • Our data suggest that an IL-6 autocrine self stimulation confers on B cells a selective growth advantage and results in the induction of progression of the malignant state of B cells [6].
  • A fusion protein containing a B cell lymphoma idiotype (Id) and granulocyte-macrophage colony-stimulating factor (GM-CSF) is a potent stimulator of tumor immunity [7].
  • Three children developed normal B cell immunity, two of whom received ablative conditioning therapy with either radiation or busulfan [8].
  • These results suggested that antigen-stimulated NKT cells might play a critical role not only in early defense mechanisms but also in early B-cell activation through IL-4 production [9].
  • Dysregulation of IL-6 synthesis is thought to play a role in the development of a number of age-related conditions, such as rheumatoid arthritis, osteoporosis, atherosclerosis, Alzheimer's disease and B cell malignancies [10].
 

High impact information on B-Lymphocytes

  • PD-1 and BTLA also are expressed on B cells and may have broader immunoregulatory functions [11].
  • Recent data indicate that Notch can also direct the differentiation and activity of peripheral T and B cells [12].
  • Pax5 restricts the developmental options of lymphoid progenitors to the B cell lineage by repressing the transcription of lineage-inappropriate genes and simultaneously activating the expression of B-lymphoid signaling molecules [13].
  • BAFF AND APRIL: a tutorial on B cell survival [14].
  • Plasma cells that result from antigen activation of B-1 and marginal zone B cells provide the first, rapid response to antigen [15].
 

Chemical compound and disease context of B-Lymphocytes

 

Biological context of B-Lymphocytes

 

Anatomical context of B-Lymphocytes

  • Therefore, CD28 receptor stimulation is required for T cell responses to antigens and for B cell responses to T-dependent antigens [26].
  • Other cells in this group participate in cognate cellular interactions with helper T cells in which the recognition of both antigen and a class II MHC molecule on the B-cell surface is key to activation [27].
  • In addition, IL-10 likely contributes to regulating proliferation and differentiation of B cells, mast cells, and thymocytes [28].
  • CD21 is also expressed by follicular dendritic cells and mediates the long-term retention of antigen that is required for the maintenance of memory B cells [29].
  • Our results indicate that Fus is essential for viability of neonatal animals, influences lymphocyte development in a non-cell-intrinsic manner, has an intrinsic role in the proliferative responses of B cells to specific mitogenic stimuli and is required for the maintenance of genomic stability [30].
 

Associations of B-Lymphocytes with chemical compounds

  • Covalent attachment of activated complement C3 (C3d) to antigen links innate and adaptive immunity by targeting antigen to follicular dendritic cells (FDC) and B cells via specific receptors CD21 and CD35 [31].
  • In both T- and B-lymphocyte activation, antigen receptor or mitogen stimulation results in phosphoinositide turnover, generation of InsP3 and diacylglycerol, and a sustained rise in intracellular Ca2+, from both intracellular Ca2+ stores release and enhanced transmembrane Ca2+ influx [32].
  • Most recent evidence suggests that complement also regulates elimination of self-reactive B cells, as breeding of mice that are deficient in C4 or CD21/CD35 with the lupus-prone strain of lpr mice demonstrates an exacerbation of disease due to an increase in autoantibodies [31].
  • In contrast, two other polyclonal B cell activators, lipopolysaccharide and phorbol myristate acetate, failed to induce any of these effects [33].
  • Functional maturation of B lymphocytes correlates with expression of the B lineage-specific cell surface glycoprotein CD22 [34].
 

Gene context of B-Lymphocytes

  • Regulation of B lymphocyte responses to foreign and self-antigens by the CD19/CD21 complex [29].
  • This complex reduces the threshold for B cell activation via the B cell receptor by bridging Ag specific recognition and CD21-mediated complement recognition [35].
  • Soluble recombinant forms of gp39 containing these mutations were unable to bind CD40 and drive normal B cell proliferation [23].
  • We further demonstrate that CD22 recognizes a second ligand, CD75, expressed predominantly on activated B cells and shown to be a cell surface alpha 2-6 sialyltransferase [34].
  • Independent regulation of the two Pax5 alleles during B-cell development [36].
 

Analytical, diagnostic and therapeutic context of B-Lymphocytes

References

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