Myeloid differentiation factor

Eisenbarth SC, Zhadkevich A, Ranney P, Herrick CA, Bottomly K IL-4-dependent Th2 collateral priming to inhaled antigens independent of Tolllike receptor 4 and myeloid differentiation factor 88. J Immunol 2004 172 4527-4534. 

Gobert, A.P., Bambou, J.-C., Werts, C., Balloy, V., Chignard, M., Moran, A.P., and Ferrero, R.L. Helicobacter pylori heat shock protein 60 mediates interleukin-6 production by macrophages via a Toll-like receptor (TLR)-2-, TLR-4-, and myeloid differentiation factor 88-independent mechanism. J Biol Chem 279 (2004) 245-250. 

Myeloid differentiation factor 88 (MyD88) Mouse Cecal ligation and puncture Yes. No protection against liver injury [205]... 

Hacker, H., Vabulas, R.M., Takeuchi, O., Hoshino, K., Akira, S. and Wagner, H. (2000) Immune cell activation by bacterial CpG-DNA through myeloid differentiation marker 88 and tumor necrosis factor receptor-associated factor (TRAF)6. J. Exp. Med., 192, 595-600. 

Another example of problems in interpreting results in knockout mice is demonstrated by the following An important role of colony-stimulating factor (CSF) in hemopoiesis of myeloid lineage cells has been demonstrated. G-CSF was knocked out, animals were neutropenic and had decreased hemopoietic progenitors in bone marrow and spleen [24]. In contrast, mice with a null mutation in GM-CSF, which acts upstream to G-CSF in myeloid differentiation, demonstrated no impairment of hemopoiesis, but develop a characteristic pulmonary pathology [25]. Therefore, we have to interpret the results of our experiments with knockout mice with caution. 

Scatena R, Nocca G, De Sole P, Rumi C, Puggioni P, Remiddi F, Bottom P, Ficarra S, Giardina B. Bezafibrate as differentiating factor of human myeloid leukemia cells. Cell Death Differ 1999 6 781-7. 

Cytokines, eg, interferons, interleukins, tumor necrosis factor (TNF), and certain growth factors, could have antitumor activity directiy, or may modulate cellular mechanisms of antitumor activity (2). Cytokines may be used to influence the proliferation and differentiation of T-ceUs, B-ceUs, macrophage—monocyte, myeloid, or other hematopoietic cells. Alternatively, the induction of interferon release may represent an important approach for synthetic—medicinal chemistry, to search for effective antiinflammatory and antifibrotic agents. Inducers of interferon release may also be useful for lepromatous leprosy and chronic granulomatous disease. The potential cytokine and cytokine-related therapeutic approaches to treatment of disease are summarized in Table 4. A combination of cytokines is a feasible modaUty for treatment of immunologically related diseases however, there are dangers inherent in such an approach, as shown by the induction of lethal disserninated intravascular coagulation in mice adrninistered TNF-a and IFN-y. 

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