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Changes in Splenic Macrophage Mac Antigen Expression During Tumor Growth: A Kinetic Study of Accessory Cell Function and Antigen‐Defined Phenotypes
Author(s) -
Garner Ronald E.,
Elgert Klaus D.
Publication year - 1986
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.40.6.709
Subject(s) - biology , spleen , antigen , epitope , microbiology and biotechnology , immunology , antibody , monoclonal antibody , t cell , immune system
Three monoclonal antibodies, anti‐Mac‐1, ‐2, and ‐3, were used to modify accessory cell activity of whole spleen cell (WSC) or splenic adherent cell (SAC) preparations from normal or tumor‐bearing hosts (TBH). Ligand activation by anti‐Mac‐1, ‐2 and ‐3 modified normal and TBH WSC lectin responses differentially; the most pronounced effect was with anti‐Mac 1, which augmented normal WSC responsiveness, whereas anti‐Mac‐2 and ‐3 augmented TBH WSC mitogenesis. Ligand interaction with Mac‐2 epitopes resulted in significantly suppressed normal host WSC responsiveness. With complement, anti‐Mac‐1 and ‐3 each reduced normal and TBH WSC proliferation. Reconstitution of blastogenesis was obtained by combining Mac‐2‐depleted with Macs‐depleted normal host WSC or by combining Mac‐1 ‐depleted with Mac‐2‐depleted TBH WSC. To evaluate the role of different types of splenic adherent cells in T cell lectin responsiveness, adherent cells were collected and depleted by antibody plus complement treatment and added back to normal T cells. Removal of TBH SAC indicated the number of Mac‐1 + SAC susceptible to lysis increased during tumor growth, whereas those susceptible to anti‐Mac‐2 and‐3 treatment decreased. Removal of Mac‐1 + normal host SAC stimulated the supportive accessory function of the remaining SAC. Enhancing accessory cell function diminished after removal of Mac‐2 + or Mac‐1 + normal and TBH SAC, respectively. T cell responsiveness was increased by adding back combinations of normal host SAC, Mac‐1‐depleted with Mac‐3‐depleted SAC or Mac‐1‐depleted with Mac‐2‐depleted SAC but not by Mac‐2‐depleted with Macs‐depleted SAC. In contrast, none of the TBH SAC combinations were completely restored in accessory activity. In summary, SAC from normal host demonstrated an accesssory cell function corresponding to a Mac‐1 ‐ phenotype, which was either replaced or obscured by the predominance of a Mac‐1 + phenotype in TBH.