Figure 4.
Figure 4. Effect of anti–TNF-α on erythroid-committed progenitor growth in FA patients. (A) CFU-Es grown in the absence of anti–TNF-α are shown (i,ii; medium alone). The size of CFU-Es cultured in the absence of anti–TNF-α but in the presence of purified Fc fragment of human IgG1 were not different (not shown). The addition of LD (1 μg/mL) anti–TNF-α (iii,iv) increased the size of CFU-Es grown from marrow MNCs of FA patients. A similar effect was seen with HD (10μg/mL) anti–TNF-α (not shown). (B) BFU-Es grown in the absence of anti–TNF-α are shown (i,ii; medium alone). The size of BFU-Es cultured in the absence of anti–TNF-α but in the presence of purified Fc fragment of human IgG1 were not different (not shown). Panel Bii shows a minor nonhemoglobinized component at the periphery. The addition of LD anti–TNF-α (iii,iv) increased the size of BFU-Es grown from BM MNCs of FA patients. A similar effect was seen with HD anti–TNF-α (not shown).

Effect of anti–TNF-α on erythroid-committed progenitor growth in FA patients. (A) CFU-Es grown in the absence of anti–TNF-α are shown (i,ii; medium alone). The size of CFU-Es cultured in the absence of anti–TNF-α but in the presence of purified Fc fragment of human IgG1 were not different (not shown). The addition of LD (1 μg/mL) anti–TNF-α (iii,iv) increased the size of CFU-Es grown from marrow MNCs of FA patients. A similar effect was seen with HD (10μg/mL) anti–TNF-α (not shown). (B) BFU-Es grown in the absence of anti–TNF-α are shown (i,ii; medium alone). The size of BFU-Es cultured in the absence of anti–TNF-α but in the presence of purified Fc fragment of human IgG1 were not different (not shown). Panel Bii shows a minor nonhemoglobinized component at the periphery. The addition of LD anti–TNF-α (iii,iv) increased the size of BFU-Es grown from BM MNCs of FA patients. A similar effect was seen with HD anti–TNF-α (not shown).

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