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.