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R E Garner

Publications and source records attributed to R E Garner.

24 records · Page 2Linked to original sources
PubMed1986

Variations in macrophage antigen phenotype: a correlation between Ia antigen reduction and immune dysfunction during tumor growth.

Variable Ia antigen expression by macrophages (M phi) was examined during tumor growth by measuring: Ia antigen masking and immunofluorescence by anti-Ia antibody, accessory cell function in concanavalin A (Con A) and mixed lymphocyte reaction (MLR)-induced T cell proliferation, and M phi stimulatory function in the MLR. Tumor-induced progressive loss of Ia antigen expression was shown by immunofluorescence and corroborated by anti-Ia blockade of MLR stimulatory activity of normal but not tumor-bearing hosts (TBH) splenic M phi. The TBH splenic M phi supported Con A-induced proliferation of syngeneic T cells (Ia antigen-independent) but did not support syngeneic T cell proliferation in the MLR (Ia antigen-dependent). Irrespective of tissue source, normal and TBH M phi differed in their MLR stimulatory capabilities. In general, splenic M phi preparations were better stimulators of allogeneic T cell blastogenesis in the MLR than thioglycollate-elicited peritoneal M phi. Kinetic studies with TBH M phi showed a significant progressive loss in MLR stimulatory activity, which was especially pronounced with peritoneal M phi. Expression of Ia antigens by normal but not TBH M phi were diminished by 24-h in vivo plating of the peritoneal M phi. Indomethacin treatment showed Prostaglandin E2 was not a direct in vitro factor in Ia antigen-mediated reduction of splenic M phi MLR stimulatory activity. Taken together, these data delineate a loss of M phi Ia antigen expression, resulting in a decrease in Ia antigen-mediated functional activities during tumor growth.

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PubMed1986

Changes in splenic macrophage Mac antigen expression during tumor growth: a kinetic study of accessory cell function and antigen-defined phenotypes.

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 Mac-3-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 Mac-3-depleted SAC. In contrast, none of the TBH SAC combinations were completely restored in accessory activity. In summary, SAC from normal host demonstrated an accessory cell function corresponding to a Mac-1- phenotype, which was either replaced or obscured by the predominance of a Mac-1+ phenotype in TBH.

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PubMed1984

In vivo assessment of tumor-induced nonspecific suppression of contact sensitivity. II. Regulation by cytokines and T cells via adoptive transfer.

Normal BALB/c mice were assessed for 2,4-dinitrofluorobenzene (DNFB)-induced contact sensitivity following adoptive transfer of macrophages (Mo). T cells, or their derived products, from normal or tumor-bearing hosts (TBH). Contact sensitivity (CS) was measured by a quantitative radioisotopic ear assay, a total in vivo system based on localization of IP-injected iodinated human serum albumin [( 125I]HSA) in the DNFB-challenged ear. Adoptive transfer of low or high doses of TBH T cells or their derived supernatants into normal recipients suppressed their responsiveness, while Mo supernatants enhanced it. Moreover, in all cases adoptive transfer of TBH cells or supernatants resulted in a lower CS response than did their normal counterparts. These results further corroborate our previous in vitro data indicating that T cells, or Mo and T cell soluble products, possess immunoregulatory capabilities in vivo.

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PubMed1984

Normal and tumor-bearing host macrophage factor-mediated modulation of mixed-lymphocyte reaction responsiveness: separation of T-lymphocyte subset susceptibility to enhancing and inhibitory factors.

The mixed-lymphocyte reaction reactivity of normal and tumor-bearing host (TBH) T-cell subsets was examined in response to normal and TBH macrophage (M phi) supernatants. Both inhibiting and enhancing activities were identified in normal and TBH M phi supernatants. The present data suggest that TBH M phi supernatants contained more inhibitory activity than normal host M phi supernatants and that enhancing activity of M phi supernatants was restricted to the Lyt 2,3+ population of cells. TBH Lyt 2,3+ cells were more responsive to the enhancing molecule(s) than their normal counterparts. These data were consistent with studies which implicate M phi as being partially responsible for the immune dysfunction seen in TBH, and extends previous findings on the ability of M phi to regulate the immune response in an attempt to achieve homeostasis.

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PubMedDate not supplied

Morphologic and biochemical studies of chitin expression in Pneumocystis carinii.

Tomato lectin, which binds oligosaccharides of N-acetyl-D-glucosamine, and an antiserum against macromolecular chitin were used to probe sections of human and murine lungs infected with Pneumocystis carinii. By light, fluorescence and electron microscopy, lectin and antiserum binding patterns indicated that both human and murine strains of P. carinii express chitin at all identifiable stages of their life cycles. Light microscopic autoradiographs of murine P. carinii cultured in vitro with 3H-glucosamine revealed dense incorporation of the radiolabel into the cell walls in a pattern analogous to those of the antiserum and lectin binding studies. These investigations offer further evidence that chitin is an integral part of the cell wall of P. carinii trophozoites and cysts.

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