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Updated: Aug 14, 2026

Murine Model of CD40-activation of B cells
Published on: March 6, 2010
Recognition of an Igh-linked histocompatibility antigen, H-40, on B-cell tumors by cytotoxic T lymphocytes
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.
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.
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