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Radiation leukemia virus (RadLV)‐induced leukemogenesis is associated with an increased number and activity of thymic macrophages
Author(s) -
Messika E.,
Gallily R.,
Yefenof E.
Publication year - 1991
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.2910480621
Subject(s) - lymphoma , biology , leukemia , antibody , macrophage , immunology , cancer research , in vitro , biochemistry
The radiation leukemia virus (RadLV) is a chronic leukemia retrovirus that induces thymlc lymphomas in C57BL/6 mice after a latency of 3 to 6 months. During the pre‐leukemic (PL) period, the number of thymic macrophages gradually increased up to 100 fold. Of the cells in a RadLV‐induced lymphoma, 0.3% were large macrophages packed with infected lymphoma cells. These thymic lymphoma macrophages (TLM) also ingested RadLV‐induced lymphoma cells in vitro . red RadLV‐induced lymphoma lines could activate and fix C3 fragments through the alternative complement pathway (ACP). C3‐bound lymphoma cells elicited an oxidatlve burst (OB) response in TLM but not in bone‐marrow macrophages (BMM). However, IL4 treatment of BMM rendered them capable of responding with an OB following triggering by C3‐opsonized cells. Thymic macrophages (TM) responded moderately with OB to C3‐opsonized cells and this response was elevated If the TMs were treated by rlL4. The OB reaction of the TLMs could be partially inhibited by anti‐LFA‐1 or anti‐MALA‐2 antibodies, and was completely inhibited by antl‐CR3 antibodies. These results suggest that IL4 can prime macrophages for triggering an OB reaction and that the interaction between C3‐opsonized cells and IL4‐primed macrophages is mediated primarily through CR3.