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TNF- and IFN- are overexpressed in the bone marrow of Fanconi anemia patients and TNF- suppresses erythropoiesis in vitro
Abstract
In Fanconi anemia (FA) C mice tumor necrosis factor alpha (TNF-alpha) and interferon gamma (IFN-gamma) have key roles in the pathogenesis of bone marrow failure. In FA subjects TNF-alpha was found to be increased in the serum and overproduced by patient-derived B-cell lines. In acquired aplastic anemia, a disease in which, similarly to FA, marrow failure occurs, TNF-alpha and IFN-gamma act as late mediators of the stem cell damage and are overexpressed in patient marrow lymphocytes. This study evaluated in marrow mononuclear cells (MNCs) of patients with FA, the expression of negative modulators of the hematopoiesis, such as TNF-alpha, IFN-gamma, macrophage inflammatory protein 1alpha (MIP-1alpha), and surface Fas ligand, and the role of TNF-alpha on FA erythropoiesis in vitro. TNF-alpha and IFN-gamma were significantly overexpressed in stimulated marrow MNCs of FA patients as compared to healthy controls. MIP-1alpha and Fas ligand were undetectable in patients and controls. In bone marrow cultures, the addition of anti-TNF-alpha increased the size and significantly increased the number of erythroid colony-forming units and erythroid burst-forming units grown from FA patients but not from healthy controls. This indicates that FA subjects have a marrow TNF-alpha activity that inhibits erythropoiesis in vitro. TNF-alpha has a relevant role in the pathogenesis of erythroid failure in FA patients.
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“Importantly, the addition of the anti-TNF-α fusion decoy protein etanercept to human bone marrow cultures was associated with a significantly increased number and size of erythroid colonies grown in vitro in FA but not in normal control samples, indicating that TNF-α inhibits FA erythropoiesis in vitro [15].”
From Finding the needle in the hay stack: Hematopoietic stem cells in Fanconi anemia (2009) · cites this paper as [15]
Citations
Cites
Interaction of the Fanconi Anemia Proteins and BRCA1 in a Common Pathway
Garcia-Higuera, I., Taniguchi, T., Ganesan, S., Meyn, M. S., Timmers, C., Hejna, J., Grompe, M., & D'Andrea, A. D. (2001) · Molecular Cell · doi:10.1016/s1097-2765(01)00173-3 · Cited by 1,198
Biallelic Inactivation of BRCA2 in Fanconi Anemia
Howlett, N. G., Taniguchi, T., Olson, S., Cox, B., Waisfisz, Q., de Die-Smulders, C., Persky, N., Grompe, M., Joenje, H., Pals, G., et al. (2002) · Science · doi:10.1126/science.1073834 · Cited by 1,149
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Fanconi Anemia Proteins Function in Mitophagy and Immunity
Sumpter, R., Sirasanagandla, S., Fernández, Á. F., Wei, Y., Dong, X., Franco, L., Zou, Z., Marchal, C., Lee, M. Y., Clapp, D. W., et al. (2016) · Cell · doi:10.1016/j.cell.2016.04.006 · Cited by 250
“Thus, FA gene deficiency could lead to increased generation of known and potential cytokine triggers of bone marrow failure in FA patients (Dufour et al., 2003; Garbati et al., 2013) through the dual effects of defective viral autophagic targeting (and increased accumulation of pathogen-associated…”
Impact of interferon-γ on hematopoiesis
de Bruin, A. M., Voermans, C., & Nolte, M. A. (2014) · Blood · doi:10.1182/blood-2014-04-568451 · Cited by 215
Hematopoietic stem cell defects in mice with deficiency of Fancd2 or Usp1
Parmar, K., Kim, J., Sykes, S. M., Shimamura, A., Stuckert, P., Zhu, K., Hamilton, A., Deloach, M. K., Kutok, J. L., Akashi, K., et al. (2010) · Stem Cells · doi:10.1002/stem.437 · Cited by 113
Chen, J., Feng, X., Desierto, M. J., Keyvanfar, K., & Young, N. S. (2015) · Blood · doi:10.1182/blood-2015-06-652453 · Cited by 97
Multiple members of the TNF superfamily contribute to IFN-γ-mediated inhibition of erythropoiesis
Felli, N., Pedini, F., Zeuner, A., Petrucci, E., Testa, U., Conticello, C., Biffoni, M., Di Cataldo, A., Winkles, J. A., Peschle, C., et al. (2005) · The Journal of Immunology · doi:10.4049/jimmunol.175.3.1464 · Cited by 96
Metadata
- Authors
- Dufour, C.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2003-09-15
- Volume
- 102
- Issue
- 6
- Pages
- 2053-2059
- ISSN
- 0006-4971
- 1528-0020
- Cited by
- 213
- References
- 2
- Language
- en
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