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Involvement of HLA‐DR+ Large Granular Lymphocytes in the Induction of Tumor Necrosis Factor by Mycobacterium avium‐intracellulare Complex
Author(s) -
MicheliniNorris M. Beatriz,
Blanchard D. Kay,
Friedman Herman,
Djeu Julie Y.
Publication year - 1991
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.50.6.529
Subject(s) - biology , tumor necrosis factor alpha , cd8 , cd16 , secretion , immunology , monoclonal antibody , macrophage , peripheral blood mononuclear cell , population , percoll , microbiology and biotechnology , immune system , antibody , cd3 , endocrinology , in vitro , medicine , biochemistry , environmental health
This study shows that normal human large granular lymphocytes (LGL) secrete tumor necrosis factor (TNF) in response to Mycobacterium avium‐intracellulare complex (MAI). Percoll density gradient fractionation of peripheral mononuclear cells showed TNF activity in the fractions corresponding to LGL and not T cells, even when 5% monocytes were added to the T lymphocytes for accessory function. TNF release was not abrogated by treatment of the crude LGL preparations with anti‐Leu M3. ‐CD4. and ‐CD8 antibodies (Ab) plus complement (C), but was abrogated by anti‐CD16 and ‐CD2 Ab, as expected. Interestingly, anti‐HLA‐DR monoclonal antibody (mAb) treatment significantly diminished TNF activity from LGL, but maintained natural killer (NK) cell function unmodified as opposed to CD2 ‐ and CD16‐ cell depletion. Panning studies demonstrated that TNF secretion upon MAI stimulation resided only in the HLA‐DR+ LGL and not the DR LGL population. These results indicate that normal fresh HLA‐DR+ LGL, as well as monocytes, are also responsible for rapid TNF secretion during early MAI infection. These DR ‐ cells appear to be distinct from those expressing NK function.