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  • Multiple myeloma  (1)
  • mice  (1)
  • 1
    ISSN: 1573-2592
    Keywords: Multiple myeloma ; CD4+ subsets ; CD8+ subsets
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The phenotypic distribution of T-lymphocyte subsets in peripheral blood from multiple myeloma (MM) patients shows a reduced proportion of CD4+ cells and a normal proportion of CD8+ cells. The decrease in CD4+ cells could be due to a random process, with all types of CD4+ cells being equally affected, or it could reflect a nonrandom process with selected subsets preferentially reduced. In order to distinguish between these possibilities, double immunofluorescence analysis was performed on blood samples from patients with MM, patients with monoclonal gammopathy of unknown significance (MGUS), and age-matched normal donors, using monoclonal anti-CD4 or anti-CD8 paired with antibodies to the common leukocyte marker Lp220 (CD45R) or 4B4 (CDw29). Normal peripheral blood lymphocytes (PBL) include two phenotypically and functionally distinct CD4+-cell subsets, identified as CD4+ Lp220+ 4B4-and CD4+ Lp220- 4B4+, whereas the majority of CD8+ cells expresses Lp220 (70–85%). MM patients had a highly significant selective reduction of the CD4+ Lp220+ subset compared with normal controls (P〈0.001). Although the percentage of CD4+ Lp220- cells was also reduced in some MM patients relative to normal donors, most of MM patients had an elevated Lp220-/Lp220+ ratio of CD4+ cells (P〈0.001). The proportion of the two CD8+ subsets was also markedly abnormal. In the set of patients studied the abnormalities within the CD4+ and CD8+ lymphocytes were exclusive to patients with MM since patients with MGUS had normal proportion of CD4+ and CD8+ subsets.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-2592
    Keywords: Cognate activation ; X-linked immunodeficiency ; humoral immunity ; humans ; mice
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The identification of the gp39-CD40 as an essential ligand-receptor pair for TD humoral immunity offers new insights into the regulation of TD immune responses. It is apparent that alterations in the regulation of gp39 expression, either by mutations in the gp39 gene (HIM patients) or by other factors that influence expression (like cyclosporine), have an overwhelming effect on humoral immunity. Whether other arms of the immune response are targets of gp39 action is unknown at this time. However, the identification of CD40 as the receptor for gp39 provides clues as to other CD40-expressing cell types (folicular dendritic cells, thymic epithelial cells, etc.) that might be regulated by activated CD4+ T cells. The immunosuppressive effects of anti-gp39 on primary and secondary humoral immunity, as well as the beneficial therapeutic effects of anti-gp39 on the progression of autoimmune disease in animal models, suggest that this ligand-receptor pair is an ideal target for the therapeutic intervention.
    Type of Medium: Electronic Resource
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