EXPRESSION OF Ia IN MOUSE KIDNEY

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Abstract
The Ia antigen origins in perfused mouse kidney were investigated. Possible sources were considered: leukocytes in residual blood which was trapped in kidney, B cells resident in kidney, and non-B renal parenchymal or vascular cells. Leukocytes in trapped blood seemed to make no significant contribution to renal Ia expression because of the following: perfused kidney had approximately as much Ia as nonperfused kidney, even though the perfusion reduced the blood content by 90%; the estimated number of leukocytes in trapped blood was at least 3 orders of magnitude less than that needed to account for Ia expression by kidney; and 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. Most Ia in kidney must be on resident cells, either B cells or parenchymal cells. To demonstrate Ia-positive B cells, radiation chimeras of (B10 .times. B10.D2)F1 bone marrow into B10 hosts were created. Ia of (B10 .times. B10.D2)F1 bone marrow donor origin was easily detectable in kidneys of these chimeras at 4 mo. Ia of nonbone marrow donor origin was demonstrated in chimera kidney: long-term B10.A into (BALB/c .times. A)F1 chimeras and C57BL/6 into (C57BL/6 .times. DBA/2)F1 chimeras continued to express renal Ia of bone marrow recipient origin. Some renal Ia is produced by B 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 T cells because anti-Thy-1.2 was not absorbable by the same kidney preparations which absorbed anti-Ia.