Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 199, Issue 1, Pages 47-57Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20031104
Keywords
bone marrow; innate immunity; TNF alpha; hematopoiesis; neutrophilia
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Funding
- NIAID NIH HHS [AI 49326, R01 AI024335, AI 56363, R01 AI049326, U19 AI056363, AI 24335] Funding Source: Medline
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Inflammation removes developing and mature lymphocytes from the bone marrow (BM) and induces the appearance of developing B cells in the spleen. BM granulocyte numbers increase after lymphocyte reductions to support a reactive granulocytosis. Here, we demonstrate that inflammation, acting primarily through tumor necrosis factor alpha (TNFalpha), mobilizes BM lymphocytes. Mobilization reflects a reduced CXCL12 message and protein in BM and changes to the BM environment that prevents homing by cells from naive donors. The effects of TNFalpha are potentiated by interleukin 1beta (IL-1beta), which acts primarily to expand the BM granulocyte compartment. Our observations indicate that inflammation induces lymphocyte mobilization by suppressing CXCL12 retention signals in BM, which, in turn, increases the ability of IL-1beta to expand the BM granulocyte compartment. Consistent with this idea, lymphocyte mobilization and a modest expansion of BM granulocyte numbers follow injections of pertussis toxin. We propose that TNFalpha and IL-1beta transiently specialize the BM to support acute granulocytic responses and consequently promote extramedullary lymphopoiesis.
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