Document Detail


Characterization of the suppressor activity in lymphocytes from patients with common variable hypogammaglobulinemia: evidence for an associated primary B-cell defect.
MedLine Citation:
PMID:  6309448     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The pathogenetic mechanisms responsible for the impaired immunoglobulin production in common variable hypogammaglobulinemia (CVH) are diverse with abnormalities in both B cells and immunoregulatory T cells. Production of IgG, IgM, and IgM-rheumatoid factor (IgM-RF) was measured in pokeweed mitogen (PWM) or Epstein-Barr virus (EBV)-stimulated cultures using various combinations of CVH, cord blood mononuclear cells (CBMC), and normal adult control B and T cells. The following results were obtained. First, the proportion of OKT3+ and OKT8+ cells were increased in CVH patients. Second, the T cells from four CVH patients and CBMC suppressed PWM-induced IgG, IgM, and IgM-RF production by normal B cells. Furthermore, major suppressor activity was found in the OKT8+ T-cell subpopulations in CBMC and three out of four CVH patients. There was no significant difference in relative suppression by OKT8+ cells from normal adults, CVH patients, or CBMC. However, in one CVH patient suppressor T cells were found in both OKT4+ as well as OKT8+ fractions. In the CVH patient with OKT4+ suppressor cells, X irradiation (1250 rads) abrogated suppressor activity and restored helper activity in the OKT4+ T-cell fraction. Irradiation of normal OKT4+ cells did not increase helper activity. When non-E-rosetting cells from normal subjects, CVH, and CBMC were stimulated with EBV it was observed that normal adult B cells could be induced to secrete IgG, IgM, and Ig-RF whereas CVH and CBMC could only produce IgM and IgM-RF but not IgG. The present study demonstrates for the first time that a radiosensitive OKT4+ suppressor cell is present in some CVH patients.
Authors:
M A Rodriguez; A D Bankhurst; R C Williams
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Clinical immunology and immunopathology     Volume:  29     ISSN:  0090-1229     ISO Abbreviation:  Clin. Immunol. Immunopathol.     Publication Date:  1983 Oct 
Date Detail:
Created Date:  1983-10-28     Completed Date:  1983-10-28     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0356637     Medline TA:  Clin Immunol Immunopathol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  35-50     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Agammaglobulinemia / immunology*
Antibodies, Monoclonal
Antigens, Surface / analysis*
B-Lymphocytes / immunology*
Fluorescent Antibody Technique
Herpesvirus 4, Human / immunology
Humans
Immunoglobulin G / genetics
Immunoglobulin M / genetics
Lymphocyte Activation
Pokeweed Mitogens
Rheumatoid Factor / genetics
Rosette Formation
T-Lymphocytes / immunology*
T-Lymphocytes, Regulatory / immunology*
Grant Support
ID/Acronym/Agency:
AM13690/AM/NIADDK NIH HHS; CA-24873/CA/NCI NIH HHS; M01-RR00997/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Antibodies, Monoclonal; 0/Antigens, Surface; 0/Immunoglobulin G; 0/Immunoglobulin M; 0/Pokeweed Mitogens; 9009-79-4/Rheumatoid Factor

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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