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Bone marrow cells from A/J mice do not proliferate in interleukin‐3 but express normal numbers of interleukin‐3 receptors
Author(s) -
Hapel Andrew J.,
Fung MingChiu,
Mak NaiKi,
Morris Carolyn,
Metcalf Donald,
Nicola Nicos
Publication year - 1992
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1992.tb06457.x
Subject(s) - bone marrow , biology , immunology , interleukin 3 , receptor , spleen , microbiology and biotechnology , t cell , immune system , antigen presenting cell , biochemistry
Summary. Haemopoietic cells from A/J mice do not form colonies (proliferate) in response to interleukin‐3 (multi‐CSF. IL‐3). We have examined different populations of cells from A/J mice and shown that, despite their failure to proliferate in response to IL‐3, cells from bone marrow, spleen and the peritoneum all bound 125 I‐labelled IL‐3. A wide variety of cell types bound IL‐3 as determined by autoradiography, including promyelocytes, myelocytes, metamyelocytes, polymorphs, promonocytes, monocytes, eosinophils and lymphocytes, but not nucleated erythroid cells, and the proportion of each cell type binding label was similar when cells from A/J mice were compared with those of C57B1/6 and Balb/c mice. Bone marrow cells from A/J mice internalized interleukin‐3 with normal kinetics and mRNA extracted from these cells contains the same species of IL‐3 receptor and IL‐3 receptor‐like mRNAs as are found in the other strains. Collectively the data suggest that the failure of haemopoietic cells from A/J mice to proliferate in response to IL‐3 is related to a selective defect in signalling to proliferation specific genes. This defect is apparently not related to internalization or processing of the IL‐3/IL‐3‐receptor complex, but may be due to failure to activate appropriate accessory molecules in the cell.