| First Author | Forman J | Year | 1985 |
| Journal | Surv Immunol Res | Volume | 4 |
| Issue | 1 | Pages | 41-7 |
| PubMed ID | 3923586 | Mgi Jnum | J:7887 |
| Mgi Id | MGI:56356 | Doi | 10.1007/BF02918585 |
| Citation | Forman J, et al. (1985) Recognition of an Igh-linked histocompatibility antigen, H-40, on B-cell tumors by cytotoxic T lymphocytes. Surv Immunol Res 4(1):41-7 |
| abstractText | This article reviews our data on H-40, a histocompatibility antigen controlled by a locus linked to Igh structural genes but telomeric to Tsu. The antigen is detected by rejection of H-40+ tumor cells in vivo and by the activity of H-2 restricted anti-H-40 cytotoxic T lymphocytes in vitro. H-40 is expressed on lipopolysaccharide stimulated B cells and B cell tumors that express surface(s) IgM and not on sIgM- tumors or other neoplastic cells. Its expression on the sIgM,D+ BALB/c (Igha, H-40a) derived leukemia, BCL1, prevents its transplantability across the Ig heavy chain (and H-40) barrier into C.B-20 (Ighb, H-40b) mice; whereas, BALB/c tumors that do not express H-40 can be transplanted into this allotype-congenic recipient. Although irradiated C.B-20 animals are susceptible to the BCL1 tumor, adoptive transfer of a mixture of Lyt-2+ and Lyt-2- effector cells (anti-H-40) from C.B-20 animals that have previously rejected BCL1 protect such recipients. However, the same effector cells will not protect irradiated BALB/c or (BALB/c X C.B-20)F1 recipients from this tumor. Since normal BALB/c sIg+ cells express H-40, either the effector cells are diverted from interacting with and destroying the tumor, or recognition of H-40 on non-tumor cells elicits a suppressor mechanism. |
