PubMed Health⌕ Search

Biomedical subjects

S K Stylianos

Publications and source records attributed to S K Stylianos.

9 recordsLinked to original sources
PubMed1980

Expression of Ia in mouse kidney.

Expression of Ia antigens in mouse kidney was studied by absorption of diluted anti-Ia sera with crude suspensions of kidney issue. Specific absorption of anti-Ia activity was seen for all Ia specificities tested: Ia.1,2, Ia.3, Ia.4,5,12, Ia.7, Ia.8, Ia.9, Ia.15, and Ia.16. Certain polyspecific antisera (against the I-Ak products Ia.1,2,3,15) were more difficult to absorb than oligo-specific antisera against other Ia specificities (e.g., Ia.7 and Ia.9). This observation may indicate that polyspecific sera are less absorbable by limited numbers of antigenic sites because of steric hindrance, although differences in the extent of antigen expression in kidney have not been excluded. Ia absorption could be demonstrated either in microcytotoxicity or in 51Cr release assays. Both mechanically disrupted and enzyme-disrupted kidney tissue suspensions absorbed Ia specifically, although the former method was used routinely. As estimated from the efficiency of absorption, the amount of Ia in kidney was small, about 2 to 5% of that in spleen. One kidney was equivalent in absorptive capacity to about 3 X 10(6) splenocytes, and to greater than 3 X 10(6) buffy coat cells. Comparisons of the rates of absorption indicated that the amount of Ia in kidney was less than the amount of an H-2K or D alloantigen. Ia was expressed in kidney in an immunogenic form, since animals immunized repeatedly with I region-incompatible kidney tissue produced anti-Ia antibodies. Thus, Ia antigens are expressed in and are immunogenic in mouse kidney and can be studied by conventional serological techniques.

Animals↗
PubMed1980

Expression of Ia in mouse kidney. II. Evidence for expression on resident marrow-derived and nonmarrow-derived cells.

The origins of Ia antigens in perfused mouse kidney were investigated. Three possible sources were considered: leukocytes in residual blood which was trapped in kidney, bone marrow-derived cells resident in kidney, and nonbone marrow-derived renal parenchymal or vascular cells. Leukocytes in trapped blood seemed to make no significant contribution to renal Ia expression because (1) perfused kidney had approximately as much Ia as nonperfused kidney, even though the perfusion reduced the blood content by 90%; (2) the estimated number of leukocytes in trapped blood was at least three orders of magnitude less than that needed to account for Ia expression by kidney; and (3) perfused kidney, volume for volume, absorbed more anti-Ia than did whole blood, so that no amount of blood contamination could account for all renal Ia expression. Thus most Ia in kidney must be on resident cells, either bone marrow-derived or parenchymal. To demonstrate bone marrow-derived Ia-positive cells, we created radiation chimeras of (B10 X B10.D2)F1 bone marrow into B10 hosts. Ia of (B10 X B10.D2)F1 bone marrow donor origin was easily detectable in kidneys of these chimeras at 4 months. However, we also demonstrated Ia of nonbone marrow donor origin in chimera kidney: long-term B10.A into (BALB/c X A)F1 chimeras and C57BL/6 into (C57BL/6 X DBA/2)F1 chimeras continued to express renal Ia of bone marrow recipient origin. Thus, some renal Ia is produced by bone marrow-derived cells, and some is produced by cells which are nonmarrow derived (or are marrow derived but are resistant to replacement in bone marrow chimeras). The cells expressing Ia in kidney were unlikely to be thymus derived because anti-Thy-1.2 was not absorbable by the same kidney preparations which absorbed anti-Ia.

Animals↗
PubMed1979

Macrophage-alloantibody-target cell interactions. II. Nonphagocytic effects.

Two nonphagocytic effects of macrophages on antibody-coated lymphocyte target cells were studied: antibody-dependent cell-mediated cytotoxicity (ADCC) and abrogation of complement lysis (ACL) by nonphagocytic mechanisms. Macrophages did not mediate ADCC, and actually inhibited K cell-mediated ADCC, presumably by direct interactions with the antibody-coated target cells. These interactions were studied in the ACL assay previously described, in which macrophages, antibody, and 51Cr-labelled target cells were incubated for 1 hr. Then complement lysis (as measured by 51Cr release) was performed to assess the status of the target cells. The nonphagocytic component of ACL could be distinguished from the phagocytic component by the addition of a second antibody during the complement lysis phase. This procedure revealed that some of the target cells which were resistant to the original antibody were susceptible to lysis by a second antibody and were therefore not phagocytized. Such cells had apparently been stripped of their antibody and the associated antigen by the macrophages. In support of this interpretation, specific antigen alterations were demonstrable on these stripped cells under certain conditions. These alterations were produced more consistently when the macrophages were less than maximally stimulated, and were detected better by guinea pig complement than by rabbit complement. The mechanism of stripping may involve inactivation, redistribution, or removal of target cell-bound antibody by the macrophages. Possible in vivo roles for the stripping mechanism, for example, in the enhancement of tumours or allografts, are discussed.

Animals↗