Abstract
Interleukin-2 (IL-2)-deficient (IL-2-/-) mice develop anemia and colonic inflammatory bowel disease. To elucidate the mechanism of this disease, we have bred IL-2-/- mice to two strains of immunodeficient mice, RAG-2-deficient (RAG-2-/-, lacking B and T cells) and JH-deficient mice (JH-/-, lacking B cells). IL-2-/-, RAG-2-/- double-mutant mice are disease free, while IL-2-/-, JH-/- double-mutant mice succumb to bowel disease at the same rate as IL-2-/- littermates. IL-2-/-, JH-/- mice do not, however, succumb to anemia. Thus, spontaneous intestinal inflammation in IL-2-/- mice requires mature T cells, not B cells, while anemia is dependent on B cells.
MeSH Terms
Anemia, Hemolytic, Autoimmune/etiology,immunology
Animals
Autoantibodies/analysis
Autoimmune Diseases/etiology,immunology,pathology
B-Lymphocytes/immunology
Colon/pathology
DNA-Binding Proteins
Immunoglobulin Heavy Chains/genetics
Immunoglobulin J-Chains/genetics
Immunologic Deficiency Syndromes/complications,genetics
Inflammatory Bowel Diseases/etiology,immunology,pathology
Interleukin-2/deficiency,genetics
Mice
Mice, Knockout
Mice, Transgenic
Models, Immunological
Opportunistic Infections/complications
Proteins/genetics
Specific Pathogen-Free Organisms
T-Lymphocytes/immunology
Chemicals
Autoantibodies
DNA-Binding Proteins
Immunoglobulin Heavy Chains
Immunoglobulin J-Chains
Interleukin-2
Proteins
Rag2 protein, mouse
V(D)J recombination activating protein 2
Authors & Affiliations
5 authors, click to expand affiliations / ORCID
Ma A
Center for Blood Research, Harvard Medical School, Boston, Massachusetts 02115, USA.
Datta M
Margosian E
Chen J
Horak I
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